Linked from
The 49 pages that link to Cancer, each with the reason it gives.
ApoptosisRelated: Cancer cells can evade apoptotic signals, while many treatments aim to restore cell death.
Gene expressionRelated: Disrupted expression of growth, survival, and identity genes contributes to tumor development.
Cell cycleRelated: Cancer commonly involves mutations that weaken restraints on cell-cycle progression.
MitosisRelated: Disrupted controls over mitotic entry and division contribute to tumor growth.
Cell theoryRelated: Cancer shows how changes in individual cells can disrupt an organism’s larger organization.
AutophagyRelated: Autophagy can suppress tumor initiation yet support established tumors under stress.
Somatic mutationRelated: In animals, accumulated somatic mutations can contribute to cancer development.
AneuploidyRelated: Aneuploidy is common in many cancers, but its role in tumor development varies.
Gene regulatory networkRelated: Disrupted regulatory networks can alter growth, survival, and cell identity.
CellRelated: Cancer arises when cellular growth and division escape normal regulation.
DNA damage responseRelated: Accumulated mutations from failed damage control can drive cancer development.
Cell polarityRelated: Disrupted epithelial polarity can accompany tumor progression and loss of tissue organization.
CytokinesisRelated: Cytokinesis errors can contribute to chromosome instability in some cancers.
Group selectionRelated: Multicellular organisms face conflict between selection among cells and cooperation at organism level.
Theodor BoveriRelated: Boveri’s 1914 theory proposed that abnormal chromosome combinations could initiate cancer.
Cell divisionRelated: Cancer can arise when controls on cell division fail.
Cell-cycle checkpointRelated: Checkpoint defects can enable damaged cells to keep dividing.
Programmed cell deathRelated: Cancer can arise when cells evade death signals, and many therapies aim to restore their sensitivity.
CentrosomeRelated: Centrosome abnormalities are common in tumors and can contribute to chromosome instability.
Guanosine triphosphateRelated: Mutations that impair GTP hydrolysis can keep Ras signaling active and promote cancer.
TelomeraseRelated: Many cancers activate telomerase to maintain telomeres during continued cell division.
Elizabeth BlackburnRelated: Many cancers reactivate telomerase, enabling continued cell division.
Somatic cellRelated: Many cancers originate when somatic cells acquire changes that disrupt growth regulation.
Paul NurseRelated: Disrupted cell-cycle regulation is a common feature of cancer.
Leland H. HartwellRelated: Hartwell’s cell-cycle research helped clarify how disrupted division control can contribute to cancer.
NucleolusRelated: Many cancers alter ribosome production and show changes in nucleolar size or activity.
Raymond DamadianRelated: His early experiments compared magnetic resonance signals from cancerous and normal tissue.
Jack W. SzostakRelated: Many cancers activate telomerase, linking chromosome-end maintenance to sustained cell division.
Tim HuntRelated: Disrupted cyclin and cell-cycle control is a common feature of cancer.
Regulation of gene expressionRelated: Cancer can arise when oncogenes are overexpressed or tumor-suppressor genes are silenced.