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Related Concept Videos

Cancers Originate from Somatic Mutations in a Single Cell02:21

Cancers Originate from Somatic Mutations in a Single Cell

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Cancer arises from mutations in the critical genes that allow healthy cells to escape cell cycle regulation and acquire the ability to proliferate indefinitely. Though originating from a single mutation event in one of the originator cells, cancer progresses when the mutant cell lines continue to gain more and more mutations, and finally, become malignant. For example, chronic myelogenous leukemia (CML) develops initially as a non-lethal increase in white blood cells, which progressively...
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The Ras-gene-encoded proteins are regulators of signaling pathways controlling cell proliferation, differentiation, or cell survival. The Ras-gene family in humans constitutes three primary members—the HRas, NRas, and KRas. These genes code for four functionally distinct yet closely related proteins—the HRas, NRas, KRas4A, and KRas4B. The involvement of mutant Ras genes in human cancer was first discovered in 1982 and is among the most common causes of human tumorigenesis.
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Mutations01:39

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Mutations01:35

Mutations

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Mutations are changes in the sequence of DNA. These changes can occur spontaneously or they can be induced by exposure to environmental factors. Mutations can be characterized in a number of different ways: whether and how they alter the amino acid sequence of the protein, whether they occur over a small or large area of DNA, and whether they occur in somatic cells or germline cells.
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Mutagenicity and carcinogenicity refer to the ability of drugs to cause genetic defects and induce cancer, respectively. The International Agency for Research on Cancer (IARC) classifies agents into four groups based on their carcinogenic potential. Group 1 agents are known human carcinogens; group 2A agents are probably carcinogenic to humans; group 3 agents lack data to support their role in carcinogenesis; and group 4 includes agents for which data support that they are not likely to be...
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Genes usually encode proteins necessary for the proper functioning of a healthy cell. Mutations can often cause changes to the gene expression pattern, thereby altering the phenotype.
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Related Experiment Video

Updated: Apr 24, 2026

An Oncogenic Hepatocyte-Induced Orthotopic Mouse Model of Hepatocellular Cancer Arising in the Setting of Hepatic Inflammation and Fibrosis
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Gene mutations in hepatocellular adenomas.

Marie B Raft1, Ernö N Jørgensen1, Ben Vainer1

  • 1Department of Pathology, Rigshospitalet, University of Copenhagen, Copenhagen, Denmark.

Histopathology
|September 9, 2014
PubMed
Summary

Hepatocellular adenomas (HCA) are benign liver tumors classified into four subtypes based on genetic mutations. Understanding these subtypes, like HNF1α-inactivating and β-catenin activating HCA, aids diagnosis and treatment.

Keywords:
adenomadiagnosis, differentialfocal nodular hyperplasiahepatocellularhepatocellular carcinomaliverliver neoplasmsmutation

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Area of Science:

  • Hepatology
  • Oncology
  • Genetics

Background:

  • Hepatocellular adenomas (HCA) are rare, benign liver tumors often linked to oral contraceptive use.
  • Increased incidence in older women and men suggests links to metabolic syndrome.
  • Genetic classification identifies four HCA subtypes: HNF1α-inactivating, β-catenin activating, inflammatory, and unclassified.

Purpose of the Study:

  • To review gene mutations associated with hepatocellular adenomas.
  • To discuss the diagnostic and prognostic value of HCA subclassification.

Main Methods:

  • Review of reported gene mutations in hepatocellular adenomas.
  • Discussion of immunohistochemical analyses for HCA subclassification.

Main Results:

  • HNF1α-inactivating HCA shows TCF1 gene mutations and steatosis.
  • β-catenin activating HCA involves Wnt/β-catenin pathway activation and potential malignant transformation.
  • Inflammatory HCA is linked to JAK/STAT pathway alterations and inflammation.

Conclusions:

  • HCA subclassification based on genotype and phenotype is crucial for diagnosis and prognosis.
  • Immunohistochemical analysis is key for classifying HCA subtypes.
  • Understanding genetic mutations improves treatment choices and patient assessment.