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cancer
tumor that is a tissue overgrowth; independent of the laws governing the body; serves no useful purpose*
tumor
new growth; neoplasm; not all tumors are cancer*
characteristics of malignant tumor
rapid growth; microscopic alterations; lack of capsule; invasion into blood vessels, lymphatics, surrounding structures; anaplasia*
metatstasis
spreads to other parts of the body*
anaplasia
without form, inability of tumor cells to differentiate and orient to one another and to blood vessels, clinically recognized as increase in size of nucleus*
suffix \\\'oma\\\'
lipoma, glioma, leiomyoma, chondroma*
carcinoma
malignant epithelial tumor*
adenocarcinomas
arise from glandular or ductal tissue*
sarcoma
malignant connective tissue*
rhabdomyoscacroma
cancer of skeletal muscle*
lymphoma
lymphatic tissue*
leukemia
blood forming cells*
carcinoma in situ (CIS)
early stage tumors, preinvasive epithelial tumors of glandular or squamous cell origin; have not broken through the basement membrane or invaded surrounding stroma
stages of cancer spread 1-4
1 cancer confined to organ of origin; 2 locally invasive; 3 spread to regional structures (lymph); 4 spread to distant sites; CIS (special case) reinvasive epithelial tumors of glandular or squamous cell origin
biopsy required
tissue brushing; fine needle aspiration, open biopsy; then examined
clinical staging
combination of physical findings, lab testing, and imaging studies reveal whether cancer has spread
autonomy
cancer cell\\\'s independence from normal cellular controlls
anaplasia
loss of differentiation
pleomorphic
anaplastic cells are this, of variable size and shape
undifferentiated cells
pluripotent; precursor; stem; they can differentiate into multiple different cell types. cancer cells are like precurser cells, less differentiated and divide rapidly
tumor cell markers
biological markers, substances produced by cancer cells found on tumor plasma membranes, in the blood, CSF or urine and include hormones, enzymes, antibodies and antigens
tumor cell markers used to
screen and identify individuals at high risk, diagnose specififc types of cancer, obseve clinical course of cancer; nonmalignant diseases als oproduce them
clonal proliferation (expansion)
as a result of a mutation, a cell acquires characteristics that allow it to have selective advantage over its neighbors (increased growth rate or decreased apoptosis)
mutations in progrowth isgnals
proliferate in absense of growth signals; increased growth factor receptors; signal cascade from cell-surface receptor is always on
mutations in antigrowth signals
inactivation of Rb tumor suppressor; activation of protein kinases that drive the cell cycle; disabling of apoptosis pathway;
p53 gene
mutation of this gene confers resistance to apoptosis
angiogenesis
growth of new blood vessels; limited to wound healing and proliferative phase of menstrual cycle
angiogenic factors (VEGF)
vascular endothelial growth factor; advanced cancers secrete
hallmarks of cancer
self-suffic. in growth signals; insensitive to antigrowth signals; evading apoptosis; limitless replicative potential; sustained angiogenesis; tissue invasion and metastasis
telomere
multicopy DNA sequence at the ends of chromosomes; they become smaller and smaller with each cell division and when they are too small the cell dies
teomerase
enzyme that maintains telomeres; found in germ cells and stemm cells, cancer cells reactivate teomerase-can divide indefinitely
oncogenes
mutant genes that in their nonmutant state direct protein syntheses and cellualr growth
tumor-suppressor genes
encode proteins that in their normal state negatively regulate proliferation, also reffered to as anti-oncogenes
point mutations
changes in one or a few nucleotide base pairs; point mutations chang ras into an oncogene
chromosome amplification
duplicaiton of a small piece of choromosome over and over; 10s-100s of copies(normal is 2); result in increased expression of an oncogene
chromosome translocations
a piece on one chromosome is tranferred to another, can create oncogene
chromosome tranaslocation mutation activates oncogenes by
causing excess and inappropriate prodcution of a proliferation factor; can lead to production of novel proteins
tumor-suppressor genes
slow the cell cycle, inhibit proliferation from growth signals; stop cell dividsonwhen cells are damamged; must be inactivated for cancer to occur, two copies of each gene, both must be inactivated, two separate events
mutated tumor-suppressor genes
allow unregulated cellular growth
retinoblastoma gene
inhibits cell cycle
tumor-suppressor gene inactivation
first copy- often inactviated by point mutation; second copy-usualy lost because entire regions of the chromosome are lost
loss of heterozygosity (LOH)
loss of a region on one chromosome that corresponds to a mutated region on the other chromosome; both are inactivated
gene silencing
gene regulation in a heritable manner; happens in specific tissues; epigenetic mechanism shuts off whole regions of chromosomes
cancer cells and gene silencing
the boundaries of the silenced regions can spread, important way that tumor-suppressor genes are inactivated
how mutations occur
during DNA synthesis, during mitosis, by damage from external mutagens
caretaker genes
rapair mechanisms are directed by; encode for proteins that are involved in repairing damaged DNA; loss of these genes leads to increased mutation rates
cancer prone genetics
mutations in germline cells, tumor suppressor genes and caretaker genes
viruses and cancer
hepB and C viruses - liver cancer; EBV- Bcell lymphomas; kaposi\\\'s sarcoma herpesvirus (KSHV)
Human T cell leukemia-lymphoma virus (HTLV)
retrovirus that can be transmitted horizontally, breastfeeding, blood transfusions, sexual intercourse, needles
bacterial cause of cancer
h pylori; infects 1/2 the words pop; chronic infections assoc with peptic ucler disease, stomach carcinoma, mucosa-assoc lymphoid tissue lymphomas
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