Hallmarks of Cancer Overview

Mutation of TP53, a gene, is found in about 50% of cancers.

Cancer cells bypass normal growth limits to keep dividing indefinitely.

Reactivation of telomerase in cancer cells prevents telomere shortening.

The process leading to cellular senescence once telomeres are too short.

Cancer cells invade tissues and spread via blood or lymphatic systems.

E-cadherin is downregulated while N-cadherin is upregulated in invasive cancers.

The formation of new blood vessels to supply tumors with nutrients and oxygen.

Cancer cells reprogram their metabolism to support rapid growth.

Key features driving cancer development, identified in 2000.

Cancer cells produce growth signals or bypass control mechanisms.

Overexpression of the HER2 receptor in certain breast cancers leads to targeted therapy sensitivity.

Cancer cells ignore signals that normally inhibit growth.

Cancer cells evade apoptosis, allowing survival despite damage.

An anti-apoptotic protein often overexpressed in cancers.

Genes that regulate the cell cycle to prevent excessive growth.

Cancer caused by RB gene inactivation, leading to uncontrolled cell cycle progression.

RB protein regulates cell cycle by forming complex with E2F to control transcription during G1/S and G2/M transitions.

Downregulation or deletion of RB leads to growth suppression evasion, common in cancer cells.

Cancer commonly evades apoptosis, a natural cell death process, through various signaling pathways.

Intrinsic is triggered by internal signals, while extrinsic is triggered by external signals to regulate apoptosis.

Genes that sense apoptotic signals; important for determining if a cell undergoes apoptosis.

Proteins that regulate apoptosis; overactivation is linked to tumorigenesis in cancers.

TP53 senses DNA damage and is a negative regulator of apoptosis; mutated in many cancers.

BCL2 fused to IGH leads to inappropriate expression and is associated with cancer.

Mutations in RAS are linked to several cancers, including pancreatic and bowel cancers.

The process where cancer cells spread to adjacent tissues from the primary tumor.

The spread of cancer cells to distant organs via blood or lymphatic systems.

A protein that helps cells stick together, often reduced in metastatic cancers.

A protein upregulated in aggressive cancers, aiding cell migration.

Altered metabolism in cancer, providing energy for growth and division.

Cancer cells avoid destruction by the immune system, aiding their survival.

Increased mutations and instability in cancer, leading to more aggressive behavior.

A gene that can be amplified in some cancers, influencing treatment with Herceptin.

A drug prescribed for patients with high HER2 amplification (3+).

Assessment of HER2 gene expression levels: 0 (none), 1+ (low), 3+ (high).

A method used to investigate borderline cases of HER2 amplification.

Fluorescence in situ hybridization used to evaluate HER2 amplification status.

A metric used to determine HER2 gene amplification, needing at least 2:1.

Genes that normally restrain cell growth; often mutated or suppressed in cancer.

What Herceptin does to Her2, stopping cancer signals from spreading.

Propagation of a competitive cell line within a tumor.

Genomic changes that enhance the competitiveness of a tumor clone.

Increased mutation rates and chromosomal abnormalities in cancer cells.

Tumor suppressor genes linked to breast and ovarian cancer risk.

High-fidelity repair pathway for DNA double-strand breaks.

Mechanisms that fix DNA errors to maintain genomic integrity.

Substances causing damage to DNA, increasing mutation rates.

Aggressive cancer that spreads widely throughout the body.