CANCER 101
These neoplastic cells have not yet become invasive; removing the mass usually achieves a cure
BENIGN
EPITHELIAL CELL CANCER
CARCINOMA
Normal genes that, when mutated, can be converted into cancer-promoting oncogenes
PROTO-ONCOGENE
The hallmark of Chronic Myelogenous Leukemia (CML), resulting from a translocation between chromosomes 9 and 22
PHILADELPHIA CHROMOSOME
The tendency of tumor cells to de-emphasize oxidative phosphorylation and consume massive amounts of glucose
WARBURG EFFECT
This term describes cells that have acquired the ability to invade surrounding tissues
MALIGNANT
WHITE BLOOD CELL CANCER
LEUKEMIA
To contribute to cancer, both copies of this type of gene must usually be removed or inactivated
TUMOR SUPPRESSOR GENE
A defect in the repair system for UV-induced DNA damage leads to this skin cancer-prone condition
XERODERMA PIGMENTOSUM
Cancer cells escape replicative senescence by producing this enzyme
TELOMERASE
The process by which cancer cells break loose, enter blood vessels, and form secondary tumors at other sites
METASTASIS
CONNECTIVE TISSUE OR MUSCLE CELL CANCER
SARCOMA
Mutations that are the actual causal factors in the development of cancer, as opposed to "passenger" mutations
DRIVERS
The first tumor suppressor gene was discovered through the study of this rare childhood eye cancer
RETINOBLASTOMA
This critical pathway for cell growth control is often activated by mutation to allow growth without external signals
P13/AKT/MTOR PATHWAY
Cancer is described as this type of "process" because it involves successive rounds of random inherited change followed by natural selection
MICROEVOLUTIONARY PROCESS
BONE MARROW CANCER
MYELOMA
This type of mutation creates a hyperactive version of this monomeric GTPase that cannot hydrolyze GTP
RAS ONCOGENE
A rare hereditary predisposition to colorectal cancer where thousands of polyps develop in the colon
FAMILIAL ADENOMATOUS POLYPOSIS
Often called the "guardian of the genome," cancer cells depend on the inactivation of this pathway to avoid apoptosis under stress
P53
These specific colonies of cancer spread and multiply at new sites in the body
MICROMETASTASES
MALIGNANT CANCER OF THE PIGMENT CELS IN THE SKIN
MELANOMA
Heritable changes in gene expression that result from modifications of chromatin structure rather than DNA sequence alterations
EPIGENETIC CHANGES
This condition involves an increased risk of colon cancer due to mutations in the DNA mismatch repair system, without an increase in polyps
Hereditary Nonpolyposis Colorectal Cancer
The loss of this specific tumor suppressor gene results in excess β-catenin and uncontrolled expansion of stem cells in the colon
APC