Some Cancer Nomenclature Terminology - Biology of Cancer | BIMM 134, Study notes of Biology

Download Some Cancer Nomenclature Terminology - Biology of Cancer | BIMM 134 and more Study notes Biology in PDF only on Docsity! 4/6/04 Some cancer nomenclature/terminology Cancer = “crab” in latin 2 biggest divisions of cancer types: Carcinoma – cancer of epithelial origin - e.g. adeno-carcinomas - note: prefix is usually the tissue type (adeno = secretory cell type) Sarcoma – cancer from mesenchymal origin (muscle, fat, cartilage) The suffix – in most cases: - oma = benign tumor - sarcoma = malignant (some exceptions: melanoma, leukemia, lymphoma) benign – tumor at a stage preceding malignant malignant – full blown cancer tumor hyperplasia – growing group of cells (proliferating) neoplasia/neoplasm – malignant group of cells anaplasia – de-differentiated group of cells (no longer looks like the original cell type) “de-differentiated”: - stem cells (un-differentiated cells) typically differentiate to become a specialized cell type (skin cells, blood cells, etc) - de -differentiation refers to the apparent reversal of this process (such that the cell no longer appears to possess the properties of a stem cell, blood cell, etc), thus the confusing term, de-differentiation. Differences in solid tumors: Benign Malignant Edges: encapsulated irregular (basement membrane still intact) (hasn’t broken through) OO /////////////////// ////////OOO/// OOOOOO OOOOOO OOOOOO OOOOOO Metastatic: never have the capacity To metastasize Invasive: no yes - capacity to break through basement membrane Differentiated: yes – like normal no – de-differentiated (may become fully anaplastic) Nuclei: small large, irregular, unusual Lethal: no yes AML - Most common adult leukemia Some causes of AML: t(8;21) - ~15% of AML patients have the translocation t(8;21) - results in a fusion of 2 different genes: CBF and ETO o CBFand  are transcription factors involved in regulating genes that regulate myeloid differentiation ( and  function as a dimer) o Fusion of CBFwith ETO results in a dominant negative form of CBF  Dominant negative – an altered form of a protein that somehow negates the function any of the normal form of the protein in the cell o Dominant negative CBF “soaks up” all the normal functional CBF and  such that:  Myeloid regulatory genes not transcribed anymore  Loss of myeloid regulation results in development of AML Inversion 16 - knocks out proper production of CBF - also results in loss of myeloid regulatory gene transcription These types of AML have good prognoses – treatable Cytotoxic drugs/therapies (induction therapy) - drugs that specifically kill proliferating cells o cause DNA damage o fast replicating cells like tumor cells particularly succeptible - treatment is effective, but there is a risk of leukemias later in life (due to DNA damage) Treatment By Pulsed intermittent therapy - Relies on fractional cell kill hypothesis: o If you have 109 cancerous cells to kill o Cytotoxic therapy will kill 109 of them (as well as some of the body’s normally replicating cells) o 109 cancerous cells  106 cancerous cells o Wait until normal cells recover o Pulse therapy again o 106  103 o In theory, you should be able to achieve: 109  106  103  100 o But in practice it doesn’t always work this way In > 50% patients under 50, cancer goes into remission - since you can’t see less than 109 white blood cells by microscopy - if you have under 109 cells you’re in what’s called cytologic remission - new methods by PCR analysis allow for detection of as low as 105 cells - if you can’t see by PCR methods (under 105 cells) you’re in cytogenic remission X-inactivation and leukemia There is the debate over the clonal theory of cancer: Does a cancer result from a single cell (clonal) or multiple cells (nonclonal) X-inactivation – in females, the random inactivation of one of the X-chromosomes in every cell This phenomenon allows for a simple test of the clonal theory of cancer: G6PD is a gene on the X chromosome - has two different isozymes (alleles) - the two different isozymes can be differentiated by size on an electrophoresis gel Typically a single cell will show only one isozyme of G6PD (because the other is inactivated) A group of cells will show both isozymes (because each cell randomly inactivates one or the other) Thus, if leukemias result from a single cell (clonal) you should see only one isozyme in all leukemic cells. Conversely, if leukemias result from multiple cells, you should see a population of both isozymes in leukemic cells Leukemic cells show only one isozyme of G6PD, supporting a clonal origin of cancer