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Cancer, McCance

Cpt 11,12

QuestionAnswer
tumor new growth, neoplasm. not all tumors or neoplasm are cancerous
cancer malignant tumor, grow rapidly, not encapsulated, invade local structure/tissue, poorly differentiated, high mitotic index, can mets
benign neoplasm can be life threatening depending on their location. slow growing, well-defined, well-differentiated, low mitotic index, do not metastasize
anaplasia loss of cellular differentiation, loss of normal tissue structure result in cancer
adenocarcinoma arise from or form ductal or gladular structures
sarcoma cancer from connective tissue
lymphomas cancer of lympatic tissue
leukemia cancer of blood forming cells
CIS carcinoma in situ, preinvasive epithelial tumors of glandular/squamous cell origin) NOT broke basement membrane!common in the cervix, skin, oral cavity, esophagus, bronchus. ex: ductal CIS of the mammary ducts.
transformation (autonomy) process by which normal cells become cancerous
characteristics of transformed cancer cells autonomous, immortal, anchorage independent, anaplasia, pleomorphism, defective differentiation
pleomorphic variable size and shape of anaplastic cells
tumor cell markers substances produced by cancer cells, found in/on tumor, or in blood, spinal fluid, or urine. Table 11-3, p. 368. hormones, enzymes, genes, antigens, antibodies
AFP alpha fetoprotein, secreted from liver & germ cells ; tumor marker
neoplasia abnormal / uncontrolled growth of cells which result in neoplasm
naming tumors named according to the cell type from which they originate, -oma if benign. -carcinoma if cancer. Review table 11-2, p. 364
carcinoma cancer arising from epithelial cells
adult stem cell 1)self renew, 2) multipotent-differentiate. asymmetrical division-divide into another stem cell and the other one is differentiates depending on need.
cancer stem cells cells that propogate cancer/tumor growth; cancer grows back if stem cell isn't killed during treatment
mesenchymal stem cell normal adult stem cell that theoretically can differentiate into all body cell types
advantage of TCM (tumor cell markers) 1) screen/ identify high risk pt. 2) help in diagnosis 3) follow clinic cours of disease-should be < if tx effective. NOT used alone to dx.
disadvantage of TCM can't be used soley for diagnosis b/c nonmalignant conditions can > TCM
> catecholamines suggest pheochromocytoma (adrenal medullary tumor)
PSA prostate specific antigen; prostate
epigenetics heritable changes in gene expression
clonal proliferation or clonal expansion; as a clone with a mutation grows, it may become an early stage tumor
stepwise accumulation accumulation of more genetic hits; the more mutations a cell has-the bigger the neoplasm/cancer
causes of cancer cell growth 1) secrete growth factor, 2)increase in growth factor receptors, 3) mutated to "on" position, 4) RAS, 5) mutated antigrowth signal, 6) disabled apoptosis
autocrine stimulation cancer that secrete growth factor that stimulate their own growth
RAS signaling protein; stimulate cell growth even when growth factors are missing
angiogenesis advanced cancer that stimulate new blood vessels
angiogenic factors vascular endothelial growth factor-VEGF, platelet-derived growth factor-PDGF, basic fibroblast growth factor-bFGF; recruit endothelial cells and intiate proliferation of existing blood vessel cells that allow sm ca cells to become lg ca.
Hayflick limit non-immortal cells; limited # of times a cell can normally divide.
telomerase normally only in germ cells , but cancer cells activate to restore shortened telomeres so that cells can continue to grow (immortality of ca cells.)
proto-oncogenes normal, nonmutant state of a gene; regulate growth & development by encoding growth factors or growth factor receptors
oncogenes mutant genes that encode protein that promote growth by overexpression, amplification, gain of function. Dominant-one hit activates- 1) point mutation, 2) amplification 3) translocation
tumor suppressor genes recessive oncogene; encodes protein that inhibit proliferation and prevent or repair mutations. require loss of both alleles to be inactivated and mutation/cancer to form-recessive; 1)point mutation, 2)silenced or LOH
point mutation small scale changes in DNA
RAS protein normally a proto-oncogene-inactive RAS exchanges GDP for GTP and is activated-active RAS sends growth signals. normally turns off when GTP turns back into GDP. oncogenic RAS stays "on". common in ca; esp. pancreatic and colorectal
chromosome translocation one piece of a chromosome translocated to another chromosome.
Burkitt lymphoma ex of translocation. t(8;14) Aggressive ca of B lymphocytes. myc proto-oncogene (8) and Ig (14) translocate & myc oncogene causes ca of B cells b/c myc doesn't turn off
MYC protein part of positive signal for cell differentiation
myc gene chromosome 8; on in growing lymphocytes-off when they mature
Ig B cell immunoglobulin; actice in maturing lymphocytes;
ex of translocation mutations Burkitt lymphoma, t(8;14). CML, t(9;22)
gene amplification over duplication of gene, more than 2 copies. N-mic oncogene-childhood neuroblastoma. erbB2-breast ca. Also contributes to drug-resistance genes, but erbB2 breast ca responds well to targeted drug therapy
Rb gene retinoblastoma; strongly inhibits cell division cycle.
childhood retinoblastoma caused by inactivated RB gene.
loss of heterozygosity loss of a chromosome region in a tumor; unmasks inactivation mutations in recessive tumor suppressor genes. 2nd copy is not there?
silencing epigenetic; inherited gene expression that causes DNA methylation that turns off whole sections of chromosome. doesn't require mutation of gene-it's inherited that way. changes in gene silencing contribute to ca: > methylation in tumor suppressor gene
genetics and cancer genetic ca events occur in somatic cells-they are not inheritable; but can inherit the mutation that predispose to ca. (usually affect tumor-suppressor gene such as LOH or silencing.
inheritable cancer retinoblastoma-Rb gene; Wilms tumor-kidney; neurofibromatosis; inheritable breast ca-BRCA-1; familial ademoma of colon ca-APC. all inactivated tumor suppressor genes
Chronic inflammation & ca ulceritive colitis; hepatitis; chronic asthma. cytokines: TNF-a, IL-6, IL-10 enhance tumor growth, angiogenesis, mets & suppress anti-tumor immunity. chronic-no stop in wound healing process. tumors activate same factors=tumor growth/angiogenesis.
anti-tumor immunity IL-12= NK cells, CTL (cytotoxic T lymphocytes), IL-12 & IL-23=cytotoxic cytokines( IFN, TRAIL, TGF-b)
ROS reactivce oxygen species in chronic inflammation-promote mutation and block DNA repair
COX-2 enzyme cyclooxygenase-2-generates prostaglandins during inflammation. assoc w/ colon ca. NSAIDS block COX-2
TRAIL TNF-related apoptosis inducing ligand. antitumor
TNF tumor necrosis factor
Invasion local spread; prereq for mets. 1)ca proliferation 2)protease digest connective tissue capsule 3) adhesion changes (cadherins, integrins) 4) increased motility of ca cells
METS promotion deatach, & invasion by neoangiogensis and lymphangiogenesis; survival in circulation; attach & grow in new site. most ca cells can't cause mets; those that do have > heterogeneity
detachment of ca cells proteases and protease activators-digest extracellular matrix & basement membrane-pathway for ca to move; MMP-matrix metalloproteinase, plasminogen activators; also many protease that block cancer
EMT epithelial-mesenchymal transition; loss of E-cadherin so that ca cells can detach for easier migration
anoikis form of apoptosis that occurs when cells seperate from extracellular matrix (ECM). but tumor cells can resist apoptosis
WHO staging cancer Tumor, Nodes, Metastases
Carcinoma in situ staging 1) organ confined 2)locally invasive 3) regional structure-lymph nodes 4) distant sites
paraneoplastic syndrome symptoms triggered by cancer, but not caused by tumor; hormones released by the tumor, table 11-12, p. 389 may be earliest sx of ca and life-threatening
fatigue most frequent reported symptom of ca and treatment. consequence of metabolc products, of cancer treatment and muscle loss from cytokines (TNF, IL-1)
cachexia anorexia, early satiety, wt loss, anemia, asthenia (marked weakness), alt taste/ metabolism. servere form of malnutrition even with adqut diet. alt metabolism r/t cytokines: TNF-a, IL-6, IFN-y and tumor metabolites. hyperinsulinemia, IR, hyperglycemia.
anemia hgb < 9; chronic bleeding, iron deficiency. lack of iron transfer from storage pool to blood precursors-> IL6, hepcidin. defect in erythropoietin
erythropoeitin stimulate production of erythrocytes; reserved for significant ca-related anemia due to risk of blood clots.
leukopenia < total WBC, invasion of tumor to bone marrow or toxic side effect of chemo
thrombocytopenia < platelets-invasion of bone marrow, chemo S.E.; cause hemorrhage-need platelet transfusion, accompany DIC w/ acute promyelocytic leukemia
granulocytopenia neutropenia-no neutrophils. radiation or chemo tx. lessen w/ recombinant human granulocyte colony-stimulating factor (rhG-CS, filgrastim) stimulates WBC to proliferate and differentiate faster < 500: > infection chances
stomatitis oral ulcers; < cell turnover from chemo/radiation
serotonin 5-HTP antagonist ondasetron (Zofran) PO, IM, IV; dolasetron (only po form) for nausea symptoms r/t treatment
reproductive affect of tx affect gametes-< fertility, early menopause. alkylating chemotherapy agents-greatest risk. craniospinal irradiation: CNS tumors-affect hypothalamus-pituitary gland: gonad failure r/t no GRH, LH, FSH.
tobacco use r/t what type of ca lower urinary tract, upper aerodigestive tract, liver, kidney, pancreas, cervix, uterus, myeloid leukemia. squamous and small cell adenocarcinoma. Lack evidence of breast, prostate & endometrial ca.
Diet and ca < folate r/t development of colorectal ca, but after tumor folate causes growth. Diet affects mylenation changes in DNA. SFN can inhit histone modifications: sulforaphane found in cruciferous vegetables: broccoli/sprouts
Obesity and ca insulin resistance, hyperinsulinemia, increase growth factors, increased steroids, hormones, cytokines. Adipose tissue releases fatty acids. insulin & IGF promote growth, and inhibit apoptosis. Colon, breast, prostate, pancreatic, endometrial ca.
insulin resistance > fatty acids, resistin, TNF-y, < adiponectin
Alcohol and ca risk oral cavity, pharynx, hypopharynx, larynx, esophagus, liver. possible breast and colorectal ca. > interaction with smoking. early 60's laryngeal ca.
atomic bomb exposure thyroid, breast ca, as well as lung, stomach, colon, esophagus, urinary tract & acute leukemia: latent period of 20 yrs. ex of ionizing radiation, same as x-rays, radioisotopes.
UV radiation sunlight CAUSES basal cell ca (p53)(head/neck; light complex, burn easily, high sun exposure), squamous cell ca(p16)(outdoor working men, head, neck, arms.) mutate TP53 gene, release TNF-a in epidermis-reduces immune, ROS
carcinoma cancer of epithelial tissue (ex: squamous cell line major organs)
ACTH hormone tumor marker-pituitary adenoma
PSA antigen tumor marker-protate
CEA carcinoembryonic antigen, GI, pancreas, lung, breast
b-HCG germ cell tumor marker
catecholamines tumor marker-adrenal medulla; pheochromocytoma
p-53 most common mutation that causes resistance to apoptosis, UV light can mutate p53
pain none or little in beginning stages, but affect terminally ill.
infection most significant cause of complication/death in individual w/ malignant disease.
irradiation affect fertility. (prepubertal-most resistant). brain rad: affect hypothalamus/pituitary-cause gonad failure
HPV-16 account for 50-60% of cervical ca
Created by: Sniffen group