Chapter 4 - Cellular Oncogenes (flashcards)

Vocabulary flashcards covering key concepts about endogenous and retroviral oncogenes, mechanisms of activation, and clinical examples.

Proto-oncogene

Normal cellular gene that can become an oncogene via mutation, amplification, or overexpression.

Oncogene

Mutated or abnormally expressed gene that drives uncontrolled cell growth.

Endogenous oncogenes

Cellular (host) oncogenes that can be activated into oncogenes and are related to retroviral transforming factors.

Endogenous oncogenes related retroviral transforming factors

Cellular oncogenes homologous to viral oncogenes; can be activated by retroviruses to transform cells.

Retroviral transforming factors

Viral oncogenes carried by retroviruses that can transform infected cells.

Viral capture

Process by which a retrovirus acquires a host proto-oncogene to form a viral oncogene (v-onc).

Proviral insertion

Insertion of a provirus near a proto-oncogene causing misexpression of the gene.

Amplification

Increase in copy number of a proto-oncogene, leading to higher expression and oncogenic potential.

Chromosomal translocation

Rearrangement that moves a gene to a new chromosomal context, altering regulation or creating fusion genes.

Promoter substitution

Translocation or rearrangement where a promoter drives expression of another gene, altering regulation.

MYC gene family

Group of related genes (c-MYC, n-MYC, l-MYC) involved in cell proliferation and frequently dysregulated.

c-MYC

MYC family member often amplified or translocated; drives cell growth and proliferation.

N-MYC

MYCN gene; amplification associated with poor prognosis in neuroblastoma.

L-MYC

MYCL gene; member of the MYC family involved in transcriptional regulation.

H-ras (HRAS)

RAS family GTPase; mutations can lock signaling in an active state promoting proliferation.

G12V mutation

A point mutation in HRAS (glycine to valine at position 12) that causes constitutive activity.

MAP kinase pathway

Ras downstream signaling cascade promoting cell growth and division.

PI3K/AKT pathway

Survival and growth signaling pathway downstream of Ras and other RTKs.

BCR-ABL fusion

Chimeric tyrosine kinase created by BCR-ABL fusion; constitutively active and oncogenic.

Philadelphia chromosome

Translocation t(9;22) generating BCR-ABL; hallmark of chronic myeloid leukemia.

HER2/ERBB2 amplification

Increased copies of the HER2 gene leading to overexpression and aggressive breast cancer.

Herceptin (trastuzumab)

Monoclonal antibody that inhibits HER2 signaling and improves outcomes in HER2-positive breast cancer.

EGFR mutation lacking extracellular domain

EGFR mutation that yields constitutive, ligand-independent signaling (∼30% GBMs).

EGFR amplification in glioblastoma

Increased EGFR signaling due to gene amplification or mutation in glioblastoma.