Ch 7 Carcinogenic Agents and Their Cellular Interactions Flashcards
initiation
exposure of cells to sufficient dose of a carcinogenic agent making it potentially capable of giving rise to a tumor, not sufficient for tumor formation
permanent DNA damage, rapid and irreversible, non memory
promotors
can induce tumor to arise from initiated cells, but they are non tumorigenic by themselves
direct acting carcinogens
require no metabolic conversion to become carcinogenic
indirect acting carcinogens
chemicals that require metabolic conversion to become active carcinogens
aflatoxin B1
produced by mold called aspergillus
leads to hepatocellular carcinoma
UV rays
associated w/ increased incidence of squamous cell carcinoma, basal cell carcinoma, melanoma of the skin
nonmelanoma skin cancers
associated w/ total cumulative exposure to UV radiation
melanomas
associated w/ intense intermittent exposure
UVB
responsible for the induction of cutaneous cancer
carcinogenicty is due to the formation of pyrimidine dimers in DNA
HTLV-1
causes adult T cell leukemia/lymphoma
after long latent period leukemia/lymphoma involving CD4+ cells due to acquisition of mutations of host genome
TAX- increased pro growth signaling and cell survival through PI3K and AKT - polyclonal expansion of T cells
HPV
integration of viral DNA is important for malignant transformation
E6-p53
E7-Rb
both allow progression through the cell cycle
EBV
most common associated tumors are derived from B cels and nasopharyngeal carcinoma
associated w/ Burkitt lymphoma
absence of T cell immunity will lead to EBV positive B cell lymphomas which can be reversed
HBV and HCV
70-85% of hepatocellular carcinomas
oncogenic effects are multifactorial
dominant effect is immunologically mediated chronic inflammation and hepatocyte death leading to regeneration and over time genomic damage
HBx gene can activate transcription factors and signal transduction pathways
H. pylori
implicated in genesis of gastric adenocarcinomas and gastric lymphomas
pathogenesis - multifactorial, chronic inflammation, reparative gastric cell proliferation
CagA - gastric adenocarcinoma, penetrates into gastric epithelial cells where it initiates signaling cascade that mimics uregulated GF stimulation
chronic - polycolonal B cell proliferation leading to B cell tumor of the stomach
cancer cachexia
progressive loss of body fat and lean body mass accompanied by profound weakness, anorexia, and anemia
paraneoplastic syndromes
signs and symptoms that cannot readily be explained by the anatomic distribution of the tumor or by the elaboration of hormones indigenous to the tissue from which the tumor arose
endocrinopathies
not of endocrine origin and the secretory activity of the tumors is referred to as ectopic hormone production
hypercalcemia
MOST COMMON
osteolysis induced by cancer
neuromyopathic paraneoplastic syndrome
peripheral neuropathies, cortical cerebellar degeneration, polymyopathy resembling polymyositis, myasthenic syndrome
acanthosis nigricans
gray black patches of thickened hyperkeratotic skin w/ velvety appearance
hypertrophic osteoarthropathy
perosteal new bone formation at distal end of long bones, metatarsals, metacarpals, proximal phalanges
migratory thrombophlebitis
associated w/ deep seated cancers (pancreas and lung)
disseminated intravascular coagulation
associated w/ promyelocytic leukemia and prostatic adenocarcinoma
grading
cytologic
behavior and differentiation are related
pathologist
staging
surgical
based on size of primary lesion, extent of spread to regional lymph nodes, presence or absence of blood borne metastases
clinical
