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  • Monostotic Fibrous Dysplasia Wikipedia
    When symptoms are present, they often are nonspecific, including pain, swelling, or pathologic fracture. [5] It most often affects the ribs (28%), proximal femur (23%), tibia , cranio facial bones (10-25%) and humerus (10-25%). [6] See also [ edit ] Polyostotic fibrous dysplasia References [ edit ] ^ Alves, Raphael Vicente; Souza, Anderson Rodrigo; Silva, Alessandra dos Santos; Cardim, Vera Lúcia Nocchi; Godoy, Roberto (September 2009).
    GNAS
  • Hereditary Persistence Of Fetal Hemoglobin Wikipedia
    .; Fausto, Nelson; Aster, Jon (2009-05-28). Robbins and Cotran Pathologic Basis of Disease, Professional Edition: Expert Consult - Online (Robbins Pathology) (Kindle Locations 33411-33412).
    HBB, HBG1, HBG2, HBA2, KLF1, CAD, DHODH, HAMP, CACNA1H, UMPS, TFRC, TFR2, HBB-LCR, LCN2, EPO, HBA1, HBFQTL2, HPFH2, HBD, POU2F1, YY1, GATA1, DLL1, ZBTB7A, BCL11A, HBB-3'HS1, PSMB6
  • Juvenile Xanthogranuloma Wikipedia
    BMC Ophthalmology 14 (2014): 24. PMC. Web. 28 May 2016 ^ a b c d e Cypel, Tatiana Karine Simon, and Ronald Melvin Zuker.
    BRAF, NF1, MAPK1, TRBV20OR9-2
    • Juvenile Xanthogranuloma Orphanet
      Juvenile xanthogranuloma is the most common type of non-Langerhans cell histiocytosis (see this term) characterized by the occurrence of one or more reddish or yellowish self-limiting and benign papules or nodules of several millimeters in diameter, usually appearing on the head and neck (but sometimes on the extremities and trunk) during the first year of life (or rarely in adulthood) and usually regressing spontaneously. Extracutaneous involvement has also been reported, involving most commonly the eye (uveal tract) but with other locations including the central nervous system, lung, liver, bones and endocrine glands, and may be associated with considerable morbidity.
  • Cayler Cardiofacial Syndrome Omim
    Caksen et al. (2004) reviewed 35 cases of asymmetric crying facies (28 children and 7 adults) and found additional abnormalities in 16 (45%) of them, including cerebral and cerebellar atrophy, mental and motor retardation, cranial bone defects, facial dysmorphism, musculoskeletal abnormalities, and genitourinary anomalies.
    EYA1, RREB1, JMJD1C, COMT, SEC24C, UFD1, GP1BB, ARVCF, HIRA, TBX1, KCNMA1-AS1, CHD7, PIGN, KCNMA1, MIR122, AR, MMP9, MMP2, FASN, DES, CRYAB, CMA1, CASP3, BAX, FOXO4
    • Congenital Unilateral Hypoplasia Of Depressor Anguli Oris Orphanet
      Congenital unilateral hypoplasia of depressor anguli oris is a congenital anomaly, characterized by the unilateral hypoplasia/agenesis of the depressor anguli oris muscle, resulting in an asymmetric crying facies in neonatal period/ infancy (drooping of one corner of the mouth during crying) while eye closure, nasolabial fold and forehead wrinkling are symmetric. While it can be isolated, this anomaly is also seen in 22q11.2 deletion syndrome (see this term) and can be accompanied by other major congenital anomalies of the cardiovascular system, as well as less frequently the musculoskeletal, cervicofacial, respiratory, genitourinary, and, rarely, endocrine systems. When isolated, the condition is cosmetically insignificant as the infant gets older (as the muscle does not contribute significantly to facial expression in childhood/ adulthood).
    • Asymmetric Crying Facies Wikipedia
      Asymmetric crying facies Other names Cayler cardiofacial syndrome Specialty Medical genetics Asymmetric crying facies ( ACF ), also called partial unilateral facial paresis and hypoplasia of depressor angula oris muscle , [1] is a minor congenital anomaly caused by agenesis or hypoplasia of the depressor anguli oris muscle , one of the muscles that control the movements of the lower lip. This unilateral facial weakness is first noticed when the infant cries or smiles, affecting only one corner of the mouth and occurs on the left side in nearly 80% of cases. It is only rarely associated with other birth defects . When the hypoplasia of the depressor anguli oris muscle is associated with congenital cardiac defects, the term 'Cayler cardiofacial syndrome' is used. Cayler syndrome is part of 22q11.2 deletion syndrome . [2] It was characterized by Cayler in 1969. [3] References [ edit ] ^ Online Mendelian Inheritance in Man (OMIM): 125520 ^ Shashi V, Berry MN, Hines MH (September 2003). "Vasomotor instability in neonates with chromosome 22q11 deletion syndrome".
  • Caudal Regression Syndrome Medlineplus
    Some researchers believe that a disruption of fetal development around day 28 of pregnancy causes caudal regression syndrome.
    VANGL1, PCSK5
  • Hypotrichosis–lymphedema–telangiectasia Syndrome Wikipedia
    Archived from the original on 2012-02-08 . Retrieved 2011-01-28 . CS1 maint: archived copy as title ( link ) ^ Downes M, François M, Ferguson C, Parton RG, Koopman P (August 2009).
    SOX18
    • Hypotrichosis-Lymphedema-Telangiectasia Syndrome Omim
      A number sign (#) is used with this entry because of evidence that hypotrichosis-lymphedema-telangiectasia syndrome (HLTS) is caused by homozygous mutation in the SOX18 gene (601618) on chromosome 20q13. Heterozygous mutation in the SOX18 gene causes the related disorder HLTS with renal defect (HLTRS; 137940). Description Hypotrichosis-lymphedema-telangiectasia syndrome is an autosomal recessive disorder characterized by these 3 features, which begin at birth or in early childhood and are progressive (summary by Irrthum et al., 2003). Clinical Features Irrthum et al. (2003) described 2 families with an unusual association of hypotrichosis, lymphedema, and telangiectasia. In the first family, previously reported by Devriendt et al. (2002), a boy and girl, offspring of first-cousin Belgian parents, were affected.
    • Hypotrichosis-Lymphedema-Telangiectasia Syndrome Gard
      Hypotrichosis-lymphedema-telangiectasia syndrome (HLTS) is a rare condition that, as the name suggests, is associated with sparse hair (hypotrichosis), lymphedema , and telangiectasia , particularly on the palms of the hands. Symptoms usually begin at birth or in early childhood and become worse over time. HLTS is thought to be caused by changes (mutations) in the SOX18 gene. It can follow both an autosomal dominant or an autosomal recessive pattern of inheritance, depending on the affected family. There is currently no cure for the condition. Treatment is based on the signs and symptoms present in each person.
  • Focal Cortical Dysplasia Wikipedia
    "Technology-based educational therapy for developmental delays caused by focal cortical dysplasia" . ResearchGate . Retrieved 28 February 2019 . External links [ edit ] Classification D ICD - 10 : Q04.6 ICD - 9-CM : 742.4
    MTOR, TSC1, TSC2, AKT1, PIK3CA, PIK3CB, PIK3CD, PIK3CG, SMUG1, ANXA1, FANCD2, HMGB1, RHEB, TLR4
    • Isolated Focal Cortical Dysplasia Orphanet
      Isolated focal cortical dysplasia is a rare, genetic, non-syndromic cerebral malformation due to abnormal neuronal migration disorder characterized by variable-sized, focalized malformations located in any part(s) of the cerebral cortex, which manifests with drug-resistant epilepsy (usually leading to intellectual disability) and behavioral disturbances. Abnormal MRI findings (e.g. abnormal white and/or grey matter signal, blurred gray-white matter junction, localized volume loss, cortical thickening, abnormal gyral pattern, abnormal hippocampus) and variable histopathologic patterns are associated.
  • Myopathy, Myosin Storage, Autosomal Recessive Omim
    Clinical Features Onengut et al. (2004) reported 2 brothers with hyaline body myopathy; 1 of the brothers recalled weakness from childhood, but did not become severely symptomatic until age 28, whereas the other brother was asymptomatic until age 33 years.
    MYH7
  • Amelogenesis Imperfecta, Type Ib Omim
    AI was of the hypoplastic form in 72% and of the hypomineralization form in 28% of the individuals. Autosomal dominant inheritance was found in 89% of the cases with the hypoplastic form and in 44% of the cases with the hypomineralization form.
    ENAM, LTBP3, FAM83H, AMTN, MMP20, PEX1, WDR72, TUFT1, COL17A1, RELT, ITGB4, LAMC2, PEX26, TMEM165, KCNJ1, AMELX, AMELY, AMBN, KLK4, FAM20A, DLX3, CNNM4, LAMB3, ITGB6, STIM1, ORAI1, SLC24A4, ODAPH, ACP4, SLC10A7, ROGDI, SLC13A5, LAMA3, DNAJC21, MMP25, TP63, CKAP4, SLC24A3, FAM20C, CLDN19, CRX, CLDN16, HEXIM1, CSNK1G2, CSNK1G3, DSPP, GH1, HPX, HTN1, MSX2, NHS, COL1A2, RPGR, RPE65, UVRAG, VIS1, GPR68, CSNK1D, BMP4, ARHGAP6, ADAM10
    • Amelogenesis Imperfecta Gard
      Amelogenesis imperfecta (AI) (amelogenesis - enamel formation; imperfecta - imperfect) is a disorder that affects the structure and appearance of the enamel of the teeth . This condition causes teeth to be unusually small, discolored, pitted or grooved, and prone to rapid wear and breakage with early tooth decay and loss. These dental problems, which vary among affected individuals, can affect both primary (baby) teeth and permanent teeth. People with this disease my also have problems involving the tissues surrounding teeth (periodontal tissues) such as gums, cementum, ligaments, and alveolar bones in which the tooth root rests. Teeth are also sensitive to either hot or cold exposures, and sometimes both.
    • Amelogenesis Imperfecta, Type If Omim
      A number sign (#) is used with this entry because of evidence that amelogenesis imperfecta type IF (AI1F) is caused by homozygous mutation in the ameloblastin gene (AMBN; 601259) on chromosome 4q13. Description Amelogenesis imperfecta type IF is characterized by hypoplastic enamel of the primary and secondary dentition. The teeth may appear rough and discolored, and the tooth enamel may be absent, pitted, or of varying thickness (Poulter et al. (2014)). Clinical Features Poulter et al. (2014) described a consanguineous Costa Rican family with generalized hypoplastic amelogenesis imperfecta involving the primary and secondary dentitions. Clinical examination of the 3 affected sisters revealed enamel that was hard, but discolored and rough.
    • Amelogenesis Imperfecta, Type Ih Omim
      A number sign (#) is used with this entry because of evidence that amelogenesis imperfecta type IH (AI1H) is caused by homozygous or compound heterozygous mutation in the integrin beta-6 gene (ITGB6; 147558) on chromosome 2q24. Description Amelogenesis imperfecta type IH is characterized by hypoplastic and hypomineralized tooth enamel that may be rough, pitted, and/or discolored (Wang et al., 2014 and Poulter et al., 2014). Clinical Features Wang et al. (2014) reported 2 Hispanic families segregating amelogenesis imperfecta. In Family 1, a 7-year-old girl had enamel malformations in the absence of other symptoms. She had mixed dentition that was yellow, with anterior open bite and class III malocclusion.
    • Amelogenesis Imperfecta, Type Iiia Omim
      AI was of the hypoplastic form in 72% and of the hypomineralization form in 28% of the individuals. Autosomal dominant inheritance was found in 89% of the cases with the hypoplastic form and in 44% of the cases with the hypomineralization form.
    • Amelogenesis Imperfecta, Hypoplastic/hypomaturation, X-Linked 2 Omim
      For a description of hypoplastic/hypomaturation amelogenesis imperfecta, see 301200. Mapping See 301200 for description of findings in a family suggesting that one form of amelogenesis imperfecta is determined by a mutation in a gene in the Xq22-q28 region (Aldred et al., 1992). This gene may be another reflection of homeology of portions of the 2 arms of the X chromosome resulting from an ancient duplication. INHERITANCE - X-linked HEAD & NECK Teeth - Amelogenesis imperfecta, hypoplastic ▲ Close
    • Amelogenesis Imperfecta, Type Ia Omim
      A number sign (#) is used with this entry because of evidence that amelogenesis imperfecta type IA (AI1A) is caused by heterozygous mutation in the beta-3 laminin gene (LAMB3; 150310) on chromosome 1q32. Description Hypoplastic amelogenesis imperfecta IA is characterized by enamel that may not develop to normal thickness. The enamel may have pits on the labial or buccal surfaces that are often arranged in rows and columns (see Witkop, 1989). Clinical Features Kim et al. (2013) described 2 unrelated families of Turkish and Iranian descent, respectively, with autosomal dominant hypoplastic amelogenesis imperfecta. The proband in Family 1 was a 6.5-year-old girl who presented with sensitive teeth.
    • Amelogenesis Imperfecta, Type Iv Omim
      A number sign (#) is used with this entry because amelogenesis imperfecta, hypomaturation-hypoplastic type, with taurodontism can be caused by mutation in the DLX3 gene (600525). Clinical Features Congleton and Burkes (1979) and Crawford et al. (1988) described amelogenesis imperfecta of the hypomaturation-hypoplasia type with taurodontism. The dental findings were apparently identical to those of trichodentoosseous syndrome (TDO; 190320), from which it differed only by the lack of changes in the hair and bones. Crawford and Aldred (1990) reviewed all reported cases of these disorders, obtaining additional information from the original authors. They concluded that 'if the teeth are affected in the absence of hair or bone changes, either in the individual or within the family, then the diagnosis should be deemed to be AI H-H T.'
    • Amelogenesis Imperfecta Wikipedia
      ISBN 978-3-540-71690-7 . Retrieved 28 December 2010 . ^ Kida M, Ariga T, Shirakawa T, Oguchi H, Sakiyama Y (November 2002).
    • Amelogenesis Imperfecta Orphanet
      A rare genetic odontal or periodontal disorder that represents a group of developmental conditions affecting the structure and clinical appearance of the enamel of all or nearly all the teeth in a more or less equal manner, and which may be associated with morphologic or biochemical changes elsewhere in the body. Epidemiology The prevalence varies from 1:700 to 1:14,000, according to the populations studied. Clinical description The enamel may be hypoplastic, hypomineralised or both, and affected teeth may be discoloured, sensitive or prone to disintegration. Amelogenesis imperfecta (AI) exists in isolation or associated with other abnormalities as part of a syndrome. Etiology In families with an X-linked form, it has been shown that the disorder may result from mutations in the amelogenin gene, AMELX .
    • Amelogenesis Imperfecta, Type Ic Omim
      A number sign (#) is used with this entry because autosomal recessive local hypoplastic amelogenesis imperfecta (AI1C) is caused by homozygous mutation in the enamelin gene (ENAM; 606585) on chromosome 4q13. Clinical Features In the course of an extensive survey, Chosack et al. (1979) found several families with autosomal recessive local hypoplastic amelogenesis imperfecta. Characteristics included horizontal pitting and grooving more pronounced in the middle third of the crowns of most teeth of both dentitions. In a study of 50 patients with amelogenesis imperfecta, Rowley et al. (1982) found that anterior open-bite malocclusion occurred in 24%, and was always associated with a severe discrepancy in the vertical relationship of the jaws. Vertical dysgnathia also occurred in a further 20% of the patients who did not have anterior open-bite malocclusion.
  • Tinea Imbricata Wikipedia
    Clinical and Experimental Dermatology . 28 (3): 332–3. doi : 10.1046/j.1365-2230.2003.01281.x .
  • Mondor's Disease Wikipedia
    "Superficial thrombophebitis" . MedScape . Retrieved 28 August 2012 . ^ Henri Mondor: Tronculite sous-cutanée subaiqure de la paroi thoracique antero-laterale, In: Mem.
    • Mondor Disease Gard
      Mondor disease is a rare condition that is characterized by scarring and inflammation of the veins located just beneath the skin of the chest. The affected veins are initially red and tender and subsequently become a painless, tough, fibrous band that is accompanied by tension and retraction of the nearby skin. In most cases, the condition is benign and resolves on its own; however, Mondor disease can rarely be associated with breast cancer. Although the condition most commonly affects the chest, Mondor disease of other body parts (including the penis, groin, and abdomen) has been described, as well. Mondor disease is thought to occur when pressure or trauma on the veins causes blood to stagnate.
  • Non-Small-Cell Lung Carcinoma Wikipedia
    NEIL1 42% base excision repair [22] WRN 38% homologous recombinational repair, nonhomologous end joining , base excision repair [23] MGMT 13% - 64% direct reversal [22] [24] [25] ATM 47% homologous recombinational repair [26] MLH1 48% - 73% mismatch repair [26] [27] MSH2 42% - 63% mismatch repair [26] [27] BRCA2 42% homologous recombinational repair [28] BRCA1 30% homologous recombinational repair [28] XRCC5 ( Ku80 ) 20% nonhomologous end joining [28] FEN1 100% hypomethylated (increased expression) microhomology-mediated end joining [29] The frequent deficiencies in accurate DNA repair, and the increase in inaccurate repair, likely cause the high level of mutation in lung cancer cells of more than 100,000 mutations per genome (see Whole genome sequencing ). ... "The DNA damage response: ten years after". Molecular Cell . 28 (5): 739–45. doi : 10.1016/j.molcel.2007.11.015 . ... Archived from the original (PDF) on 28 September 2011. ^ "National Cancer Institute Non-Small Cell Lung Cancer Treatment (PDQ®)" . 1 January 1980 .
    EGFR, KRAS, MET, NFE2L2, ALK, CDKN2A, CHFR, BRAF, ERBB2, CASP8, PIK3CA, PTEN, MAP2K1, STK11, CLPTM1L, AKT2, NRAS, ROS1, RET, RRM1, E2F1, KEAP1, KDR, TP53, RAF1, APC, NOTCH3, AKT1, MIR126, EML4, MMP9, ABCB1, RASSF1, MIR145, MYC, AXL, MDM2, NQO1, MIR205, CXCL8, TERT, FHIT, TGFA, FGFR1, SOX2, SMARCA4, FOXM1, VEGFA, STAT3, IL10, ERCC1, ENO2, NKX2-1, GSTP1, HIF1A, MTOR, KIT, DAPK1, AREG, SLC34A2, RECK, CDH13, KDM1A, CA9, CSF3, CYP2E1, PXN, FOXO3, MIR29A, PPIA, ITGB1, FGFR2, KIF5B, CD74, CHGA, FGF9, BIRC5, PYCARD, RB1, XPC, MMP1, MIR30C1, MIR638, E2F3, MIR1246, LGALS1, FASLG, NDRG1, CAT, MS4A1, RRAD, UCHL1, CD9, MMP11, GSTM2, NCOA3, BAP1, SOD2, ENO1, TP53BP1, ITGB4, AKR1C1, MXRA5, E2F6, PTHLH, E2F2, GCLC, IL6R, MAP2K2, NEK2, PRR13, PGAM1, ATF3, PHGDH, ERGIC3, GIPR, PRAME, MIR346, SYP, LAMC2, PRDX1, MT3, E2F7, PSAT1, E2F8, ADAMTS1, DUSP3, NNAT, SELENOS, SDC4, LRRC59, RHEB, SLC22A10, OSMR, CCNH, E2F5, OXTR, HES1, TRMT11, CERT1, AVEN, IL12A-AS1, MACIR, SHMT2, ZNF462, CORO1C, CARD18, GRIK2, TMEM135, DEUP1, CST6, CYLD, RBM7, PLBD1, PHLDA2, COL7A1, ROBO1, HRAS, HLA-A, EGFR-AS1, TERC, NRG1, BPTF, IRF1, CHRNA5, XXYLT1, CYP2A6, VTI1A, CAMK2D, JAK2, TMED7-TICAM2, OGG1, EIF4E, KLF4, XKR6, EGF, EPHA2, ALB, GADL1, APEX1, XIAP, EPAS1, MBD2, IL17A, MUL1, FBXW7, EPHB2, MCCD1P1, MIR497, DCBLD1, HOTAIR, CXCL12, PTGS2, MTA1, MIR451A, ISG20, S100A2, TICAM2, ALDH1A1, PPP1R2C, MIR210, CYP1A1, COL18A1, STMN1, MIR223, RARB, MVP, TUBB3, CD274, DAB1, BCL2L11, RAD51, RAC1, PVT1, EPCAM, HDAC9, KRT19, DNMT1, ABCC4, MALAT1, SMAD4, GSTK1, CTNNB1, EIF4E2, CTLA4, CYP19A1, CTAG1B, FOXP3, TMED7, ABCG2, GRAP2, TIMM8A, COPD, ERBB3, POU5F1P4, XRCC1, PDCD1, XRCC3, TGFB1, MPZL3, ACTB, SLCO6A1, CXCR4, SCLC1, AIMP2, MIR21, ZEB1, TAZ, ADAM17, POU5F1P3, HMGA2, GABPA, MIR200C, AURKA, FUS, GLI1, XIST, TGFBR2, TIMP2, HGF, TP73, H3P10, TTF1, TOP2A, TWIST1, SAXO1, TYMS, PCNA, H3P23, GSTM1, CBLL2, TNF, GSK3B, GRP, HMGB1, PRKN, VEGFC, VIM, HSPA4, MIR203A, HSPB1, IGFBP3, TNFSF10, PARP1, IL1B, IL2RA, TNFRSF10B, EZH2, IL6, PROM1, MKS1, MAPK14, SLC2A1, FCGBP, ESR2, ESR1, ERCC5, SKP2, NEAT1, MTDH, ERCC2, AZIN2, ABCC3, HSP90AA1, BECN1, MIR195, MIR486-1, FN1, SRC, FLT1, SPP1, FOXO1, SOX9, TP63, IFI27, GDE1, CTAG1A, IFNG, MTCO2P12, IGF1, IGF1R, IGF2, UCN3, FGF2, YAP1, ZEB2, MEG3, CHRNA4, CEACAM7, CAV1, CASP9, FOXP4-AS1, SIRT2, LILRB1, MGMT, CASP3, MAPK3, PIK3CB, POU5F1, CALCR, MIR143, EPB41L3, PIEZO2, MIR148A, TBC1D9, MIR150, MAPK8, COX2, MTHFR, SIRT1, MIR155, MIR15A, CEACAM3, CCK, MUC1, CD44, CDK2, CDK4, CDK6, CDH1, MMP7, CDA, CDKN1A, CDKN1B, MIR137, MIR140, MMP2, ABCC1, MAPK1, MSH2, BAZ1A, HPGDS, CEACAM5, MSH3, WIF1, MIR141, PRKCA, MLH1, TUSC2, PPARG, DCTN6, MIR146A, BAX, BMI1, RNF19A, MDM4, PSMD9, LATS2, MIR17, PSG2, CCND1, CIB1, COL11A2, BCL2, MIR125A, CADM1, ME1, NOTCH1, MIR182, POSTN, ANKRD7, MCL1, ZNRD2, MIR30A, MAP2K7, BRCA1, CMKLR1, ATM, PLK1, CRK, PIK3CD, POLDIP2, PIK3CG, CRP, MIR34A, AHSA1, SMUG1, SMAD2, TUG1, HDAC1, MIR449A, PECAM1, CD28, BRMS1, CSF2, IDO1, GAS5, MIR25, RRM2, MIR214, EGR1, SLC12A9, PTPN11, MIR204, ARHGAP24, MIR133B, LGALS3, MIR193A, TIMP1, NES, FGFR3, HOXA5, MIR149, NTRK1, DNMT3B, MIR34B, DKK1, PAEP, CCND2, HSPA5, UBE2C, MIR338, USP22, SERPINE1, AKR1B10, INSR, WEE1, ERBB4, THBS2, PKM, RUNX3, NRP1, CFLAR, UVRAG, MIR144, BDNF, SOX4, HMOX1, GSTT1, TMPRSS4, CD34, SPARC, MIR96, FASN, IL24, KLF2, RPE65, AURKB, PRKAA1, PDK1, MIR221, PDCD1LG2, ANXA2, MIR186, CTNND1, PTK2, CKAP4, DUSP6, AFAP1-AS1, DPYD, CHEK1, NME1, MIR107, MIR375, MIR361, BSG, CD276, PPM1D, MIR152, COMMD3-BMI1, DDR1, ZNF654, RELA, MIR98, MIR206, IL22, CHPT1, ELAVL2, CCR7, ABCC2, MIR335, BAG1, DLC1, MIR330, HK2, SMAD3, WNK1, MARCKSL1, HMGA1, VDR, CYP1B1, VIP, MIR148B, MIR224, WNT5A, DHDDS, TGFBR1, MIR615, XPA, PAK1, F3, WLS, STAT1, MIR106A, PDCD4, SPHK1, ADIPOQ, PDGFRB, CD40, AGER, PTPA, MIR185, HSPB3, EPO, PRKAA2, ANKRD36B, XPR1, SOCS3, PRKAB1, CCL2, MIR142, MIR212, S100B, MIR27B, LINC00673, S100A4, HOXA9, CDC42, JAK1, MIR27A, FSTL1, DLEC1, ACKR3, XRCC5, MIR10B, SYT1, MIR200B, SLC1A5, SQSTM1, YBX1, SLC7A5, NOS1, PAX6, LOX, CLDN1, SLC31A1, TLR1, EIF5A2, MIR498, MIR216B, MIR30C2, CEACAM1, UBE2N, MIR31, TIMP3, LINC01194, NOB1, CYP2D6, PDGFRA, VTCN1, GLS, HAVCR2, MIR1290, MIR132, MIR139, IL4, GORASP1, LIN28B, CD82, PPP1R13L, NOX4, PRKCB, ATP2C1, MIR424, TNFRSF12A, SOAT1, SEMA6A, FSCN1, SIRT6, ZMYND10, RUNX2, DDR2, ZHX2, BRMS1L, SNCA, SNAI1, MST1R, CIP2A, ATG5, MST1, CCNB1, RPL17, SMARCA1, KIDINS220, KHDRBS1, MIR494, CALR, ID1, HSPB2, MIR29C, DHFR, RPL17-C18orf32, SPATA2, CHRNA3, PTCH1, MFAP1, MIR30D, PRKDC, RAP1A, MIR495, PIM1, STAT5A, MIR222, NOTCH2, MIR29B2, MIR30B, MDK, CCL21, MIR503, PGR, NEDD9, MAD2L1, RPSA, STAT6, TOP1, NCL, MIF, NUDT1, TGFBI, TLR4, HNRNPA2B1, MIR29B1, MUC5AC, MIR34C, PDPK1, MIR26B, PLAU, SRSF1, TGM2, SLC6A8, THBS1, SFRP1, ICAM1, MIR377, MIAT, FENDRR, UCA1, LIMK1, NOS2, MIR20A, MIR183, MIR378A, ROCK1, S100A1, MIR134, MIR296, MIR197, DKK3, FOLR1, ANPEP, HDAC6, FGFR4, ANGPT2, IRS2, NUP62, SPHK2, RBM5, BRD4, SIRT3, SPOP, KLRC4-KLRK1, MIR661, DICER1, USP9X, CRYZ, DCTN4, ATF2, CCDC6, GAPDH, GAS6, GATA2, HDGF, DAP, SNHG1, DCK, PTTG1, EEF1B2P2, CD163, BHLHE22, ARRB1, CDKN2B-AS1, SGSM3, EPHB6, PTGES, ATN1, APOBEC3B, FSD1L, KDM4A, ERCC4, FAS, APRT, MYDGF, ETFA, BID, PTK2B, APAF1, FSD1, LINC00460, MIR590, GJA1, KLRK1, CFL1, ROMO1, TFPI2, RALBP1, CDX2, EHD1, CDKN2B, CDH2, PCAT6, GTF2H1, TXN, CDC25A, AFAP1, MIR421, CD68, CD47, MICA, LAT, USP7, LOC110806263, TMX2-CTNND1, KLF6, ATG7, DNMT3A, MIR4435-2HG, MERTK, LRIG1, SH2B1, MMP12, MIR425, ROPN1L, AIM2, NBN, SULF2, MIR130B, KCNQ1OT1, ITGA11, SESN2, CDKN1C, SOX7, CREBBP, GOLPH3, MMP14, COL11A1, LAG3, CIB2, MIR488, ITGB3, MIR328, EFNA1, MIR410, ACE2, MIR93, MIR122, CCDC54, LONP1, TYMP, CLDN7, DVL3, ATP7A, MIR363, RPS6KB1, MACC1, NTN1, DUSP1, SOX2-OT, NEU1, RPL36A, L1CAM, MIR30E, MAP1LC3B, MIR339, BMP4, HAGLR, PLG, LPL, LRP1, CASP7, PTPRC, MIR367, SYBU, TRAP1, HTATIP2, CLU, KLF5, CXCR6, C3, PMAIP1, CTSL, CELF1, TXNIP, MIR340, MIR100, CYP24A1, USP28, TUBA1B, MXI1, METTL3, COX8A, SETDB1, SPRY4-IT1, TACC3, PLAAT4, NUAK1, MIR337, PLA2G4A, MIR106B, SUB1, BMP2, SCO2, MKI67, LGALS9, MYBL2, DACH1, ZFAS1, MOK, MIR33A, ADAM28, MIR326, LIG4, BBC3, NTS, OPRM1, AHR, MLRL, FUT8, ALCAM, EGFL7, STAT5B, NR5A2, RMDN1, MIR187, SSRP1, SRPK1, CUL4B, CUL4A, HOXA11-AS, NT5E, TRAT1, MUC5B, TRIM59, FOXC1, WRAP53, A1CF, NTRK2, VEGFD, SNX1, IL27, MIR504, POTEF, NLRP3, FEN1, TUSC3, OTUD4, UGT1A1, GEM, HDAC2, KRT20, TOP2B, RMDN2, LINC00342, MIR19A, SUMO1, MIR196A1, TLR3, VCAM1, VCP, MIR542, HMGB3, ABL1, GRB2, EZR, LINC00261, HNF4A, THY1, MIR200A, ERRFI1, WNT7A, DLL4, IL17D, XRCC2, SPA17, SIX4, GHRH, WWOX, RMDN3, FOXC2, FBP1, SLC29A1, PGK1, EPS15, IL18, EPOR, ILK, MAP3K14, SGK1, STYK1, ARG1, SFRP2, LYPD5, IL13, USP14, LMLN, SERPINA1, CXCL5, BLACAT1, IRS1, NEURL1, ASIP, SNHG12, ASPA, PGF, MRC1, FOXQ1, PRRT2, MIR23A, SLC19A1, IL7, CYTOR, SMARCA2, BRF2, ASPM, MIR499A, IL2, SETD2, DNER, TBK1, NR1I2, ADAM9, IGFBP7, MIR23B, NLRP1, AKIP1, TMEM97, PUF60, PPARD, CDK14, PHB, RABGEF1, PLA2G2A, INTS6, MIR18A, SOX18, UHRF1, NLRP2, CDK16, MIR184, TERF2IP, CHEK2, CXCL16, PTP4A3, HHLA2, MCAT, MIR154, TLR9, GOLM1, COTL1, MIR191, ING4, LINC00328, NEDD4L, TNFAIP8, SATB2, LAPTM4B, FBXW11, PRDX5, PLCE1, TP73-AS1, MIR192, PART1, DGCR5, PBK, BPIFA1, RIF1, WWTR1, MCTS1, NLK, UIMC1, PIK3R1, RSF1, KDM6B, PHLPP2, RAD18, PRPF31, ZBTB7A, PEBP4, ADAMTS8, PEA15, SLC16A1, DLK1, SNAI2, SMO, RIPK1, SMS, EIF3A, MUC16, TNKS, SOCS1, SOS1, AKR1C3, PDXK, MAP4K3, EGLN2, DLEU2, NR0B2, SFTPB, CXCL11, LATS1, ABCC10, MAP2K4, SET, GPRC5A, SFTPD, SLC3A2, HNF1A-AS1, CPNE3, SIX1, SBF2-AS1, SCGB3A1, SLC2A3, SST, ULK1, SNORD14D, VWF, XRCC4, TGFB2, XK, WT1, RSS, WNT1, VDAC1, ZFX, NR1H2, SCGB1A1, UBE2I, TNFRSF1B, TTK, CRISP2, YWHAZ, TFAP2C, MIR198, TAP1, FZD4, DVL1P1, CCNY, TAM, SYK, NCOA4, PRSS55, BTG2, TBX1, TBX5, DEK, CRTC2, TRBV20OR9-2, TERF1, SNORD14E, SNORD14C, DNAJB4, TRIM13, PIAS3, RACK1, MIRLET7C, PAK4, LILRB2, MIRLET7B, TSHZ1, MCRS1, PTPN6, PTPN13, PTPRA, LRPPRC, NANOG, HIPK3, PRMT5, CAP1, LINC00668, CD3EAP, MIR136, KLK11, BTG3, VSIR, MIR130A, PPARGC1A, KDM5B, SEMA4B, ATG3, SIX2, PINK1, SIVA1, KLK10, PSMD4, TUBA4B, FRAT1, SNORD14B, COX5A, USP17L2, TCHP, NAPSA, HOPX, SNORD35B, SPZ1, FOXD2-AS1, TMPRSS13, SNHG7, NAT2, ARHGEF2, SERPINB3, FAM83A, CCL5, CLOCK, SNORD15A, AKT3, TRIM66, BCAR4, CPEB4, SRCIN1, RASA1, RASGRF1, USP17L9P, FARP2, BRD2, NECTIN4, RASSF5, IKBKE, REV3L, KMT5A, PRDX6, SPARCL1, RALA, IL12RB2, MIR92B, ITGAE, MIR1179, EIF4A2, MCM7, IGFBP1, MIR935, CD40LG, IFNB1, HOXB5, HMMR, IFNA13, MAGEA4, HOXB7, MIR650, XRCC6, IFNA1, NORAD, ANGPT1, CYP2B6, MIR146B, HOXA1, ADAM10, CCR2, ACTN4, ELK1, CUX1, CDC25C, BIN1, HNRNPA1, KITLG, ELF3, VPS51, CDK1, KRT5, CXADR, ATF4, EIF4G1, ITGA5, GATA6, MIR485, JUN, TACSTD2, HPRT1, LEP, CALCA, LDHB, LDHA, ANXA1, DSG3, KIR3DL1, HSPA1B, KRT18, MIR455, MIR379, HSP90AB1, MIR381, MIR382, DUXAP9, TNC, AGAP2-AS1, PRMT1, BCL6, DCN, CRNDE, MIR708, ACE, DCR, ECT2, LOXL2, GADD45A, MIR372, FER, CCNE1, IDH1, FOS, FOLR2, DECR1, DVL1, MIR374A, MIR448, MIR663A, FOXA1, MIR135B, ARSF, IL6ST, MIR520A, PANDAR, MIR411, NFKB1, MIR301A, GPT, ACACA, BTK, HELLS, NM, NCAM1, MIR454, CPOX, MIR32, MIR320A, CXCL10, HIP1, CFTR, ING2, NR3C1, MIR199B, OCA2, GYPA, CLPTM1, CMA1, IL16, PEBP1, BRS3, GSN, GRPR, KLF9, NMBR, MIR3127, H2AX, CXCR2, IL9, MIR219A1, CDR1-AS, NOS3, ING1, MIR605, CFH, MIR608, HLA-C, ASCL1, MSMB, IL1A, MIR95, EIF3E, CDK5, ETS2, MPO, SNHG14, MPG, HNRNPA1P10, MIR7-3, MIR613, ATP7B, CCN2, MIR17HG, TP53COR1, MIR7-1, IKBKB, HK1, MIR7-2, MIR744, MIR761, SFTPA2, ERN1, DDX58, POLA2, USP17L25, MIR769, FOXF2, DYNLL1, BPI, HTRA3, BCYRN1, USP17L24, PRDM1, MAGED4, CYGB, BRCA2, IL18R1, TMEFF2, USP17L26, ESD, USP17L28, ADAM15, EFEMP1, MIR671, USP17L30, KRT8P3, IL17F, TNFSF13, IQGAP1, USP17L29, BMP7, SMYD2, CMTM7, BMP6, ETV4, MAPK8IP2, USP17L27, BNIP3, MIR758, PER3, TNFRSF11A, SLC46A1, EGLN3, F2R, ARHGEF7, FGF13, EIF3D, DIABLO, PC, FOXD1, YY1, GLUL, GLI3, GLI2, FOXR2, GLDC, MIR616, GPC3, GJB2, MIR621, YES1, MIR625, MMP26, MIR628, TRIM25, ZYX, GDNF, TRIM71, MIR630, AVP, GDF10, SEMA3B, KAT2A, GML, BTBD7, GNAS, SFN, FOXD3, HBP1, GSPT1, PDIK1L, UCP2, MIR577, LINC-ROR, BANCR, UMPS, ALDH7A1, CHUK, MIR582, MIR584, GRN, GRIA3, GPX4, VHL, MIR593, GPR42, MIR598, MIR600, MIR635, KLK13, GATA4, PLA2G10, MIR660, FOSB, FOLH1, DYRK2, FLT4, CUL3, BCL3, GEMIN2, FLOT2, SNORD118, PCAT1, NUS1, TRPV5, BARX2, API5, CTHRC1, IL17RA, NNT-AS1, KHSRP, TNFSF11, KLF7, BCL2L2, MMD, ARHGEF5, RAB26, GATA3, NR4A3, B2M, MIR641, MIR5702, RASSF7, SYF2, KMT2D, FXR1, YEATS4, SIN3A, ST8SIA2, BAK1, MIR652, FUT4, AXIN1, FRZB, BCL2A1, BCL2L1, FZD1, ARMC8, NIPBL, EIF5A, CPNE1, KIF14, LGR6, LUCAT1, FAM13A, CBLL1, EBI3, TRIM28, TGIF2, CYBB, TNK2, MAGI2-AS3, NUS1P3, FLOT1, MSLN, RABEPK, SNIP1, CTSS, CTSD, LIN28A, CTSB, LANCL1, CENPU, CNPY2, HEATR6, NAMPT, HRH4, MIR1304, FAM107A, RASSF8, KLK8, CD27, MIR1258, MED12, NR1I3, CD80, HNRNPDL, MIR1204, CD55, CD38, CD63, CYP27B1, ENTPD1, CHAF1A, MIR1271, ABCC5, DNM1L, IL21, MIR1253, DENND2D, CYP3A4, CTNND2, TP53AIP1, PRDM14, MRPL41, AGR2, ROBO3, FRS2, OLFM4, CXCL13, COL4A3, MRPL28, CCT4, CDK15, COL1A1, TRIM16, PDE10A, SOX17, PDPN, NPRL2, MIR1260B, IGF2BP3, MAP3K2, CCR4, CCR1, MIR4286, CHRNB4, COMT, MIR4319, CSTF2, EHMT2, TUBB4B, EBNA1BP2, STIP1, CSK, CDK9, PCNA-AS1, CSF1R, MIR3940, CENPE, TINAGL1, CRKL, CHKA, CREB1, CR1, CARM1, MMS19, DERL1, SMR3B, NMU, KAT5, HPSE, STK33, DCC, KLF8, TIMELESS, AKR1C2, SLC28A1, ABCC11, SCAF11, LPAR2, EIF4EBP1, RTN4, MIR873, PPP1R13B, MTA2, MIR936, CACNA2D2, EFNB3, PHF5A, SALL4, CA8, MIR940, EEF1A2, EDNRA, SLC9A3R2, LHX2, PPIG, KL, MIR543, ELAVL1, NEMF, ELN, ANGPTL2, EREG, NR2F6, MIR4500, CIAPIN1, EPS8, IL33, EPHX1, MIR770, TWSG1, PCBP4, ARTN, CCNE2, PRC1, PAPSS1, MIR675, TARDBP, SNHG8, MIR875, USP8, WNT3A, PDSS2, C5AR1, CA11, MIR874, CEMIP, SPRY4, CASR, PUM1, JAM3, SARDH, DYNLRB1, DPP10, CCAT1, NUF2, CBLB, CILK1, RASSF2, CASP10, CCND3, MTSS1, BMS1, CKAP5, DHX15, MAGED4B, GAB2, DDIT3, LIMD2, TLK1, MMRN1, RGS6, DANCR, NT5C2, MIR889, TMPO-AS1, LINC00968, CAPN2, AKT1S1, BIRC6, GDF15, TBPL1, MINCR, KDM2A, TP53I3, ABCG1, TPX2, CHD1L, MTA3, DRD2, PTGR1, CASP2, DPP4, CASP4, NCALD, TATDN1, SIK1, CXCL1, NFAT5, TRA2B, SELE, MIR181D, PRSS3, INPPL1, MIR125B1, ADA, SRSF2, SRSF5, MEF2D, XRCC6P5, APIP, MIR128-2, ILF2, ALOX15B, RAB8A, SIAH2, PARD6A, AMELX, PINX1, SDHC, IRAIN, PRTN3, MIR202, HOXA-AS2, MIR493, RGMB, CCL18, CCL19, RABL3, IRF5, MDH1, HSPA14, CXCL6, IRF4, IRF3, COMMD8, ALDH3A1, MIR325, MNS16A, IL15, MAPK9, SPOCK1, MIR509-1, MIR502, MME, IGFBP2, RAD9A, MMP3, MMP10, MIR506, MMP15, SOX1, MIR522, MIR510, SOX5, IDH2, MOS, MRM2, SP1, SPG7, LINC00312, FOXO4, RICTOR, PRKACG, SOX8, IL12A, MAPK7, CXCR1, SLC5A5, NCR3, TAB3, RRM2B, CXCL9, ACVRL1, MIR500A, PRKCI, BCL11A, SLPI, PRKAR1A, IGKC, CASC2, CCN1, SNHG15, SRL, DLX6-AS1, MIR384, RASD1, REN, REST, TRIM27, MIR376C, MIR345, KRT8, MIR383, RING1, PSMD7, LYN, KPNA2, PRRX2, MIR422A, MAGEC2, TM4SF1, KISS1, ESRP1, TRIM44, PTRH2, RAB14, MIR370, RAD23B, PIAS4, LIPC, MIR196B, ADH1A, RAB27B, SUMO1P3, RAP1GDS1, RAB27A, RARA, RARRES2, LCK, LASP1, KRT81, PYCR1, CASC15, LY6K, MIR342, RPA1, MIR31HG, PTGS1, PTGER4, MAPT, S100A8, ITGAV, MARS1, S100A11, MBL2, ARMH1, MIR331, MIR10A, MCC, PHF20, CMTM6, ZFR, MCM2, GTF2B, PSMD8, MAOB, MIR452, PTPN3, MIR433, SMAD6, RPL22, PTN, MIRLET7E, MIRLET7G, SMAD7, GINS2, MIR429, RPLP0, MAGEA1, RPS6, KCNK3, RPS6KB2, ADRA1A, NANOS3, MAGEA3, ADRA2B, SIK1B, IGF2R, IRF8, FOXA2, NFKB2, NFKBIA, ARR3, STS, TREM1, NHLH1, DDX53, SERPINB5, NMB, NEDD4, NR4A1, TK1, SEC62, HLA-G, TLR2, SNORA80E, TSPAN7, NNMT, NFATC1, HNRNPC, TMPO, PITX2, MYD88, CXADRP1, DCUN1D1, TFRC, SLCO1B3, PCAT7, MYLK, SFTPA1, RHOB, THBD, PITX1, GHET1, SNHG20, HNRNPK, PIK3R2, TGFBR3, TGIF1, THAS, TM7SF2, HLA-DOA, MYCN, MIR19B1, TNFRSF11B, MIR211, PAQR3, FOXP1, HAS2, SERPINB2, LYPD3, SGO1, H3P28, ODC1, PAX5, GZMB, PELP1, MIR574, PBX1, PLB1, TNFRSF4, TXNRD1, TRAF6, MIR215, H3P9, TRIM36, CLDN5, NOTCH4, TNFAIP1, SPAAR, MIR22, PFKFB3, HIC1, NTSR1, IL37, TRAF1, AGO2, ABCA3, INVS, FEZF1-AS1, MIR217, TPO, MIR216A, HSP90B1, TFDP1, PIN1, AR, PRSS50, MIR99A, MIR9-3, MT1JP, ABCC8, CT83, POMC, TAC1, MT1X, NXT1, TAPBP, TMEM100, ANXA5, TAT, MTAP, BIRC3, HOXD13, MED19, HSPA1A, HSPA2, MIR99B, IARS1, MARCHF8, ZEB1-AS1, DDIT4, SRPK2, SRY, ICOS, SENP1, MSI1, MIR484, SSTR2, SSTR4, ST13, HSPD1, ROBO4, TBP, LMO1, DROSHA, MMUT, MTHFD1, TCF19, TCF21, MTR, HOXC8, MTRR, PRDX2, ACHE, TCF7, PLAUR, MYCL, TEK, AQP3, TERF2, AQP4, RGCC, TCF7L2, TRPM2-AS, APP, PML, COX1, FBRS, NECAB3, MIR642B, TMEM106B, MIR210HG, LINC02605, PRMT7, TRIB3, INO80, CRLS1, MIR3619, HHIP, TBILA, SCUBE2, JAM2, SNORD138, UGT1A7, PXN-AS1, MIR4299, MIR3163, LINC02602, EPG5, SHTN1, CCNJ, DDX56, FBXL19, LNCRNA-ATB, RBAK, HIF3A, GAS5-AS1, AZI2, LINC01234, LINC01088, CREBZF, RNF25, SCAF1, L1TD1, ZNF71, NGB, DSCAM-AS1, LINC01133, ABCG4, MIR3666, EPB41L4A-DT, MIR4257, LINC01672, LINC00963, LINC00958, MIIP, NOD2, ELAC2, SLAMF7, MIR4262, GAPLINC, LSM2, PCAT19, RAB17, DHX29, UGT1A9, COMETT, LINC01852, SLC29A3, MIR6754, IMP3, APOM, MIR6507, ACSS2, LNCNEF, IATPR, MESP1, ZNF395, ALG1, HIF1A-AS1, ERVK-18, HJURP, ASH1L, USE1, MIR5100, BRK1, IMPACT, SLC38A7, PCDHB13, LGR4, SLC2A4RG, ELP3, MIR4677, TCEAL7, RBM23, MSTO1, RFWD3, MIR4735, DDH2, SHQ1, MOB1A, MIR4443, CEP55, SBNO1, SETD5, LINC00702, DPPA4, H3P12, KIAA1217, WWC3, CAND1, PHRF1, LINC01436, CEP72, DOK4, NDC1, CCDC88A, IARS2, IL17RB, YEATS2, URGCP, FALEC, DDX43, RBM38, PRPF40A, SOX6, SLC39A4, ASAP3, KIF16B, CHRNA9, TENT5A, SAGE1, TRPV6, MIR5195, PRNCR1, PAG1, PIDD1, FOXJ2, HEIH, TRERF1, DNM1P50, GATA2-AS1, DEPDC1B, RIOK2, LSINCT5, MBD5, ERVK-25, TDP1, ERVK-24, ZNF331, YOD1, PRR11, CNDP2, HEATR1, PRPF38B, ANO1, RBM14-RBM4, CRACD, SAMD9, SYTL2, NDRG3, SCYL1, ALKBH5, SPC25, RAB22A, WSPAR, RNF111, RAB4B-EGLN2, S100A14, INO80D, RHOJ, AICDA, CASZ1, NKILA, ADGRG6, TET2, MTUS1, NDUFA4L2, KLHL1, LINC01354, SLC35F2, LINC00665, MPHOSPH8, KIAA1522, XAF1, ZSWIM5, SNHG16, CFAP97, XPO5, CRAMP1, FBLIM1, PCDH10, CCEPR, PCSK4, ZNF398, SERINC1, PPP1R12C, NSD3, MCOLN1, ERVK-19, POGLUT1, TESC, FOXC2-AS1, LINC01288, LAMTOR1, MARCHF1, MIR4782, EPN3, ATG16L1, CASC19, LINC01614, GABPB1-IT1, OTUD7B, FEZF2, ATG2B, RALGPS2, XAB2, MFF, PNO1, PLSCR4, CASS4, MIR4465, TIGAR, SEMA4C, MICOS10-NBL1, ERVK-10, ERVK-9, YTHDF1, TRIM54, PHTF2, DUS2, RASIP1, LIME1, LINC01638, COMMD4, SDHAF2, RAB25, ERVK-21, GACAT3, MIR4458, CD177, BMF, CPEB1, NME1-NME2, MNX1-AS1, DAND5, MLKL, GAS6-AS1, PAOX, ARID2, DTX3, XAGE1B, ZNF367, PGAM5, XAGE1A, PDIA3P1, TRIM65, MIR539, MIR545, RHOV, COMMD6, LINC00858, OXER1, TRPV3, FSIP1, TMTC3, SNORA78, SNORD66, TMEM17, RDM1, MIR505, DDIAS, MIR507, ZNRF2, LINC00589, KCTD20, FAM83B, GPRC6A, ERVK-8, ALKBH3, MIR483, HEPACAM, LTO1, VWCE, RASSF10, SFTA1P, SNORA3A, ECSCR, CERNA2, FLVCR1-DT, NAIF1, LGI3, NR2F2-AS1, MT1IP, TUBB, CMYA5, FAM201A, SNORD76, RDH10, AFAP1L1, MIR585, MIR589, MIR592, MIR599, MIR612, UBE2F, DYNLL2, CHODL, CKS1BP7, STXBP5, GPR151, MIR629, SNORD78, CRYBG3, KCNH8, OSR1, RBM45, C20orf85, DRAM2, ARHGEF19, KLF17, MIR647, EDARADD, HMGB4, CACUL1, SESN3, PIWIL4, PRIMA1, MIR33B, ZNF746, CNKSR3, DAB2IP, KLB, SHISA3, RNF38, MIR449B, MIR561, LBX2-AS1, GPBAR1, MIR575, HORMAD2, GNAS-AS1, MIR576, RNF187, IL23R, LINC00337, SPC24, KLC3, TRIM16L, ARHGAP27P1, PWAR1, PELI3, FNDC5, TTTY15, PLF, MIR1-2, MIR105-1, MIRLET7A2, MIR369, GASAL1, LINC00243, MBNL1-AS1, MIR373, LINC00511, TOB1-AS1, ERVK-7, FBXW5, MIR124-2, PCNX3, HES3, OR3A4P, USP27X, FEZF1, OGFRP1, SNHG17, HES5, TNFAIP8L3, IL31, LINC-PINT, MIR124-1, MIR124-3, CERS6, BLID, MIR196A2, MIR208A, MIR188, MIR26A1, MIR299, MIR302A, MIR181C, MIR16-1, MIR15B, MIR147A, HPC4, ZYG11A, MIR324, TRIM67, LINC01123, THUMPD3-AS1, NRARP, VN1R17P, MIR129-2, OR2J3, GPR166P, MIR129-1, MIR125B2, MIR302B, RGMB-AS1, DUXAP8, LINC01116, IFNL1, MIR520E, PICART1, MIR520F, FBXL19-AS1, LINC00641, CHAMP1, LINC00346, MIR526B, RASSF3, MIR519D, CSNK2A3, MIR527, DUXAP10, ADGRF1, MRGPRX1, SGMS1, GCSAM, FRMD3, TINCR, GK5, PCSK9, MIR501, CACNA1G-AS1, ANGPTL5, CISD3, CAVIN1, ZNF326, MIR193B, JPX, LINC01193, SERINC2, MIR362, NMRAL2P, BARHL2, MIR20B, ZNF677, MIR409, VSIG1, TSPAN33, S100A7A, MIR489, LINC00221, SNAI3, RAB37, CELIAC2, DDX51, MIR491, STPG4, MIF-AS1, LINC00319, MIR496, NR2C2AP, WTIP, SPNS2, FUZ, SLC44A4, MIR1298, TNKS2, ULBP1, MIR1256, TET1, MED28, MTERF2, TRIM45, NAA50, ALPK1, MUS81, MIR1914, MIR1297, CTC1, ZNF703, TRIM46, MIR1976, NRSN2, NAA25, MINDY3, GRHL2, MIR1238, LINC00472, ITIH5, SETD7, PAQR4, CRISPLD2, FAM83A-AS1, HOXA-AS3, CCDC8, RASSF4, CD24, KDM7A-DT, KLLN, MARVELD1, LINC00426, ITCH, ATG10, LINC02418, MIR1287, CASC11, LINC00173, LOXL1-AS1, CDCA3, ZNF205-AS1, RNF146, LINC00630, TSPAN14, MIR1183, MIR1275, MIR1182, MIR1197, LPCAT1, MIR1908, MIR3188, BIRC7, HMGN5, PPDPF, MIR449C, MAPKAP1, FTO, HOTTIP, RHPN1-AS1, OTUB2, H3P41, WNK2, MIR4317, RABEP2, MIR4293, MIR4301, RTN4R, MIR4270, MIR3120, LPIN3, PCDH20, KLC2, IL25, ILRUN, PDIA2, MIR762, PAGR1, SLC52A2, MIR718, ALG13, MIR1305, VASH2, MIR548L, HAND2-AS1, SHCBP1, GSDMD, ELMO3, ZNF668, PALB2, TBL1XR1, RTL10, NEIL1, ARHGAP10, MCPH1, MIR1244-1, GALNT14, BABAM2-AS1, ADIPOR2, TCTN1, FAS-AS1, CHPF, ZEB2-AS1, HORMAD1, USP44, KAT8, HULC, UHRF2, FBXO17, MARCHF3, LINC01433, ZBED9, CARD16, TRIM9, FAM83F, CMTM1, TUBA3D, CDCA5, CT45A2, MIR802, NBAT1, STXBP5-AS1, LOC730101, FOXP2, ORAI3, TDRG1, H2AW, DTD1, MAFG-DT, TIMM50, CHMP4C, CASC8, TNFRSF13C, ALPK2, BATF2, MTFMT, TPPP2, C12orf54, INS-IGF2, TMEM132D, MIR653, CYP2R1, ANKRD22, C10orf90, MIR655, PRAP1, MRGPRX4, MRGPRX3, AGAP2, ARAP2, LRG1, SNAP47, HSPA12B, ANIB1, MRGPRD, OLIG1, FOXP4, DNTTIP1, TMEM88, TIMD4, ZCCHC9, MIR939, IL17RC, MIR942, HINT2, MIR944, IL1F10, KISS1R, MT4, MAP1LC3A, MIR190B, MAK16, MIR760, ACSS1, CABLES1, MIR365A, TNK2-AS1, SYVN1, LZTS2, C15orf48, VPS9D1-AS1, SARNP, C20orf181, GINS4, RPAIN, SYCE1L, LMNB2, ZNF503, ORAI1, ARHGEF39, RCCD1, TRIM47, DPP9, JPT2, PAGE5, LINC00473, STARD13, HPP1, TSPAN18, TRIM15, ATG16L2, MIR300, MIR541, MIR147B, TRIM4, SLC22A16, NKD1, MIR877, DISP1, MIR665, MIR301B, RITA1, MASTL, NAT1, DCLK1, MOV10L1, MT1E, MMP19, CD200, MPST, MSR1, MSRA, MT1A, MT1B, MT1F, MUTYH, MT1G, MT1H, MT1M, MT1L, MTNR1A, MUC2, MUC4, MMP16, MMP13, KMT2A, MAP3K11, MCAM, MCM4, MCM6, MDFI, MDH2, ME2, MECP2, MAP3K3, MEN1, MEOX1, MEOX2, MEST, CD99, MICB, MAP3K10, TRIM37, MYB, MARK1, NTRK3, CNOT3, NOVA1, NPAS2, NPM1, SLC11A2, NTF3, NTHL1, ROR1, GADD45B, ROR2, NUP98, OAT, OAZ1, OGN, OPCML, OPRK1, NME4, NME2, NKTR, NIT1, MYH9, MYH11, MYO6, MYO10, NAP1L1, NBL1, NCBP1, NDUFS1, NDUFS8, NEFL, NEUROD1, NF2, NFE2, NGF, NID1, MB, MAOA, IFN1@, ITGAM, IREB2, IRF7, ITGA1, ITGA2, ITGA2B, ITGA7, ITGA9, ITGB2, KCNN4, EIF6, ITPR3, JAK3, JUNB, JUND, KARS1, KCNA5, IRAK2, INSM1, INSL4, INPP5D, IFNA17, IFNGR1, IFRD1, IGFBP4, IGFBP6, RBPJ, IL1RN, IL7R, IL11, IL12B, TNFRSF9, FOXK2, INHBA, INHBC, INPP4A, KCNJ3, KCNQ1, MAGEA10, LOXL1, LECT2, LEPR, LETM1, LIG1, LIMK2, LLGL1, LMO7, LRP6, KHK, LRP5, LTA, CYP4F3, LTBR, LTF, SMAD1, SMAD5, LDHC, LAMP1, LAMB3, KRT17, KIR2DL1, KIR2DL2, KIR2DL4, KIR2DS1, KIR3DL2, KLRB1, KLRD1, KNG1, KIF11, KIFC1, KIF22, KRT6B, KRT7, KRT14, KRT16, OPRL1, SIX6, SLC22A18, RORA, RFC1, RFX5, RGS3, RGS4, RMRP, RNASE3, ABCE1, RORB, RPS27A, RORC, RPL19, RPL32, RPL34, RPN2, RPS3, RPS6KA1, REG1A, RECQL, OPN1LW, RCN1, PTPRH, PTPRK, PEX19, PYGB, RAB5A, RAC2, RAD17, RAD51B, RAD52, RAG2, RAP2B, RASGRF2, KDM5A, RBM3, RBP2, RPS15A, RXRG, ORM1, SH3GL2, CX3CL1, SDHA, SEA, SEL1L, SELENOP, SFRP5, SFTPC, SHC1, S100A6, FBXW4, SHOX2, ST6GAL1, SIM2, SIPA1, SKIL, SLC1A2, CCL25, CCL22, CCL20, CCL17, S100A7, S100A9, S100A12, S100A13, SAA1, SAA2, SAI1, SAT1, SATB1, ATXN7, SERPINB4, SCD, CCL4, CCL7, CCL8, PTPRF, PTPRD, PTPN4, PKP2, PER1, PFN2, PIGR, PIK3C2B, PIK3C3, PKD1, PKNOX1, PLA2G1B, PTPN1, PLCB3, PLCB4, PLOD2, PLP2, PMCH, PNOC, PRRX1, SERPINF1, PDYN, PDE4D, PDE3A, P2RX5, P4HB, FURIN, PAFAH1B1, PAH, PAK2, PAPPA, PARN, PAWR, PBX2, PCDH7, PCK2, PDB1, PDC, PDCD2, POLE, POLR2A, PON1, PROP1, PRSS8, PSG1, PSMA4, PSMB6, PSMD10, PSPH, PTAFR, PTBP1, PTGDR, PTGER2, PTGIS, PTK7, TWF1, PTMA, PTMAP4, PROS1, PRL, POU2F1, EIF2AK2, POU3F1, PPA1, PPARA, MED1, PPBP, PPIB, PPP2R2A, PPP5C, PPT1, PRCC, SRGN, PRG2, PRKCD, PRKD1, MAP2K3, IFNA2, IFIT2, ANLN, CEBPA, SEPTIN7, CDC25B, CDH3, CDH5, CDK8, CDKN2C, CDKN3, CEBPB, CNR1, CETN1, CGA, CHI3L1, CHKB, CHRM3, CHRNB3, CKS1B, CD151, CD70, CD69, CD59, CALM2, CALM3, CAMP, CAPNS1, CASP1, RUNX1, CBL, CBR1, CCNA2, CD1D, CD14, CD19, CD86, CD33, CD36, CCR6, CNTN1, CALB1, CYP27A1, CYP2A13, CYP2C19, CYP2C8, CYP2C9, CYP3A5, CYP3A51P, CYP17A1, DAB2, COL1A2, DAPK3, BRINP1, DBN1, DDB1, DDB2, DDT, DDX3X, CYP1A2, CX3CR1, CTBP2, CSTA, COL10A1, COL17A1, MAP3K8, COX7A1, CP, CLDN4, CPS1, CRABP2, CRMP1, CRYAB, CSF1, CSH1, CSH2, CSNK2A2, CST1, CALM1, CACNA1B, CFI, AMPH, AHSG, ALDH1B1, ALDH1A3, ALDH3A2, ALOX5, ALOX15, AMFR, ANCR, ARAF, ANK1, SLC25A5, ANXA4, BIRC2, APOA1, APOE, AQP1, AGT, JAG1, AGL, ADM, SERPINA3, AAMP, ABCA1, ABCA4, ACLY, ACTG1, ACY1, ADARB1, ADCYAP1, ADCYAP1R1, ADD1, ADD3, ADH1B, ADH1C, ADH7, AQP5, RND3, CACNA1A, BTF3P11, TNFRSF17, BCR, BCS1L, CXCR5, BMP1, BMX, BOK, BTG1, ARHGAP1, BUB1, C4BPA, C4BPB, FMNL1, PTTG1IP, CA1, CA4, BCL9, BCAT2, BARD1, BAGE, ARHGAP5, RHOH, ASNS, ASS1, ZFHX3, ATD, ATF1, ATOX1, ATP5F1A, ATP6V1E1, ATR, ATRX, AVPR2, BAAT, BAD, DDX5, DHX9, DEFB1, GPX1, GOT1, CXCR3, UTS2R, GPER1, GPR35, GRK5, MKNK2, GPX3, HABP2, GRIA2, GRIN2B, GRM1, PDIA3, GSR, GSTT2, GZMA, GNA15, GNA12, GLRA1, GCLM, FRK, GAST, G6PD, GAGE1, GAB1, GALC, GALNS, GAP43, GART, NIPSNAP2, GDI2, GFAP, GFRA3, GHSR, GJB1, H2AZ1, HAGH, DES, AGFG1, HOXC11, HOXD8, HOXD10, HP, HPD, HPGD, HPR, HRG, HAS3, HSD11B2, HSD17B1, HSPA9, DNAJB1, HTC2, HYAL1, MRPL58, HOXC6, HOXB9, HOXB2, HOXA13, HBE1, CFHR1, HINT1, HIVEP1, HLA-DMB, HLA-DRA, HLA-DRB1, HMGB2, HNRNPAB, HNRNPD, HOXA@, HOXA3, HOXA4, HOXA10, HOXA11, FPR2, FOSL2, FLT3, EFNA3, DUSP2, DUSP4, DUT, DYRK1A, ECM1, EDN1, EDNRB, EGR2, FLNA, EGR3, EGR4, EIF2S1, EIF2S3, EIF4A1, ELANE, EMD, DTX1, HBEGF, SLC26A2, DSPP, DHCR24, DLG3, DLX6, DMBT1, DMRT1, DNAH8, DNASE2, DNTT, DOCK3, DPYSL2, DRD4, DSC2, DSC3, DSG2, DSP, MARK2, EMP1, EMP3, FAAH, FAP, FBN2, FCGR3A, FCGR3B, FCGRT, FDX1, FGF5, GPC5, FGG, FHL1, FKBP3, FOXG1, FOXE1, FOXD2, FLI1, FANCG, EZH1, CTTN, EYA2, EN2, ENPEP, EP300, STOM, EPHA7, EPHB3, EPHB4, EYA4, ERG, ESRRA, ESRRB, ESRRG, ETS1, MECOM, EXTL3, SLC2A5, SLC5A1, SLC5A2, RAB11FIP2, TP53TG1, CD300A, PARK7, VSIG4, CBX3, U2AF2, NID2, SEC31A, ATF6, MLXIP, MORC2, ANKRD6, CLSTN1, FOXJ3, SBNO2, CD93, PDCD10, HPS5, ANXA10, PKP3, DSTN, RIPK3, SOX30, CYB561D2, TOPBP1, ESM1, ADAMTS13, ADAMTS5, CIT, FGFR1OP, PTPRT, FAF1, KIF3A, TREH, MAP4K1, MAPRE1, RAB18, CCDC85B, RYBP, LARP1, SIK3, LARS2, SIRT5, SIRT4, COMMD3, KCNH4, SF3B3, KIN, ABCB9, CBX5, SEC61G, CBX7, HEY2, RPL13A, SRRM2, ESYT1, BICD2, MGA, OTUD3, CCT5, TRIM32, LIMCH1, PLCH1, SPEN, FAIM2, KDM4B, NFASC, PHF8, MPRIP, DIP2A, MLC1, JMJD6, XPO6, PHLPP1, GLIPR1, KIF2C, SLC6A2, NDC80, CLEC4M, TFG, TRIM22, SEMA3A, ANAPC10, ATP8A1, MYL9, CPQ, FBLN5, RBM14, LYPLA1, TAB1, TADA3, CRTAP, SEMA4D, APPBP2, B3GNT3, AKR1A1, DLEU1, APC2, ARL4C, PDIA6, YAF2, TOB1, G3BP1, ZNF197, PSME3, TOPORS, CTDSPL, TRIB1, NBR2, SPRY2, IRX5, STUB1, NET1, MYBBP1A, DDX17, SLC38A3, NEU3, PTTG2, CHL1, PLAC1, NCKAP1, MTHFD2, CCR9, FRS3, LYVE1, IPO8, GADD45G, RNPS1, FASTK, SPIN1, SF3A3, COPS5, METAP2, RFPL3, PTGES3, GMEB1, DLL3, NEBL, BATF, ANP32B, LAMTOR5, IFI44, TXNRD2, MTHFS, SLCO1B1, SPAG5, RAD51AP1, IGF2BP1, IGF2BP2, YKT6, SPINT2, CELF2, NNT, SEC14L2, SEZ6L, ASCC1, KLK14, G0S2, SYCP3, IL20, IL21R, F11R, STMN3, ADIPOR1, CLDN18, ANGPTL4, CHCHD2, SDF4, LEF1, HERC5, CKLF, CPA4, STOML2, ERVW-1, VSX1, TBX21, MYLIP, BRD7, CLEC2D, RACGAP1, USP25, CARD10, YPEL1, STRN4, CCDC106, EEF2K, PADI1, LRP12, OBP2A, ERO1A, EFEMP2, NUSAP1, IGF2-AS, TSPAN12, ERAP1, TRIM33, OTUD6B, RTRAF, YPEL5, TPPP3, CPSF3, CMPK1, MYOZ2, MZB1, ADA2, LRP1B, MBD3, ADAM22, PTOV1, IL20RA, IL20RB, AZIN1, TDP2, ARMCX3, HDAC7, TBC1D7, NRN1, PLAC8, WT1-AS, HOOK1, UBR5, ATRAID, UCHL5, POLK, GULP1, DCDC2, LARS1, TRMO, SIRT7, IL23A, COMMD9, LINC00339, ASAP1-IT1, SOSTDC1, KLK5, NOCT, ARIH1, MOB4, USP49, TMEM158, ZDHHC5, FAM98A, HIPK2, ADGRA2, CHMP2B, ACOT11, ATRNL1, CHD5, HERC4, SERBP1, BAMBI, GCA, SLC39A6, QPCT, LPAR3, PADI4, PRG1, LEMD3, AMACR, BACE1, CBLC, LDOC1, TRIM29, SLC7A11, SMPX, RAB38, KIF4A, TFIP11, FBXO7, TES, ZBTB20, FBXL3, SND1, B3GAT1, DKK4, SIGLEC9, DISC1, IL17B, GPKOW, DHDH, RBMS3, RBMX, STK39, HTRA2, DLL1, TMEM14A, FLVCR1, COMMD5, MTBP, OPLAH, TIAM2, STEAP1, PTTG3P, NKX2-8, FBXO8, FBXO6, MYCBP, LHX6, NUPR1, PLEK2, SLC17A5, HEYL, RGS17, MYEOV, HAVCR1, SNORA71A, RNU1-1, KIF20A, RAD50, TSPAN1, XBP1, VAV2, VCL, VEGFB, VSNL1, VTN, WNT3, WNT2B, XDH, FZD5, XPO1, YWHAG, ZFP36, ZNF124, ZBTB16, PCAP, LEPQTL1, USP1, USF1, UQCRFS1, UNG, TUBA3C, TUBB2A, TNFSF4, TYR, UBA52, UBB, UBC, UBE2L3, UBE3A, UCN, UCP1, UCP3, UGCG, UGP2, UGT1A, PAX8, BAG6, HSD17B6, PIK3R3, PLA2G6, SLC25A11, SNHG3, CAVIN2, FOXN1, SMARCA5, PKP4, ELP1, TFEB, IFITM1, CBX4, CAMK1, LGR5, BHLHE40, PIAS1, DENR, FZD9, FZD8, EOMES, CDC45, MAFK, MTERF1, PSCA, LHX3, SLC25A16, SHOC2, FOSL1, USP5, PABPN1, COIL, CDR3, SLC14A2, GDF5, CHAF1B, H3-4, TUBA4A, TTN, TSC2, ITPRID2, SPINK1, SPINT1, SPN, SPTB, SREBF2, SRF, SSBP1, SSR1, TSN, STAT2, STC1, STIM1, NEK4, SUV39H1, MAP3K7, TARBP1, SOX10, SOS2, SOD1, SNRPD3, SLC6A3, SLC10A2, SLC11A1, SLC12A2, SLC12A3, SLC15A1, SLC25A1, SLC22A1, HLTF, SMARCD1, SMARCE1, SMN1, SMN2, SMPD1, SNRPB, TARBP2, CNTN2, TBX2, TLR5, TM4SF4, TMSB4X, TNFAIP3, TNNC1, TNNI1, TNNI3, TOP3A, TP53BP2, TPD52L1, TPM3, NR2C2, TRAF2, TRE-TTC3-1, TRPC1, TRPC6, TSPAN8, TJP1, TCF4, TIE1, TBX3, HNF1A, TCN1, PPP1R11, TEAD1, TF, TFAM, TFAP2B, TFE3, TFPI, TG, TGFB3, THOP1, TIA1, TIAM1, PSMG1, NUMB, EDIL3, PPIP5K1, RBM39, CYTIP, RIN1, NCOR1, TRAF4, TESMIN, ISG15, GREB1, KMT2B, BZW1, UBE3C, ESPL1, ULK2, DCAF1, SART3, PHACTR2, SOX13, BABAM2, SPAG6, BCAR1, DDX23, ZNF264, NCR1, MED23, MAP4K4, EIF2AK3, ROCK2, ONECUT2, SLC4A7, MAGED1, EEF1E1, BAG4, BAG3, EI24, CXCL14, STARD8, HDAC4, PDE5A, SRA1, AMMECR1, HS3ST3B1, HS3ST2, USP15, RBX1, DMTF1, ACOT8, HDAC5, LZTS3, PDCD6IP, PDCD6, RANBP9, UBA2, NR1H3, COX17, HUWE1, WDR1, MAGEC1, GFPT2, RBM8A, SUSD6, PCLAF, EIF4A3, DLGAP5, CUL7, TRIM14, GINS1, LRIG2, MAGI2, PJA2, FCHSD2, RBM19, ARNT2, ZBTB5, MFN2, TMPRSS11D, SELENOF, TSIX, PER2, CCN6, CCN4, HDAC3, TSC22D1, AKAP4, ALDH1A2, APLN, ZPR1, ITGBL1, NAE1, EIF2S2, BCL10, HERC2, MBD4, SKAP2, TOP3B, SOCS2, FGF18, TRIM24, TNFRSF10C, EIF3B, EIF3C, EIF3H, EIF3J, MARCO, B3GALNT1, ADAM19, TNFSF14, TNFSF12, TNFSF9, ADAM23, RAB11A, FADD, TNFRSF18, TNFRSF10D, USP13, NOL3, RNF8, EXO1, TMSB10, SLC16A7, LGI1, NOLC1, DLGAP2, GCNT3, PDLIM7, MAPKAPK2, PIWIL1, GPR55, SOCS6, CD83, TRIP10, TGM5, SLIT2, EBAG9, SLC6A5, TM4SF5, DYRK1B, SEMA5A, SPAG9, RPL14, SYT7, CLDN6, CLDN2, PKMYT1, DNAJA3, USP10, RGN, SLC16A4, SLC16A3, CCNB2, CBFA2T2, ATG12, H3P40
  • Liver Cancer Wikipedia
    Within two years, there is a risk for cancer arising from these nodules of 30–40%. [25] Obesity has emerged as an important risk factor, as it can lead to steatohepatitis . [15] [26] Diabetes increases the risk for HCC. [26] Smoking increases the risk for HCC compared to non-smokers and previous smokers. [26] There is around 5-10% lifetime risk of cholangiocarcinoma in people with primary sclerosing cholangitis . [27] Liver fluke infection increases the risk for cholangiocarcinoma, and this is the reason why Thailand has particularly high rates of this cancer. [28] Children [ edit ] Increased risk for liver cancer in children can be caused by Beckwith–Wiedemann syndrome (associated with hepatoblastoma), [29] [30] familial adenomatous polyposis (associated with hepatoblastoma), [30] low birth weight (associated with hepatoblastoma), [31] Progressive familial intrahepatic cholestasis (associated with HCC) [32] and Trisomy 18 (associated with hepatoblastoma). [30] Diagnosis [ edit ] Further information: Hepatocellular carcinoma § Diagnosis Many imaging modalities are used to aid in the diagnosis of primary liver cancer. ... China has 50% of HCC cases globally, and more than 80% of total cases occur in sub-Saharan Africa or in East-Asia due to hepatitis B virus. [28] [53] Cholangiocarcinoma also has a significant geographical distribution, with Thailand showing the highest rates worldwide due to the presence of liver fluke. [28] [54] India [ edit ] The number of new cases of hepatocellular carcinoma per year in India in males is about 4.1 and for females 1.2 per 100,000. ... Archived from the original on 2017-07-28. ^ a b c d e f g h i j k World Cancer Report 2014 . ... "Serum markers of intrahepatic cholangiocarcinoma" . Disease Markers . 34 (4): 219–28. doi : 10.1155/2013/196412 . PMC 3809974 . ... Archived from the original on 17 October 2014 . Retrieved 28 October 2014 . ^ Xu, Jiaquan (July 2018).
    TP53, CDKN2A, MYC, TERT, GNMT, PPARA, TGFA, IGF2, FHIT, NR1H4, KRAS, ASNS, APC, STAT3, TNF, CTNNB1, TNFSF10, CCND1, NFE2L2, MALAT1, PPARG, IL2, JUN, IFNA1, AHR, NR1I3, HULC, CYP2E1, ANXA2, HGF, SCD, RAF1, BRAF, NEAT1, ATP7B, MIR29A, IFT88, ANXA7, TCF4, MAPK14, SLC2A1, TOP1, DACT2, ATF3, PTPRO, HRAS, ESR1, FOSB, NDRG1, CDKN1B, HCFC1, OAT, SNX10, GSTM1, LARGE1, PHGDH, HEBP2, CRABP1, DICER1, EXOSC2, PTER, CCNH, TOX3, NCOR1, CPT1B, NUDCD3, WSCD1, TTC39A, ESM1, YIF1A, CGREF1, CHN2, HERC3, TNK2, FST, CCR4, CIDEA, EFNB2, CSF3, LTF, MYO5B, GJB1, GPC3, GPX2, GPX3, GRIK2, KRT18, NAT2, KRT8, HIF1A, ITIH1, IL12B, IL12A, HMOX1, SLC11A2, SERPINE1, ABCB1, PLS1, PRKCE, PSMA4, PTEN, PTGS2, SIX3, SRMS, ZDHHC2, TOP2A, TRIO, UGDH, XPA, XPC, BAP1, SLC40A1, CSF2, CCDC134, TMEM132D, DPP10, MACIR, FLCN, DCD, TTLL9, TRMT11, CLSTN2, WDR17, DDX54, EGLN3, SLC38A9, ZSCAN22, HIGD2A, ADAMTS17, PDRG1, PRICKLE2, RTP3, ASH1L, HSDL2, BTBD11, MACROD2, STAC3, ANXA4, ABL1, APCS, SNHG11, NOP16, GADL1, NUDT7, ACOT1, SPATA21, LINGO2, HNF4A, MET, CASP3, FOXM1, AKR1B1, COL18A1, CADM1, PCNA, MIR145, SRSF1, MIR25, HNF1A, RGN, G6PD, PLAU, PTK2, CASP8, CARM1, DNMT3A, SKP2, CCNE1, SAV1, IL10, FAS, DNMT1, SMAD2, GMPS, MIR93, HNRNPA2B1, ING3, IL6ST, ABCC3, ENG, CTSB, CDKN1A, CASP9, ABCB4, APRT, IQGAP2, TXNIP, SRF, SHC1, EP300, GC, MIR106B, ND5, HNRNPD, ABCA1, INSR, MIR96, SMAD4, MCM7, MECP2, MME, COX1, MIR195, PPAT, GJB2, AKT2, NFE2L1, MIR181C, MIR18A, PFAS, ALDOC, FTH1, POLG, MCM9, A2M, TEK, VAV1, XDH, CAPN3, ACOT12, CDK1, CDH1, MTHFD2, UACA, CTSL, CAD, CSK, HPRT1, PPP1R9A, LPAR1, HAMP, C3, FOXP1, SLC66A3, ASIP, TFRC, TGFBR2, DNMT3B, PIK3CD, PIK3CG, PIK3CA, SLC5A5, PROM1, EPCAM, BCL2, ALB, DLC1, AKT1, MIR122, EGFR, YAP1, CD44, AFP, MIR21, VEGFA, PIK3CB, MAPK1, TGFB1, THY1, MIR34A, COX2, EPHB2, IL6, SIRT1, PKM, GABPA, GRN, MIR221, MTCO2P12, DLEC1, E2F1, ADAM17, HOTAIR, DNLZ, DYNLL1, IL24, IFI27, MIR146A, MTDH, SPP1, HMGA2, ICAM1, ARHGAP1, TBC1D9, TRIB2, KLRC4-KLRK1, CXCL8, TMED7-TICAM2, HSPA5, MEG3, H3P23, KLRK1, ALDH2, MIR155, BMI1, TFDP1, TICAM2, EZH2, PSMD10, PSMD9, MAPK8, ANPEP, SPHK1, TMED7, PNPLA3, NANOG, DCTN6, ZNRD2, MAT2A, XRCC1, MAPK3, MDM2, MTHFR, IFNA13, COMMD3-BMI1, GASAL1, ROS1, SOX2, GOLM1, MIR200A, TAZ, AXIN2, PRKAB1, MAT1A, PRKAA2, PRKAA1, KDR, MMP9, MIR15A, MIR375, HDAC3, PHB, LDHA, MCL1, SQSTM1, MIR27A, PDCD1, SLC9A3R1, MMP2, H3P10, MTOR, GPT, HDAC2, HK2, CDK2, HFE, EGF, TBX3, ACHE, CAV1, HGS, PTPN11, DKK1, LCN2, HSPB3, NOTCH1, ALCAM, CEACAM5, JAG1, PAEP, TLR4, USP22, MUL1, MBD2, JAK1, MIR148A, STK11, REG3A, RUNX3, CCK, SETD2, POU5F1P3, POU5F1P4, UCA1, CXADRP1, SERPINB3, MIR7-3HG, SATB1, MIRLET7B, TRIM13, MEF2D, MIR449A, PPARGC1A, SPG7, GSTP1, ARR3, CCR2, CBLL2, MIR424, NDRG2, CD274, PRKN, DNAJB1, IGF1R, IGF1, MIR203A, FOXA1, FGR, STARD13, SIRT7, CXADR, POU5F1, BECN1, HSPB2, SIRT6, HSPB1, MIR214, NCOA2, CKS1B, MIR22, PLK1, OGT, LOC110806263, FSD1, FOXO1, FSD1L, GAS5, TWIST1, PRKAR1A, AKR1C2, NR1I2, HMGB1, MAP2K7, CASR, MIR33A, MIR199A2, NR1H3, DNM1L, RPL29, SRA1, CLIP1, XAF1, GSTK1, MIR152, PLXNB1, FAH, SPRY2, MIR199A1, XIAP, CCL2, CPQ, FGF19, EEF1AKNMT, RFC1, MIR183, RELA, PTK2B, GRK2, FBP1, FGFR4, MIR15B, MIR204, MSLN, FASN, MIR137, PTGER3, MIR125A, MIR149, PLAAT4, PTBP1, MIR10B, PARP1, MIR182, RDX, POMC, MFN2, RECQL, RASAL1, YOD1, AQP5, CCN2, VCAM1, TNFRSF10B, MAK16, TNFRSF10A, UGT2B7, SPZ1, TTK, KAT2B, CLIP2, HSP90B1, FUBP1, NQO1, TM4SF4, TLR1, SALL4, SMURF1, TNFRSF6B, SPRTN, ZEB2, AIMP2, NR0B2, CUL4A, AXIN1, TET1, SLC7A5, AKR1C3, HHIP, CXCR4, DCN, IRS2, VSIR, BSG, ZFP36, ALX4, RIPK1, XPO1, CDCA5, CIAPIN1, SPAG9, SLC5A2, PIN1, CALD1, APOBEC3B, LAPTM4B, FOXK1, CREB1, CTTN, IFNL3, AKR1B10, AR, EPAS1, SHMT2, EPHA3, PCLAF, EPHB6, SFPQ, SOAT1, SOD2, GDF15, APOBEC3A, DPYD, BAX, UNC119, PNO1, ZEB1, ATM, SLCO6A1, METTL3, EGR1, AURKA, ST13, ASPH, ASL, SRC, ABCG2, FOXO3, PSG2, MIR222, CD151, ATAD2, IGFBP3, GGTLC5P, MIR544A, HNRNPA1P10, MIR590, MICA, TIAM2, CCNB1, CXCR2, MKI67, CXCL9, HPGDS, KITLG, MST1, CBX5, MIR483, HMGA1, MIR503, WWP2, MIR885, MIR499A, MUC1, PES1, SUZ12, CEACAM3, MYCN, APOBEC3A_B, PRDX3, MIR490, SRRM2, RBMS3, GGTLC3, LNCNEF, KISS1, MARCKS, CDKN3, HDAC1, MIR675, SULF1, LGALS3BP, MIR300, IL17A, RPIA, MIR1247, KLRC1, MIR216B, TPX2, KDM1A, CD82, JUNB, JAK2, HLA-A, ACAT1, MXD1, HOTTIP, LATS2, SMAD3, GTF2H1, FLT4, SMAD7, GGTLC4P, ZHX2, GGT2, NUPR1, ILF2, GJA1, IFNG, CEBPA, MIR346, GAPDH, NUP62, KAT5, GATA4, WWTR1, NPC2, MIR372, HSD17B4, MLXIPL, MIR302A, MIR30A, MIR378A, MIR338, DCTN4, CPA4, CELF1, PDGFRA, KHDRBS1, GCK, PBX3, POSTN, NUSAP1, NOTCH3, MIR34B, GGT1, GH1, YTHDF2, HSPA9, PERCC1, HSPG2, CEACAM7, HPSE, CD34, FN1, FOXP3, SERPINA1, STOML2, HNRNPA1, SMUG1, FOS, RTN4R, ELOVL6, XPO5, PINK1, SLC17A5, SND1, MAVS, WNK1, BIRC6, LAT, MARCKSL1, RAB22A, LETMD1, TIGAR, AICDA, CENPM, PLXDC1, AHNAK, MMEL1, CLIC4, RNF19A, FOXL2, POLDIP2, HACE1, CTDSP1, GORASP1, CLEC7A, ZBTB20, SCPEP1, CSMD1, KRT23, PRPF31, MTMR14, BTG1, BTF3P11, ARHGAP9, XPO4, APOBEC3G, NCAPG, ATRNL1, RPRD1B, PHF19, MRPL38, CD19, JCAD, GAS8-AS1, VPS33B, SAMHD1, USP28, GOLPH3, MRPS5, SFMBT2, GPR107, PCDH20, ETNPPL, GATAD1, VPS51, B3GAT3, FNDC3B, CIP2A, DEPDC1, ACKR3, RIN2, MBD3, FXYD5, DUOX1, PPIL3, PCA3, TREM1, GEMIN4, IL22, NOX4, TERF2IP, MIEF1, SLC12A9, CAMK4, UGT1A7, UGT1A9, UGT1A1, CDHR2, SYTL2, OSGIN1, TEX10, NSD3, YTHDF1, DERL2, TM6SF2, NDUFA13, RTEL1, MAGEC2, CAPN6, UFC1, DTL, ANAPC11, AMOTL2, TRPV2, TNFRSF12A, PLAC8, CASP4, IER5, VRK3, GDE1, MED15, ZFR, LEF1, CHCHD2, ANGPTL4, NLK, WWOX, CRYL1, SARS2, TMOD3, PINX1, SLC39A4, NLRP2, URGCP, BTBD7, OGDHL, BBC3, CAND1, LDLRAD4, PBK, ZNF395, ACSS2, SULF2, TEX11, RNF17, CD14, CCL28, SPHK2, B9D1, FSTL5, TCIM, PSMG2, CHPT1, DKK4, DKK3, MARCHF1, ASAP3, TMEM176B, CCNA2, CALML3, IGHVIV-44-1, ANO1, MAT2B, MSTO1, RABGEF1, MAP1S, NAT10, YY1AP1, VPS53, DRAM1, TMEM176A, PDLIM3, PDCD4, CD5L, RBM38, PLXNA3, DKK2, DDR1, EPS8L3, GTSF1, CERS4, POTEKP, MIR26B, ADARB1, MIR27B, ADAR, MIR29C, MIR30D, MIR31, MIR32, MIR320A, ADAM10, ACYP2, ACVRL1, MIR99A, MIR17HG, MIR330, MIR24-2, MIR340, MIR342, MIR370, MIR373, CISD2, ACTG2, MIR382, DUXAP9, MIR429, MIR448, MIR363, MIR20B, MIR433, MIR451A, ADH1C, MIR23B, MIR410, BIN1, LIN28B, ZCCHC13, ST20, HAGLR, ANXA6, MIRLET7C, ANXA5, MIR107, MIR10A, ANXA3, MIR126, ANXA1, ANGPT2, MIR150, ALPP, MIR23A, ALDH1A1, MIR185, MIR186, MIR196A1, MIR196A2, MIR199B, MIR20A, MIR205, MIR210, MIR181A1, MIR217, MIR219A1, ADORA2B, MIR224, MIR409, MIR493, HMBOX1, LINC00554, MIR1258, MIR1307, MIR1228, BAALC-AS1, MIR3664, LUCAT1, THORLNC, LINC00665, SNHG16, MINCR, GMDS-DT, ACADL, ACACA, HEIH, ZNF385D-AS2, CD24, LINC-ROR, LINC00210, ROR1-AS1, PCBP2-OT1, LOC102724197, TP53COR1, WSPAR, CCEPR, ABO, LOC108004545, CNE-2, MAPK6-DT, LNCARSR, SERPINA3, TSPY10, ACTA2-AS1, MIR193B, MIR637, MIR498, MIR525, MIR500A, MIR506, MIR486-1, ACTG1, POTEM, SNHG6, PURPL, CRNDE, MIR421, MIR589, MIR608, MIR613, MIR639, MIR760, MIR92B, MAFIP, TSPY3, MAGED4, ACTB, ACOX1, MIR454, MIR766, CDKN2B-AS1, MIR665, MIR374B, MIR920, MIR935, MIR543, TMEM82, APEX1, BIRC3, HAVCR2, TLN2, SESN2, MARVELD1, ZNF484, LOXL4, SETD3, BGLAP, RPAIN, ACRBP, AFAP1L2, KISS1R, RNASE7, USP30, RIOX2, MASTL, CDCA3, UBASH3B, NKD1, WNT3A, KCNK17, SLC25A21, BCL2A1, PYGO2, IL33, DEPDC7, GGTLC1, BCHE, MTG1, TP53INP1, BCAT1, CEACAM1, TCF7L1, ASPG, CEBPA-DT, GALNT14, TNFAIP8L2, SUV39H2, LIN28A, HAND2-AS1, VASH2, CPSF7, BMPR2, HDAC11, BMPR1A, DHDDS, PDZD7, WLS, SVEP1, ASRGL1, KIF18A, PREX2, CPEB4, BMP4, SRCIN1, BMP2, DUSP16, MOB2, MAGED4B, TXNDC5, BLVRA, MAP1LC3B, NUAK2, SLCO5A1, SHARPIN, CYTOR, CMTM7, NLRP3, TIPRL, TIGD1, ALG1L, RHOA, MPEG1, LTO1, OTUD1, ZEB1-AS1, HOXA11-AS, GPC2, CTAG1A, ARF6, TMEM9, AREG, SERPINA11, AQP9, CYGB, SLC13A5, DLX6-AS1, FAM83H, SCARA5, MT1DP, ABCB5, RSPO2, APOE, ACTBL2, H3P44, PCNAP1, IRF2BP2, NDUFS7, NCR3LG1, ARID2, ARNT, STS, ARSF, VASN, ZNF689, TOP1MT, MRGPRF, THEM4, BAG1, ATRX, PRDX5, ATR, MSI2, OSCP1, KLF17, ALDH7A1, DIS3L2, KCNH8, ATHS, CKS1BP7, FUNDC1, BRI3BP, ATF4, PRICKLE1, E2F7, GSC, SPC24, RNF187, LRATD1, SERPINC1, TMEM74, DEUP1, FBXL2, HOXA7, RAD54B, RASA1, RIT1, RHO, RHEB, RET, KDM5A, RASA2, RARB, NECTIN2, RARA, RAP1A, RAN, RALA, ERCC2, RAC1, RNASE3, ROBO1, ERBB2, RPA1, RPE, RPS27, RRBP1, S100A6, S100B, SAFB, ACSM3, SARS1, SERPINB4, EPS8, SCT, SCTR, CCL20, PYCR1, ERG, XCL1, POLE, PPOX, FHL1, FHL2, POU2F1, POLR2E, FHL3, PRRX1, PTMAP4, FOXC1, PLEC, PIK3R1, PIM1, FOLR1, FOLR2, PPP2R3A, FGA, FER, PRKCI, MAPK6, MAP2K1, MAP2K3, PRL, ACSL1, PSMD4, FABP4, F2, PSMD12, ESRRG, ESRRA, ESR2, PTMA, CXCL11, SDC1, CD80, TAGLN, HNF1B, EDNRB, TBL1X, TBCA, TAT, TARBP1, EIF2S1, TRIM21, SYT1, SYCP1, SULT1A3, STIM1, STAT5B, STAT5A, TCF7L2, PPP1R11, PRDX2, TMBIM6, EDNRA, TERF2, ECHS1, TFCP2, NR2F2, E2F2, DVL1, DPYS, TGFB2, TGFBR1, DPP4, DLD, TIMP1, EIF2S3, SRY, CXCL12, SLC2A4, SMARCA1, SLPI, SLC22A1, SLC19A1, SLC10A1, SLC3A2, ENO1, EIF4E, ENSA, ST6GAL1, SHH, SHBG, SELENOP, SELP, SMARCA4, SMPD1, SUMO3, SUMO2, SNAI1, SNCG, FSCN1, SORD, SOX1, ELK3, SOX4, SOX10, SP1, SPINK1, ELK1, SRD5A2, ELANE, PHKB, PGM5, PGK1, KRT10, LEPR, LEP, LDLR, CFH, STMN1, KRT19, HGFAC, ITGA7, KRT6A, HIC1, KPNA2, KIT, KIR3DL1, HK1, LGALS1, LGALS9, LMNB1, LOX, SMAD1, H2AZ1, MAFG, MAGEA1, MAN2A1, GSTT1, MBL2, GSTA3, GSR, GRP, GRM5, MEN1, MFAP1, JUND, ITGA2, PGF, HSPA1B, IDH2, IDH1, ID1, HTC2, HNRNPC, HSPA4, HSF1, IRS1, AGFG1, HNRNPK, HNRNPU, HPR, HPD, HOXA13, IDUA, FOXA2, NR4A1, IFNB1, IGF2R, IGFBP1, IL1A, HMGCS2, IL2RA, HMGCR, HMGB3, CXCR1, HMBS, HLF, HLA-DRB4, ILK, HLA-DRB1, MGMT, MLH1, MAP3K10, NUP98, ORM1, OPRM1, TNFRSF11B, OGG1, ODC1, GDF2, NRAS, FOXO4, GEM, NPM1, NONO, NME1, NM, NFKBIA, OSM, P4HB, PEBP1, PRDX1, PCK1, PCK2, GATA3, PDCD2, PDE6D, PDGFRB, PDK1, PDK4, ENPP2, SERPINF1, GATA1, ATP8B1, PFKM, NFKB1, NF2, NEK2, GP1BA, GPER1, CXCR3, XCR1, MMP14, MNT, MPL, MPO, MPP1, MPST, MRC1, ABCC1, MSH2, MSI1, MT1H, GLUL, NEDD9, GLI3, GLI2, MTR, MTRR, MUC4, MUTYH, GLI1, GADD45B, MYLK, NASP, NBN, NCK1, NEDD4, SEPTIN2, TIMP2, TIMP3, TJP1, CHAF1A, LRPPRC, ARL4C, ACTR3, ABCB6, GJC1, SMC4, TROAP, CPS1, HDAC6, NR2E3, AKT3, HNRNPDL, RBX1, CLEC2B, TRAP1, BCAP31, CLDN3, PSMD14, GDF11, CD96, SF3B4, RAMP3, LILRB2, RTN3, CITED2, COMT, CCR7, RACK1, PEMT, NDC80, CLIC1, CLDN7, CPT1A, PCSK7, PPIG, NTN1, GRAP2, RECQL4, ADIPOQ, ATF2, KL, TRIP10, NUAK1, CRK, PIWIL1, MAPKAPK2, PTTG1, NOLC1, CRMP1, NCR1, GGPS1, FHL5, PCYT1B, TBPL1, CHD1L, KIF20B, WTAP, AKAP12, NUP155, ISG15, SOCS5, KDM4A, DCAF1, HDAC9, HDAC4, MAML1, CLU, CIRBP, HOXA10, MORC2, LARP4B, SEPTIN6, SCAP, ATF6, CEBPB, CARD8, TDGF1P6, SIVA1, OIP5, CBX3, ACOT7, SLCO2B1, PADI2, POLG2, SASH1, SYNE1, CDK4, CDH17, SIRT5, SIRT4, NCS1, KCNH4, GRIP1, BRD4, RBFOX2, KLHDC2, DAPK2, SNHG1, TRIM29, SLC7A11, SH3BP4, ANXA10, RASSF1, STRAP, AKR1C4, AHSA1, SLCO1B1, TRIM3, CHUK, IGF2BP1, CAMKK2, CXCR6, CTCF, CHI3L1, CHEK1, PLK4, MAP3K2, NES, PLK2, CHD4, NUDT6, CCL27, LYVE1, GADD45G, EHMT2, SPIN1, APOBEC2, ATF7, OGFR, UBE2C, CEBPD, CD160, ZWINT, HHLA2, PTP4A3, XPR1, EXO1, TLN1, ZNF224, CUL5, ADAM12, TFPI2, DEK, MANF, PAX8, ZMYM2, DGKQ, ZNF148, ZBTB16, ZIC2, ZFX, XRCC5, XRCC4, CYP19A1, CYP17A1, NCOA3, TAM, CHAF1B, AKAP17A, ARID1A, TRRAP, CYP2D6, CYP2C9, FZD6, H3C1, H3C4, H3C3, H3C6, H3C11, H3C8, XRCC3, DAPK1, CCNE2, TPT1, TSG101, TRO, DECR1, TRAF6, TRAF3, TRAF2, TPO, AKR1C1, TPM3, DEFB1, CFD, TNFRSF1A, DIO3, TMSB4X, TSPY1, TTR, TXNRD1, SUMO1, UCN, UCP1, DHX9, UGP2, UQCRB, UTRN, DDX3X, VDAC1, VDR, VHL, VRK1, WEE1, WT1, H3C12, H3C10, H3C2, SOCS2, VCAN, CTAG1B, IER3, CTBS, CCN6, CFLAR, CTLA4, MAD1L1, IQGAP1, TRIM24, DLK1, FADD, ADAM9, CTNND1, EIF2B5, EIF2S2, AP1M1, CSE1L, BTRC, H3C7, P4HA2, SOCS3, TM4SF5, PKD2L1, PRC1, CLDN1, DIRAS3, LDB2, CRYZ, LATS1, SLC16A3, TNFSF13, RNGTT, EED, PARG, PLA2G6, SLC25A11, SPOP, TAGLN2, CYP2B6, GNPAT, DYRK2, CUL3, KLF11, RAE1, RGS5, MAP4K3, PPFIA1, PIK3R3, ENC1, TNFRSF25, IKBKG, LGR5, DENR, KMO, AKR7A2, RUVBL1, NCOA1, NUMB, CYP1B1, TNKS, EIF3I, PEA15, MARCO, TRADD, LAMTOR5
    • Liver Cancer Mayo_clinic
      Overview Liver cancer is cancer that begins in the cells of your liver. Your liver is a football-sized organ that sits in the upper right portion of your abdomen, beneath your diaphragm and above your stomach. Several types of cancer can form in the liver. The most common type of liver cancer is hepatocellular carcinoma, which begins in the main type of liver cell (hepatocyte). Other types of liver cancer, such as intrahepatic cholangiocarcinoma and hepatoblastoma, are much less common. Cancer that spreads to the liver is more common than cancer that begins in the liver cells.
  • Porphyria, Acute Intermittent Omim
    Whatley et al. (1999) reported a prospective comparison of direct automated sequencing of cDNA (in 29 patients) or genomic DNA (in 28 patients) to identify HMBS mutations in 57 patients referred consecutively for mutation analysis; 39 different mutations were identified in 54 patients. ... They identified 3 different disease haplotypes among 28 Swedish AIP families. The haplotype designated 2/1/1/2 was the most frequent, segregating with AIP in 10 of 28 families. ... Genealogic data showed that 12 of the 15 were related, suggesting a founder effect. In 28 Finnish families representing 72% of all AIP families in the Finnish population of 5 million, Kauppinen et al. (1995) found 19 separate mutations in HMBS: 13 novel mutations, including 1 de novo event, and 6 previously characterized mutations.
    HMBS, ALAS1, PPOX, PRSS1, AIP, CXCR5, SPINK1, CELA1, ALAD, HLA-DRB1, UROD, TNF, AMY2A, KRAS, LTBR, FOXP3, TLR4, LTA, IL33, CFTR, IFNA1, CALCA, IFNA13, PTX3, DEGS1, TFPI2, SCT, TP53, SKI, PPIG, THY1, TGM2, TGFB1, SST, SLC15A2, TLR2, ABCF1, KNTC1, PDPN, LOC102724971, LOC102723407, CCR2, MIR181D, MIR193B, MIR34A, MIR150, LOC390714, LINC01193, FCRL3, IL21, KRT20, TLR9, IL22, CD274, IGHV3-69-1, IGHV3OR16-7, SMUG1, LILRB1, MMRN1, NTRK1, PPBP, CRP, GC, FECH, ENO1, DPAGT1, DOCK3, CYP3A5, CYP2D6, CTLA4, CPOX, HLA-A, MS4A1, CAT, CALCB, CA2, B2M, ARSA, APOA2, ALAS2, H2AX, HLA-E, MED1, MGST3, POMC, PLAT, PKD1, PEBP1, NGF, MVD, ATP8, MST1, SMAD4, HSPE1, CYP4F3, LAIR1, KCNA3, IDO1, IL13, IL10, CXCL8, IFN1@, LOC105379528
    • Acute Intermittent Porphyria Gene_reviews
      Summary Clinical characteristics. Acute intermittent porphyria (AIP), an autosomal dominant disorder, occurs in heterozygotes for an HMBS pathogenic variant that causes reduced activity of the enzyme porphobilinogen deaminase. AIP is considered "overt" in a heterozygote who was previously or is currently symptomatic; AIP is considered "latent" in a heterozygote who has never had symptoms, and typically has been identified during molecular genetic testing of at-risk family members. Note that GeneReviews does not use the term "carrier" for an individual who is heterozygous for an autosomal dominant pathogenic variant; GeneReviews reserves the term "carrier" for an individual who is heterozygous for an autosomal recessive disorder and thus is not expected to ever develop manifestations of the disorder. Overt AIP is characterized clinically by life-threatening acute neurovisceral attacks of severe abdominal pain without peritoneal signs, often accompanied by nausea, vomiting, tachycardia, and hypertension. Attacks may be complicated by neurologic findings (mental changes, convulsions, and peripheral neuropathy that may progress to respiratory paralysis), and hyponatremia.
    • Acute Intermittent Porphyria Gard
      Acute intermittent porphyria (AIP) is one of the liver (hepatic) porphyrias . AIP is caused by low levels of porphobilinogen deaminase (PBGD), an enzyme also often called hydroxymethylbilane synthase. The low levels of PBGD are generally not sufficient to cause symptoms; however, activating factors such as hormones, drugs, and dietary changes may trigger symptoms. Although most individuals with AIP never develop symptoms, symptomatic individuals typically present with abdominal pain with nausea. Treatment is dependent on the symptoms.
    • Acute Intermittent Porphyria Orphanet
      A rare, severe form of the acute hepatic porphyrias characterized by the occurrence of neuro-visceral attacks without cutaneous manifestations. Clinical description Patients suffer intermittent neuro-visceral attacks that can persist for several days and that repeat over several weeks. These attacks manifest as intense abdominal pain (>95% of cases) and neurological and/or psychological symptoms. The abdominal pain is often associated with lumbago irradiating to the thighs, and with nausea, vomiting and relentless constipation. Psychological symptoms are variable: irritability, emotionality, depression, considerable anxiety and, more rarely, auditory and visual hallucinations, disorientation, mental confusion.
    • Acute Intermittent Porphyria Wikipedia
      Some individuals may be more likely to develop paresis based on increased susceptibility of neurons to toxins. [28] Diagnosis [ edit ] The initial diagnosis of acute porphyria is confirmed by urinalysis , including the common method, the Watson-Schwartz test .
  • Abortion In Queensland Wikipedia
    Aside from expanding the scope of the section 282 exemption from criminal liability, the amendments also allow women to self-administer abortifacients in accordance with a prescription. [21] 2016 child abortion case and Pyne bills [ edit ] In the 2016 Queensland Supreme Court case of Central Queensland Hospital and Health Service v Q , [23] Justice Duncan McMeekin authorised a 12-year-old girl to undergo an abortion due to the risk of self-harm and suicide. [24] [25] The case led abortion advocates to criticise the need for court involvement in such cases, with Larissa Waters and Rob Pyne arguing it demonstrated the need to change Queensland's abortion laws. [25] The girl's treating obstetrician David Macfarlane told a Queensland parliamentary inquiry into abortion law that the case set a precedent that young girls lacked capacity to give informed consent , injecting court involvement into situations that had earlier involved just the girl and medical staff. [26] The case led Labor-turned-independent politician Pyne to propose laws decriminalising abortion to the Queensland Parliament. [26] On 10 May 2016 Rob Pyne introduced the Abortion Law Reform (Woman's Right to Choose) Amendment Bill 2016 to remove abortion from the Criminal Code. [27] [28] The matter was referred to the Health, Communities, Disability Services and Domestic and Family Violence Prevention Committee, which also considered the termination of pregnancies in Queensland more broadly. [27] In August 2016 the Committee released its report, [29] recommending that the bill not be passed. The bill left several policy issues unregulated, including gestational limits, the rights of conscientious objectors and "safe access zones" near abortion providers. [8] To address the issues on which the first bill was silent, on 27 August 2016 Pyne introduced the Health (Abortion Law Reform) Amendment Bill 2016 . [30] This bill would amend the Health Act to require the approval of two doctors to terminate a pregnancy of 24 weeks or more, allow conscientious objection unless a woman's life was at risk and block abortion opponents from protesting within 50 metres of abortion clinics. [31] On 17 February 2017, the Committee issued its report with a split recommendation. [32] Liberal National Party members of the Committee raised concerns that if the second bill passed while the first failed, it would create legal confusion by subjecting abortion to conflicting criminal and health laws. [33] On 28 February 2017 Pyne withdrew both bills after the Liberal National Party of Queensland signalled that none of its members would vote for the proposed laws. [34] The Labor Government promised to refer the matter of abortion to the Queensland Law Reform Commission for its recommendations and to introduce new laws in its next term of government if elected. [34] 2018 legalisation [ edit ] Following the withdrawal of Pyne's bills, on 19 June 2017 Attorney-General Yvette D'Ath referred Queensland's pregnancy termination laws to the Queensland Law Reform Commission to review and recommend changes. [35] [36] On 21 December 2017, the Commission released a consultation paper [37] and called for submissions from the public. [38] The Commission produced its report in June 2018. [39] On 22 August 2018 the Termination of Pregnancy Bill was introduced to Parliament and referred to the Health, Communities, Disability Services and Domestic and Family Violence Prevention Committee for consideration. [40] The bill's Explanatory Notes outlined the proposed changes and noted they were informed by the Commission's report. [41] On 5 October 2018 the Committee's report was tabled, recommending that the law be passed and that all politicians be granted a conscience vote. [42] [43] The Queensland Parliament set aside three sitting days commencing 16 October 2018 to debate the proposed law. [44] Both the Labor Party and Liberal National Party allowed their members a conscience vote on the issue. [45] Politicians spoke emotionally and passionately both for and against the bill. [46] [47] [48] The conscience vote split largely along party lines, with almost all members of the governing Labor Party voting in favour except Jo-Ann Miller who voted against and Linus Power who abstained. ... Retrieved 13 November 2018 . ^ a b O'Brien, Chris (28 February 2017). "Queensland abortion decriminalisation bills withdrawn" . ... News.com.au . News Corp Australia . Retrieved 28 November 2018 . ^ "Termination of Pregnancy Act 2018" . legislation.qld.gov.au . ^ "Proclamation made under the Termination of Pregnancy Act 2018" . legislation.qld.gov.au . ^ "Termination of Pregnancy Bill 2018 – Third Reading" (PDF) .
  • Diving Disorders Wikipedia
    Divers may develop this condition for several possible reasons: Increased work of breathing due to increased density of the breathing das with depth. [26] [27] [28] [29] Inadequate ventilatory response to exertion. [26] [27] [28] [29] Dead space of the breathing apparatus. [29] Higher inspired CO 2 due to failure of the carbon dioxide scrubber in the diver's rebreather to remove sufficient carbon dioxide from the loop. ... South Pacific Underwater Medicine Society Journal . 28 (1). ISSN 0813-1988 . OCLC 16986801 . ... The American Journal of Emergency Medicine . 28 (8): 941–6. doi : 10.1016/j.ajem.2009.08.004 . ... Alert Diver . Divers Alert Network . Retrieved 28 February 2017 . ^ Ernest S Campbell, MD, FACS.
  • Unsafe Abortion Wikipedia
    Incomplete abortions were the leading cause for OB-GYN services across the United States. [28] In the 1960s, the National Opinion Research Center found that hundreds of women were attempting to self-abort with coat hangers, knitting needles and ballpoint pens, and by swallowing toxic chemicals like bleach and laundry detergent. [28] However, the number of deaths declined significantly into the 1960s and 1970s. ... PMID 9194245 . ^ a b "Preventing unsafe abortion" . WHO . Retrieved 2014-03-28 . ^ "New findings from the WHO Multicountry Survey on Maternal and Newborn Health" . WHO . Retrieved 2014-03-28 . ^ Sedgh G, Henshaw S, Singh S, Ahman E, Shah IH (October 2007).
  • Abortion Wikipedia
    In some areas abortion is legal only in specific cases such as rape , problems with the fetus , poverty , risk to a woman's health, or incest . [24] There is debate over the moral, ethical, and legal issues of abortion. [25] [26] Those who oppose abortion often argue that an embryo or fetus is a human with a right to life , and they may compare abortion to murder . [27] [28] Those who support the legality of abortion often hold that it is part of a woman's right to make decisions about her own body . [29] Others favor legal and accessible abortion as a public health measure. [30] Contents 1 Types 1.1 Induced 1.2 Spontaneous 2 Methods 2.1 Medical 2.2 Surgical 2.3 Labor induction abortion 2.4 Other methods 3 Safety 3.1 Mental health 3.2 Unsafe abortion 4 Incidence 4.1 Gestational age and method 5 Motivation 5.1 Personal 5.2 Societal 5.3 Maternal and fetal health 5.3.1 Cancer 6 History and religion 7 Society and culture 7.1 Abortion debate 7.2 Modern abortion law 7.3 Sex-selective abortion 7.4 Anti-abortion violence 8 Other animals 9 Notes 10 References 11 Bibliography 12 External links Types Induced Approximately 205 million pregnancies occur each year worldwide. ... D&C Intact D&X Mifepr. Induced Miscarr. 0–12 wks 12–28 weeks 28–40 wks Gestational age may determine which abortion methods are practiced. ... It has been estimated that the incidence of unsafe abortion could be reduced by up to 75% (from 20 million to 5 million annually) if modern family planning and maternal health services were readily available globally. [139] Rates of such abortions may be difficult to measure because they can be reported variously as miscarriage, "induced miscarriage", "menstrual regulation", "mini-abortion", and "regulation of a delayed/suspended menstruation". [140] [141] Forty percent of the world's women are able to access therapeutic and elective abortions within gestational limits, [22] while an additional 35 percent have access to legal abortion if they meet certain physical, mental, or socioeconomic criteria. [24] While maternal mortality seldom results from safe abortions, unsafe abortions result in 70,000 deaths and 5 million disabilities per year. [15] Complications of unsafe abortion account for approximately an eighth of maternal mortalities worldwide, [142] though this varies by region. [143] Secondary infertility caused by an unsafe abortion affects an estimated 24 million women. [131] The rate of unsafe abortions has increased from 44% to 49% between 1995 and 2008. [19] Health education, access to family planning, and improvements in health care during and after abortion have been proposed to address this phenomenon. [144] Incidence There are two commonly used methods of measuring the incidence of abortion: Abortion rate – number of abortions annually per 1000 women between 15 and 44 years of age Abortion percentage – number of abortions out of 100 known pregnancies (pregnancies include live births, abortions and miscarriages) In many places, where abortion is illegal or carries a heavy social stigma, medical reporting of abortion is not reliable. [130] For this reason, estimates of the incidence of abortion must be made without determining certainty related to standard error. [19] The number of abortions performed worldwide seems to have remained stable in recent years, with 41.6 million having been performed in 2003 and 43.8 million having been performed in 2008. [19] The abortion rate worldwide was 28 per 1000 women per year, though it was 24 per 1000 women per year for developed countries and 29 per 1000 women per year for developing countries. [19] The same 2012 study indicated that in 2008, the estimated abortion percentage of known pregnancies was at 21% worldwide, with 26% in developed countries and 20% in developing countries. [19] On average, the incidence of abortion is similar in countries with restrictive abortion laws and those with more liberal access to abortion. [145] However, restrictive abortion laws are associated with increases in the percentage of abortions performed unsafely. [22] [146] [145] The unsafe abortion rate in developing countries is partly attributable to lack of access to modern contraceptives; according to the Guttmacher Institute , providing access to contraceptives would result in about 14.5 million fewer unsafe abortions and 38,000 fewer deaths from unsafe abortion annually worldwide. [147] The rate of legal, induced abortion varies extensively worldwide.
  • Abortion In The United Kingdom Wikipedia
    The Northern Ireland Parliament was suspended in 1972 and direct rule from Westminster continued until the devolution of a range of powers, including health, to the Northern Ireland Assembly in 1999. [28] [29] Criminal law, including abortion, continued to be reserved to Westminster until the devolution of policing and justice powers in 2010. [30] Between 1993 and 1999, a series of court cases interpreted the law as also allowing for abortion in cases where, for the pregnant woman, "there is a risk of real and serious adverse effect on her physical or mental health, which is either long term or permanent". [31] Statute law [ edit ] The law on abortion in Northern Ireland was radically changed by the Northern Ireland (Executive Formation etc) Act 2019 . ... This reflected fetal viability in the United Kingdom at the time of the legislation and the relevant law has not been amended since 1945. [52] In 2017–2018, a total of 81 children in Northern Ireland were born alive at less than 28 weeks of gestation. [53] The repeal of sections 58 and 59—without replacement—decriminalised the following actions, in situations where a pregnancy has not reached 28 weeks of gestation: a woman administering drugs, or using an instrument or "other means whatsoever", with intent to cause (procure) her own miscarriage ; [54] any person (whosoever) taking any of the same actions with intent to cause the miscarriage of any woman (including cases with no consent from the pregnant woman ); [54] or any person supplying or procuring drugs, any instrument or anything whatsoever, with intent to cause the miscarriage of any woman. [55] The law provides for wider access to abortion than in Great Britain, where abortions are generally permitted up to 24 weeks of gestation. [56] Sections 58 and 59 have remained part of the law in England and Wales. [57] The intention of the Act, when it was passed by Parliament, was to consolidate and amend the statute law of England and Ireland relating to offences against the person. [58] On 21 October 2019, as a result of the Northern Ireland Assembly not being restored, sections 58 and 59 of the Offences Against the Person Act 1861 were repealed, decriminalising abortion. [59] On 25 March 2020, The Abortion (Northern Ireland) Regulations 2020 were laid before the Assembly; since 31 March 2020, the regulations make provision for abortion in Northern Ireland. [3] [60] [61] Hospital access to abortions [ edit ] On 24 May 2012, the Northern Ireland Department of Health issued an order requiring an audit of clinical coding regarding abortion in health and social care hospitals. [62] On 23 January 2019, the Northern Ireland Department of Health revealed that 12 abortions were performed in Northern Ireland hospitals between 2017 and 2018. [63] On 22 January 2020, it was revealed that hospitals in Northern Ireland were able to perform eight abortions between 2018 and 2019. [64] Current regulations [ edit ] On 25 March 2020, Northern Ireland published the changes to the abortion law. [65] This law permits abortion on demand for the first 12 weeks of pregnancy, since 31 March 2020. [66] [67] However, mirroring abortion laws in other United Kingdom countries, there is no time limit on abortions which involve risk of injury to the woman's physical or mental health, rape or incest, or fatal fetal abnormalities. [66] [67] Political party positions [ edit ] The positions of the political parties contesting elections in Northern Ireland regarding abortion can be summarised as follows: Democratic Unionist Party (DUP), Traditional Unionist Voice (TUV), Aontú – opposed to abortion; Social Democratic and Labour Party (SDLP) – anti-abortion with conscience vote; [68] Ulster Unionist Party (UUP), Alliance Party , Conservative – conscience vote (i.e. no formal party position); Sinn Féin – abortion to be available "where a woman’s life, health or mental health is at risk and in cases of fatal foetal abnormality" and "without specific indication ... through a GP led service in a clinical context as determined by law and licensing practice for a limited gestational period"; [69] Green Party – decriminalisation of abortion (i.e. abortion being available for any reason). [70] Abortion policy is regularly an issue of political debate in Northern Ireland. ... This was to close a lacuna in the law, identified by Lord Darling, which allowed for infants to be killed during birth, which would mean that the perpetrator could neither be prosecuted for abortion or murder. [103] There was included in the Act the presumption that all children in utero over 28 weeks' gestation were capable of being born alive. ... Human Fertilisation and Embryology Act 1990 [ edit ] Changes to the Abortion Act 1967 were introduced in Parliament through the Human Fertilisation and Embryology Act 1990 . The time limits were lowered from 28 to 24 weeks for most cases on the grounds that medical technology had advanced sufficiently to justify the change. ... Asked if a woman wants an abortion, she should not have to continue with her pregnancy: 53% agreed 15% agreed very strongly 12% agreed strongly 27% agreed 22% neither agreed nor disagreed 17% disagreed 8% disagreed 3% disagreed strongly 5% disagreed very strongly 5% did not know 3% preferred not to answer Asked if too many women do not think hard enough before having an abortion: 37% agreed 8% agreed very strongly 8% agreed strongly 21% agreed 26% Neither agreed nor disagreed 28% Disagreed 16% Disagreed 7% Disagreed strongly 5% Disagreed very strongly 6% Did not know 3% Preferred not to answer Asked if it should be made more difficult for women to obtain abortions 23% Agreed 7% agreed very strongly 4% agreed strongly 12% agreed 23% neither agreed nor disagreed 46% disagreed 25% disagreed 9% disagreed strongly 12% disagreed very strongly 6% did not know 2% preferred not to answer Approved methods [ edit ] Methodology is time-related.
  • Electromagnetic Hypersensitivity Wikipedia
    More women believed to be electromagnetically hypersensitive than men. [23] Society and culture [ edit ] In 2010, a cell tower operator in South Africa revealed at a public meeting that the tower that nearby residents were blaming for their current EHS symptoms had been turned off over six weeks prior to the meeting, thus making it a highly unlikely cause of EHS symptoms. [27] [28] In February 2014, the UK Advertising Standards Authority found that claims of harm from electromagnetic radiation, made in a product advertisement, were unsubstantiated and misleading. [10] People have filed lawsuits to try to win damages due to harm claimed from electromagnetic radiation. ... "Prevalence of self-reported hypersensitivity to electric or magnetic fields in a population-based questionnaire survey" . Scand J Work Environ Health . 28 (1): 33–41. doi : 10.5271/sjweh.644 . ... "Development and evaluation of the electromagnetic hypersensitivity questionnaire". Bioelectromagnetics . 28 (2): 137–151. doi : 10.1002/bem.20279 . ... Retrieved 31 December 2016 . ^ a b Barrett, Stephen (August 28, 2015). " " Electromagnetic Hypersensitivity" Is Not a Valid Diagnosis" .
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