Neoplasms Part 2

The molecular basis of cancer, involving proto-oncogenes transforming into oncogenes, tumor suppressor genes preventing uncontrolled growth, and gene regulators influencing apoptosis.

Genetic alterations in cancer cells, which can be point mutations or chromosome changes, and classified as either drivers (pathogenic) or passengers.

Pathogenic mutations that directly contribute to the development and progression of cancer by altering the function of cancer-related genes.

Mutations that create genetic variants providing tumor cells with a selective advantage, especially during therapy.

New, uncontrolled growth of cells, where neoplastic cells are 'transformed' and replicate abnormally.

Tumors consist of parenchyma (transformed or neoplastic cells determining biological behavior) and stroma (supporting, host-derived connective tissue providing blood supply and support).

Tumor cells achieve growth self-sufficiency by producing their own growth factors or inducing stromal cells to produce them, or by interacting with stroma to activate supporting cells.

Most commonly mutated oncogene in human tumors, activated by point mutations affecting G+P binding or hydrolysis.

Translocation of the ABL gene from chromosome 9 to chromosome 22, fusing with the BCR gene, resulting in a hybrid BCR-ABL protein.

Most common mutated gene in cancer, encoding the p53 protein which prevents neoplastic transformation through cell cycle arrest, DNA repair induction, or apoptosis.

Changes in bowel or bladder habits, sores that don't heal, unusual bleeding or discharge, thickening or lumps, indigestion or difficulty swallowing, changes in warts or moles, and nagging cough or hoarseness.