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Hepatocellular carcinoma(HCC)

MedGen UID:
389187
Concept ID:
C2239176
Neoplastic Process
Synonyms: HCC; Hepatocellular cancer; Hepatoma; LIVER CELL CARCINOMA; Primary carcinoma of liver
SNOMED CT: Primary carcinoma of liver (187769009); Hepatocarcinoma (109841003); Hepatocellular carcinoma (109841003); Malignant hepatoma (109841003); HCC - Hepatocellular carcinoma (109841003); LCC - Liver cell carcinoma (109841003); Liver cell carcinoma (109841003); Liver carcinoma (109841003); Hepatocellular carcinoma (25370001); Liver cell carcinoma (25370001); Hepatocarcinoma (25370001); Hepatoma, malignant (25370001); Hepatoma (25370001); Primary liver cell carcinoma (1186630006); Primary liver carcinoma (1186630006); Primary hepatocarcinoma (1186630006); Primary malignant hepatoma (1186630006); Primary hepatocellular carcinoma (1186630006)
Modes of inheritance:
Not genetically inherited
MedGen UID:
988794
Concept ID:
CN307044
Finding
Source: Orphanet
clinical entity without genetic inheritance.
 
Genes (locations): APC (5q22.2); AXIN1 (16p13.3); CASP8 (2q33.1); CTNNB1 (3p22.1); IGF2R (6q25.3); MET (7q31.2); PDGFRL (8p22); PIK3CA (3q26.32); TP53 (17p13.1)
 
HPO: HP:0001402
Monarch Initiative: MONDO:0007256
OMIM®: 114550
Orphanet: ORPHA88673

Definition

Hepatocellular carcinoma is the major histologic type of malignant primary liver neoplasm. It is the fifth most common cancer and the third most common cause of death from cancer worldwide. The major risk factors for HCC are chronic hepatitis B virus (HBV) infection, chronic hepatitis C virus (HCV) infection, prolonged dietary aflatoxin exposure, alcoholic cirrhosis, and cirrhosis due to other causes. Hepatoblastomas comprise 1 to 2% of all malignant neoplasms of childhood, most often occurring in children under 3 years of age. Hepatoblastomas are thought to be derived from undifferentiated hepatocytes (Taniguchi et al., 2002). [from OMIM]

Clinical features

From HPO
Hepatocellular carcinoma
MedGen UID:
389187
Concept ID:
C2239176
Neoplastic Process
Hepatocellular carcinoma is the major histologic type of malignant primary liver neoplasm. It is the fifth most common cancer and the third most common cause of death from cancer worldwide. The major risk factors for HCC are chronic hepatitis B virus (HBV) infection, chronic hepatitis C virus (HCV) infection, prolonged dietary aflatoxin exposure, alcoholic cirrhosis, and cirrhosis due to other causes. Hepatoblastomas comprise 1 to 2% of all malignant neoplasms of childhood, most often occurring in children under 3 years of age. Hepatoblastomas are thought to be derived from undifferentiated hepatocytes (Taniguchi et al., 2002).
Micronodular cirrhosis
MedGen UID:
75640
Concept ID:
C0267812
Disease or Syndrome
A type of cirrhosis characterized by the presence of small regenerative nodules.
Subacute progressive viral hepatitis
MedGen UID:
349389
Concept ID:
C1861901
Finding

Term Hierarchy

CClinical test,  RResearch test,  OOMIM,  GGeneReviews,  VClinVar  
  • CROGVHepatocellular carcinoma
Follow this link to review classifications for Hepatocellular carcinoma in Orphanet.

Conditions with this feature

Wilson disease
MedGen UID:
42426
Concept ID:
C0019202
Disease or Syndrome
Wilson disease is a disorder of copper metabolism that can present with hepatic, neurologic, or psychiatric disturbances, or a combination of these, in individuals ranging from age three years to older than 50 years; symptoms vary among and within families. Liver disease includes recurrent jaundice, simple acute self-limited hepatitis-like illness, autoimmune-type hepatitis, fulminant hepatic failure, or chronic liver disease. Neurologic presentations include movement disorders (tremors, poor coordination, loss of fine-motor control, chorea, choreoathetosis) or rigid dystonia (mask-like facies, rigidity, gait disturbance, pseudobulbar involvement). Psychiatric disturbance includes depression, neurotic behaviors, disorganization of personality, and, occasionally, intellectual deterioration. Kayser-Fleischer rings, frequently present, result from copper deposition in Descemet's membrane of the cornea and reflect a high degree of copper storage in the body.
Acute intermittent porphyria
MedGen UID:
56452
Concept ID:
C0162565
Disease or Syndrome
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 attacks, which may be provoked by certain drugs, alcoholic beverages, endocrine factors, calorie restriction, stress, and infections, usually resolve within two weeks. Most individuals with AIP have one or a few attacks; about 3%-8% (mainly women) have recurrent attacks (defined as >3 attacks/year) that may persist for years. Other long-term complications are chronic renal failure, hepatocellular carcinoma (HCC), and hypertension. Attacks, which are very rare before puberty, are more common in women than men. Latent AIP. While all individuals heterozygous for an HMBS pathogenic variant that predisposes to AIP are at risk of developing overt AIP, most have latent AIP and never have symptoms.
X-linked agammaglobulinemia
MedGen UID:
65123
Concept ID:
C0221026
Disease or Syndrome
X-linked agammaglobulinemia (XLA) is characterized by recurrent bacterial infections in affected males in the first two years of life. Recurrent otitis is the most common infection prior to diagnosis. Conjunctivitis, sinopulmonary infections, diarrhea, and skin infections are also frequently seen. Approximately 60% of individuals with XLA are recognized as having immunodeficiency when they develop a severe, life-threatening infection such as pneumonia, empyema, meningitis, sepsis, cellulitis, or septic arthritis. S pneumoniae and H influenzae are the most common organisms found prior to diagnosis and may continue to cause sinusitis and otitis after diagnosis and the initiation of gammaglobulin substitution therapy. Severe, difficult-to-treat enteroviral infections (often manifest as dermatomyositis or chronic meningoencephalitis) can be prevented by this treatment. The prognosis for individuals with XLA has improved markedly in the last 25 years as a result of earlier diagnosis, the development of preparations of gammaglobulin that allow normal concentrations of serum IgG to be achieved, and more liberal use of antibiotics.
Alpha-1-antitrypsin deficiency
MedGen UID:
67461
Concept ID:
C0221757
Disease or Syndrome
Alpha-1 antitrypsin deficiency (AATD) can present with hepatic dysfunction in individuals from infancy to adulthood and with chronic obstructive lung disease (emphysema and/or bronchiectasis), characteristically in individuals older than age 30 years. Individuals with AATD are also at increased risk for panniculitis (migratory, inflammatory, tender skin nodules which may ulcerate on legs and lower abdomen) and C-ANCA-positive vasculitis (granulomatosis with polyangiitis). Phenotypic expression varies within and between families. In adults, smoking is the major factor in accelerating the development of COPD; nonsmokers may have a normal life span, but can also develop lung and/or liver disease. Although reported, emphysema in children with AATD is extremely rare. AATD-associated liver disease, which is present in only a small portion of affected children, manifests as neonatal cholestasis. The incidence of liver disease increases with age. Liver disease in adults (manifesting as cirrhosis and fibrosis) may occur in the absence of a history of neonatal or childhood liver disease. The risk for hepatocellular carcinoma (HCC) is increased in individuals with AATD.
Glucose-6-phosphate transport defect
MedGen UID:
78644
Concept ID:
C0268146
Disease or Syndrome
Glycogen storage disease type I (GSDI) is characterized by accumulation of glycogen and fat in the liver and kidneys resulting in hepatomegaly and nephromegaly. Severely affected infants present in the neonatal period with severe hypoglycemia due to fasting intolerance. More commonly, untreated infants present at age three to four months with hepatomegaly, severe hypoglycemia with or without seizures, lactic acidosis, hyperuricemia, and hypertriglyceridemia. Affected children typically have doll-like faces with full cheeks, relatively thin extremities, short stature, and a protuberant abdomen. Xanthoma and diarrhea may be present. Impaired platelet function and development of reduced or dysfunctional von Willebrand factor can lead to a bleeding tendency with frequent epistaxis and menorrhagia in females. Individuals with untreated GSDIb are more likely to develop impaired neutrophil and monocyte function as well as chronic neutropenia resulting in recurrent bacterial infections, gingivitis, periodontitis, and genital and intestinal ulcers. Long-term complications of untreated GSDI include short stature, osteoporosis, delayed puberty, renal disease (including proximal and distal renal tubular acidosis, renal stones, and renal failure), gout, systemic hypertension, pulmonary hypertension, hepatic adenomas with potential for malignancy, pancreatitis, and polycystic ovaries. Seizures and cognitive impairment may occur in individuals with prolonged periods of hypoglycemia. Normal growth and puberty are expected in treated children. Most affected individuals live into adulthood.
Familial porphyria cutanea tarda
MedGen UID:
75669
Concept ID:
C0268323
Disease or Syndrome
Familial porphyria cutanea tarda (F-PCT) is characterized by: skin findings including blistering over the dorsal aspects of the hands and other sun-exposed areas of skin, skin friability after minor trauma, facial hypertrichosis and hyperpigmentation, and severe thickening of affected skin areas (pseudoscleroderma); and an increased risk for hepatocellular carcinoma (HCC).
Tyrosinemia type I
MedGen UID:
75688
Concept ID:
C0268490
Disease or Syndrome
Untreated tyrosinemia type I usually presents either in young infants with severe liver involvement or later in the first year with liver dysfunction and renal tubular dysfunction associated with growth failure and rickets. Untreated children may have repeated, often unrecognized, neurologic crises lasting one to seven days that can include change in mental status, abdominal pain, peripheral neuropathy, and/or respiratory failure requiring mechanical ventilation. Death in the untreated child usually occurs before age ten years, typically from liver failure, neurologic crisis, or hepatocellular carcinoma. Combined treatment with nitisinone and a low-tyrosine diet has resulted in a greater than 90% survival rate, normal growth, improved liver function, prevention of cirrhosis, correction of renal tubular acidosis, and improvement in secondary rickets.
Phosphate transport defect
MedGen UID:
87455
Concept ID:
C0342749
Disease or Syndrome
Glycogenosis due to glucose-6-phosphatase deficiency (G6P) type b, or glycogen storage disease (GSD) type 1b, is a type of glycogenosis due to G6P deficiency (see this term).
Budd-Chiari syndrome
MedGen UID:
163632
Concept ID:
C0856761
Disease or Syndrome
Budd-Chiari syndrome (BCS) is caused by obstruction of hepatic venous outflow at any level from the small hepatic veins to the junction of the inferior vena cava (IVC) with the right atrium, 1 and occurs in 1/100,000 of the general population worldwide. The most common presentation is with ascites, but can range from fulminant hepatic failure (FHF) to asymptomatic forms. Obstruction of hepatic venous outflow is mainly caused by primary intravascular thrombosis, which can occur suddenly or be repeated over time, accompanied by some revascularization, accounting for the variable parenchymal hepatic damage and histologic presentation. Budd-Chiari syndrome is thus a disease, but since it occurs as a manifestation of several other diseases, this term is kept for the present for convenience.
Navajo neurohepatopathy
MedGen UID:
338045
Concept ID:
C1850406
Disease or Syndrome
MPV17-related mitochondrial DNA (mtDNA) maintenance defect presents in the vast majority of affected individuals as an early-onset encephalohepatopathic (hepatocerebral) disease that is typically associated with mtDNA depletion, particularly in the liver. A later-onset neuromyopathic disease characterized by myopathy and neuropathy, and associated with multiple mtDNA deletions in muscle, has also rarely been described. MPV17-related mtDNA maintenance defect, encephalohepatopathic form is characterized by: Hepatic manifestations (liver dysfunction that typically progresses to liver failure, cholestasis, hepatomegaly, and steatosis); Neurologic involvement (developmental delay, hypotonia, microcephaly, and motor and sensory peripheral neuropathy); Gastrointestinal manifestations (gastrointestinal dysmotility, feeding difficulties, and failure to thrive); and Metabolic derangements (lactic acidosis and hypoglycemia). Less frequent manifestations include renal tubulopathy, nephrocalcinosis, and hypoparathyroidism. Progressive liver disease often leads to death in infancy or early childhood. Hepatocellular carcinoma has been reported.
Citrullinemia type II
MedGen UID:
350276
Concept ID:
C1863844
Disease or Syndrome
Citrin deficiency can manifest in newborns or infants as neonatal intrahepatic cholestasis caused by citrin deficiency (NICCD), in older children as failure to thrive and dyslipidemia caused by citrin deficiency (FTTDCD), and in adults as recurrent hyperammonemia with neuropsychiatric symptoms in citrullinemia type II (CTLN2). Often citrin deficiency is characterized by strong preference for protein-rich and/or lipid-rich foods and aversion to carbohydrate-rich foods. NICCD. Children younger than age one year have a history of low birth weight with growth restriction and transient intrahepatic cholestasis, hepatomegaly, diffuse fatty liver, and parenchymal cellular infiltration associated with hepatic fibrosis, variable liver dysfunction, hypoproteinemia, decreased coagulation factors, hemolytic anemia, and/or hypoglycemia. NICCD is generally not severe and symptoms often resolve by age one year with appropriate treatment, although liver transplantation has been required in rare instances. FTTDCD. Beyond age one year, many children with citrin deficiency develop a protein-rich and/or lipid-rich food preference and aversion to carbohydrate-rich foods. Clinical abnormalities may include growth restriction, hypoglycemia, pancreatitis, severe fatigue, anorexia, and impaired quality of life. Laboratory changes are dyslipidemia, increased lactate-to-pyruvate ratio, higher levels of urinary oxidative stress markers, and considerable deviation in tricarboxylic acid (TCA) cycle metabolites. One or more decades later, some individuals with NICCD or FTTDCD develop CTLN2. CTLN2. Presentation is sudden and usually between ages 20 and 50 years. Manifestations are recurrent hyperammonemia with neuropsychiatric symptoms including nocturnal delirium, aggression, irritability, hyperactivity, delusions, disorientation, restlessness, drowsiness, loss of memory, flapping tremor, convulsive seizures, and coma. Symptoms are often provoked by alcohol and sugar intake, medication, and/or surgery. Affected individuals may or may not have a prior history of NICCD or FTTDCD.
Alagille syndrome due to a JAG1 point mutation
MedGen UID:
365434
Concept ID:
C1956125
Disease or Syndrome
Alagille syndrome (ALGS) is a multisystem disorder with a wide spectrum of clinical variability; this variability is seen even among individuals from the same family. The major clinical manifestations of ALGS are bile duct paucity on liver biopsy, cholestasis, congenital cardiac defects (primarily involving the pulmonary arteries), butterfly vertebrae, ophthalmologic abnormalities (most commonly posterior embryotoxon), and characteristic facial features. Renal abnormalities, growth failure, developmental delays, splenomegaly, and vascular abnormalities may also occur.
Hepatocellular carcinoma
MedGen UID:
389187
Concept ID:
C2239176
Neoplastic Process
Hepatocellular carcinoma is the major histologic type of malignant primary liver neoplasm. It is the fifth most common cancer and the third most common cause of death from cancer worldwide. The major risk factors for HCC are chronic hepatitis B virus (HBV) infection, chronic hepatitis C virus (HCV) infection, prolonged dietary aflatoxin exposure, alcoholic cirrhosis, and cirrhosis due to other causes. Hepatoblastomas comprise 1 to 2% of all malignant neoplasms of childhood, most often occurring in children under 3 years of age. Hepatoblastomas are thought to be derived from undifferentiated hepatocytes (Taniguchi et al., 2002).
Glycogen storage disease due to glucose-6-phosphatase deficiency type IA
MedGen UID:
415885
Concept ID:
C2919796
Disease or Syndrome
Glycogen storage disease type I (GSDI) is characterized by accumulation of glycogen and fat in the liver and kidneys resulting in hepatomegaly and nephromegaly. Severely affected infants present in the neonatal period with severe hypoglycemia due to fasting intolerance. More commonly, untreated infants present at age three to four months with hepatomegaly, severe hypoglycemia with or without seizures, lactic acidosis, hyperuricemia, and hypertriglyceridemia. Affected children typically have doll-like faces with full cheeks, relatively thin extremities, short stature, and a protuberant abdomen. Xanthoma and diarrhea may be present. Impaired platelet function and development of reduced or dysfunctional von Willebrand factor can lead to a bleeding tendency with frequent epistaxis and menorrhagia in females. Individuals with untreated GSDIb are more likely to develop impaired neutrophil and monocyte function as well as chronic neutropenia resulting in recurrent bacterial infections, gingivitis, periodontitis, and genital and intestinal ulcers. Long-term complications of untreated GSDI include short stature, osteoporosis, delayed puberty, renal disease (including proximal and distal renal tubular acidosis, renal stones, and renal failure), gout, systemic hypertension, pulmonary hypertension, hepatic adenomas with potential for malignancy, pancreatitis, and polycystic ovaries. Seizures and cognitive impairment may occur in individuals with prolonged periods of hypoglycemia. Normal growth and puberty are expected in treated children. Most affected individuals live into adulthood.
Cholestasis, progressive familial intrahepatic, 4
MedGen UID:
418976
Concept ID:
C2931067
Disease or Syndrome
Any progressive familial intrahepatic cholestasis in which the cause of the disease is a mutation in the TJP2 gene.
Hemochromatosis type 1
MedGen UID:
854011
Concept ID:
C3469186
Disease or Syndrome
HFE hemochromatosis is characterized by inappropriately high absorption of iron by the small intestinal mucosa. The phenotypic spectrum of HFE hemochromatosis includes: Persons with clinical HFE hemochromatosis, in whom manifestations of end-organ damage secondary to iron overload are present; Individuals with biochemical HFE hemochromatosis, in whom transferrin-iron saturation is increased and the only evidence of iron overload is increased serum ferritin concentration; and Non-expressing p.Cys282Tyr homozygotes, in whom neither clinical manifestations of HFE hemochromatosis nor iron overload are present. Clinical HFE hemochromatosis is characterized by excessive storage of iron in the liver, skin, pancreas, heart, joints, and anterior pituitary gland. In untreated individuals, early symptoms include: abdominal pain, weakness, lethargy, weight loss, arthralgias, diabetes mellitus; and increased risk of cirrhosis when the serum ferritin is higher than 1,000 ng/mL. Other findings may include progressive increase in skin pigmentation, congestive heart failure, and/or arrhythmias, arthritis, and hypogonadism. Clinical HFE hemochromatosis is more common in men than women.
Progressive familial intrahepatic cholestasis type 2
MedGen UID:
483742
Concept ID:
C3489789
Disease or Syndrome
The phenotypic spectrum of ATP8B1 deficiency ranges from severe through moderate to mild. Severe ATP8B1 deficiency is characterized by infantile-onset cholestasis that progresses to cirrhosis, hepatic failure, and early death. Although mild-to-moderate ATP8B1 deficiency initially was thought to involve intermittent symptomatic cholestasis with a lack of hepatic fibrosis, it is now known that hepatic fibrosis may be present early in the disease course. Furthermore, in some persons with ATP8B1 deficiency the clinical findings can span the phenotypic spectrum, shifting over time from the mild end of the spectrum (episodic cholestasis) to the severe end of the spectrum (persistent cholestasis). Sensorineural hearing loss (SNHL) is common across the phenotypic spectrum.
Progeroid features-hepatocellular carcinoma predisposition syndrome
MedGen UID:
863898
Concept ID:
C4015461
Disease or Syndrome
Ruijs et al. (2003) reported a Moroccan boy with a chromosomal breakage who died of hepatocellular carcinoma at age 17 years. The boy was noted to have growth retardation at age 3 years; at age 7 he was found to have thoracic kyphosis, frontal bossing, and a delayed bone age of approximately 3 years. He underwent surgery for severe bilateral posterior subcapsular cataracts at age 14. Examination at age 15 showed short stature and low weight, with premature graying of scalp hair, small frontotemporal diameter, small deep-set eyes, bulbous nose with high nasal bridge, small upper lip, and micrognathia. In addition, he had thoracic kyphoscoliosis, sloping shoulders, mild pectus excavatum, moderate bilateral contractures of both elbows, bilateral clinodactyly, and pes planus. At age 17, he developed abdominal pain, and ultrasonography revealed a liver mass; biopsy confirmed hepatocellular carcinoma. Because of the advanced stage, no treatment was possible, and he died 2 months later. Although his parents were not known to be consanguineous, they originated from the same small Moroccan village. Lessel et al. (2014) studied 2 brothers from a nonconsanguineous Australian family of European ancestry who exhibited low body weight, micrognathia, triangular face, muscular atrophy, lipodystrophy, bilateral simian creases, delayed bone age, and mild joint restrictions in the fingers and elbows. In addition, both brothers developed early-onset hepatocellular carcinoma, at ages 16 and 14 years, respectively. The older brother died at age 18 from complications of acute fulminant hepatic failure. Analysis of patient tumor biopsies showed strong focal accumulations of cancer biomarkers as well as a high proliferative index compared to healthy liver or to cells from idiopathic hepatocellular carcinoma.
Silver-Russell syndrome 1
MedGen UID:
1718472
Concept ID:
C5393125
Disease or Syndrome
Silver-Russell Syndrome (SRS) is typically characterized by asymmetric gestational growth restriction resulting in affected individuals being born small for gestational age, with relative macrocephaly at birth (head circumference =1.5 SD above birth weight and/or length), prominent forehead usually with frontal bossing, and frequently body asymmetry. This is followed by postnatal growth failure, and in some cases progressive limb length discrepancy and feeding difficulties. Additional clinical features include triangular facies, fifth-finger clinodactyly, and micrognathia with narrow chin. Except for the limb length asymmetry, the growth failure is proportionate and head growth normal. The average adult height in untreated individuals is ~3.1±1.4 SD below the mean. The Netchine-Harbison Clinical Scoring System (NH-CSS) is a sensitive diagnostic scoring system. Clinical diagnosis can be established in an individual who meets at least four of the NH-CSS clinical criteria – prominent forehead/frontal bossing and relative macrocephaly at birth plus two additional findings – and in whom other disorders have been ruled out.
Portal hypertension, noncirrhotic, 2
MedGen UID:
1794158
Concept ID:
C5561948
Disease or Syndrome
Noncirrhotic portal hypertension-2 (NCPH2) is an autosomal recessive disorder characterized by signs of liver dysfunction that become apparent in the first decades of life. Affected individuals have jaundice, hyperbilirubinemia, pancytopenia, including neutropenia, lymphopenia, and thrombocytopenia, hepatosplenomegaly, and esophageal varices. Some patients may have recurrent infections or features suggestive of an immunodeficiency. Liver biopsy is notable for the absence of cirrhosis and the presence of nodular regeneration. Liver sinusoidal endothelial cells (LSECs) have abnormal expression of CD34 (142230) (summary by Drzewiecki et al., 2021). For a discussion of genetic heterogeneity of NCPH, see 617068.
HEPATORENOCARDIAC DEGENERATIVE FIBROSIS
MedGen UID:
1808950
Concept ID:
C5676996
Disease or Syndrome
Hepatorenocardiac degenerative fibrosis (HRCDF) is a primarily fibrotic disease affecting the liver, kidney, and heart, with considerable variability in disease onset and expression. Affected individuals develop degenerative hepatic fibrosis in childhood or early adulthood, with variable later onset of fibrocystic kidney disease and hypertrophic cardiomyopathy (Devane et al., 2022).

Recent clinical studies

Etiology

Tang Y, Zhang H, Chen L, Zhang T, Xu N, Huang Z
Int J Mol Sci 2022 Nov 5;23(21) doi: 10.3390/ijms232113590. PMID: 36362375Free PMC Article
Deng R, Lu X, Hong C, Cai R, Wang P, Xiong L, Wang X, Chen Q, Lin J
J Transl Med 2022 Oct 23;20(1):485. doi: 10.1186/s12967-022-03690-3. PMID: 36274132Free PMC Article
Spearman CW, Dusheiko G, Jonas E, Abdo A, Afihene M, Cunha L, Desalegn H, Kassianides C, Katsidzira L, Kramvis A, Lam P, Lesi OA, Micah EA, Musabeyezu E, Ndow G, Nnabuchi CV, Ocama P, Okeke E, Rwegasha J, Shewaye AB, Some FF, Tzeuton C, Sonderup MW; Gastroenterology and Hepatology Association of sub-Saharan Africa (GHASSA).
Lancet Gastroenterol Hepatol 2022 Nov;7(11):1036-1048. Epub 2022 Jul 8 doi: 10.1016/S2468-1253(22)00041-3. PMID: 35810766
Bhushan S, Noble C, Balouch F, Lewindon P, Lampe G, Hodgkinson P, McGill J, Ee L
Pediatr Transplant 2022 Nov;26(7):e14334. Epub 2022 Jun 13 doi: 10.1111/petr.14334. PMID: 35698261
Li C, Lu X, Xiao J, Chan CWH
J Clin Nurs 2022 Nov;31(21-22):3130-3143. Epub 2021 Nov 23 doi: 10.1111/jocn.16140. PMID: 34816510

Diagnosis

Tang Y, Zhang H, Chen L, Zhang T, Xu N, Huang Z
Int J Mol Sci 2022 Nov 5;23(21) doi: 10.3390/ijms232113590. PMID: 36362375Free PMC Article
Tan K, Wang K, Zhao A, Liu Z, Song W, Cheng Q, Li X, Chen Z, Yuan Y, Yang Z
Med Oncol 2022 Nov 9;40(1):14. doi: 10.1007/s12032-022-01875-w. PMID: 36352167Free PMC Article
Spearman CW, Dusheiko G, Jonas E, Abdo A, Afihene M, Cunha L, Desalegn H, Kassianides C, Katsidzira L, Kramvis A, Lam P, Lesi OA, Micah EA, Musabeyezu E, Ndow G, Nnabuchi CV, Ocama P, Okeke E, Rwegasha J, Shewaye AB, Some FF, Tzeuton C, Sonderup MW; Gastroenterology and Hepatology Association of sub-Saharan Africa (GHASSA).
Lancet Gastroenterol Hepatol 2022 Nov;7(11):1036-1048. Epub 2022 Jul 8 doi: 10.1016/S2468-1253(22)00041-3. PMID: 35810766
Bhushan S, Noble C, Balouch F, Lewindon P, Lampe G, Hodgkinson P, McGill J, Ee L
Pediatr Transplant 2022 Nov;26(7):e14334. Epub 2022 Jun 13 doi: 10.1111/petr.14334. PMID: 35698261
Li C, Lu X, Xiao J, Chan CWH
J Clin Nurs 2022 Nov;31(21-22):3130-3143. Epub 2021 Nov 23 doi: 10.1111/jocn.16140. PMID: 34816510

Therapy

Fujimoto Y, Namisaki T, Takeda S, Murata K, Enomoto M, Takaya H, Tsuji Y, Fujinaga Y, Sawada Y, Nishimura N, Kitagawa K, Kaji K, Inoue T, Kawaratani H, Moriya K, Akahane T, Mitoro A, Yoshiji H
Anticancer Res 2022 Oct;42(10):4895-4905. doi: 10.21873/anticanres.15995. PMID: 36191983
Chen Y, Qiu X, Wu D, Lu X, Li G, Tang Y, Jia C, Xiong Z, Wang T
Genes (Basel) 2022 Aug 26;13(9) doi: 10.3390/genes13091535. PMID: 36140703Free PMC Article
Singh A, Zahid S, Noginskiy I, Pak T, Usta S, Barsoum M, Khan U
Curr Oncol 2022 Sep 8;29(9):6445-6462. doi: 10.3390/curroncol29090507. PMID: 36135076Free PMC Article
Bhushan S, Noble C, Balouch F, Lewindon P, Lampe G, Hodgkinson P, McGill J, Ee L
Pediatr Transplant 2022 Nov;26(7):e14334. Epub 2022 Jun 13 doi: 10.1111/petr.14334. PMID: 35698261
Ando W, Kaneko F, Shimamoto S, Igarashi K, Otori K, Yokomori H
Ann Hepatol 2022 Mar-Apr;27(2):100660. Epub 2022 Jan 8 doi: 10.1016/j.aohep.2022.100660. PMID: 35007770

Prognosis

Tang Y, Zhang H, Chen L, Zhang T, Xu N, Huang Z
Int J Mol Sci 2022 Nov 5;23(21) doi: 10.3390/ijms232113590. PMID: 36362375Free PMC Article
Tan K, Wang K, Zhao A, Liu Z, Song W, Cheng Q, Li X, Chen Z, Yuan Y, Yang Z
Med Oncol 2022 Nov 9;40(1):14. doi: 10.1007/s12032-022-01875-w. PMID: 36352167Free PMC Article
Fujimoto Y, Namisaki T, Takeda S, Murata K, Enomoto M, Takaya H, Tsuji Y, Fujinaga Y, Sawada Y, Nishimura N, Kitagawa K, Kaji K, Inoue T, Kawaratani H, Moriya K, Akahane T, Mitoro A, Yoshiji H
Anticancer Res 2022 Oct;42(10):4895-4905. doi: 10.21873/anticanres.15995. PMID: 36191983
Chen Y, Qiu X, Wu D, Lu X, Li G, Tang Y, Jia C, Xiong Z, Wang T
Genes (Basel) 2022 Aug 26;13(9) doi: 10.3390/genes13091535. PMID: 36140703Free PMC Article
Torimura T, Iwamoto H
Liver Int 2022 Aug;42(9):2042-2054. Epub 2022 Jan 6 doi: 10.1111/liv.15130. PMID: 34894051

Clinical prediction guides

Tang Y, Zhang H, Chen L, Zhang T, Xu N, Huang Z
Int J Mol Sci 2022 Nov 5;23(21) doi: 10.3390/ijms232113590. PMID: 36362375Free PMC Article
Deng R, Lu X, Hong C, Cai R, Wang P, Xiong L, Wang X, Chen Q, Lin J
J Transl Med 2022 Oct 23;20(1):485. doi: 10.1186/s12967-022-03690-3. PMID: 36274132Free PMC Article
Fujimoto Y, Namisaki T, Takeda S, Murata K, Enomoto M, Takaya H, Tsuji Y, Fujinaga Y, Sawada Y, Nishimura N, Kitagawa K, Kaji K, Inoue T, Kawaratani H, Moriya K, Akahane T, Mitoro A, Yoshiji H
Anticancer Res 2022 Oct;42(10):4895-4905. doi: 10.21873/anticanres.15995. PMID: 36191983
Li N, Wan X, Zhang H, Zhang Z, Guo Y, Hong D
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