Ch 7 Carcinogenic Agents and Their Cellular Interactions Flashcards

1
Q

initiation

A

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

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2
Q

promotors

A

can induce tumor to arise from initiated cells, but they are non tumorigenic by themselves

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3
Q

direct acting carcinogens

A

require no metabolic conversion to become carcinogenic

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4
Q

indirect acting carcinogens

A

chemicals that require metabolic conversion to become active carcinogens

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5
Q

aflatoxin B1

A

produced by mold called aspergillus

leads to hepatocellular carcinoma

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6
Q

UV rays

A

associated w/ increased incidence of squamous cell carcinoma, basal cell carcinoma, melanoma of the skin

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7
Q

nonmelanoma skin cancers

A

associated w/ total cumulative exposure to UV radiation

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8
Q

melanomas

A

associated w/ intense intermittent exposure

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9
Q

UVB

A

responsible for the induction of cutaneous cancer

carcinogenicty is due to the formation of pyrimidine dimers in DNA

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10
Q

HTLV-1

A

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

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11
Q

HPV

A

integration of viral DNA is important for malignant transformation
E6-p53
E7-Rb
both allow progression through the cell cycle

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12
Q

EBV

A

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

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13
Q

HBV and HCV

A

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

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14
Q

H. pylori

A

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

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15
Q

cancer cachexia

A

progressive loss of body fat and lean body mass accompanied by profound weakness, anorexia, and anemia

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16
Q

paraneoplastic syndromes

A

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

17
Q

endocrinopathies

A

not of endocrine origin and the secretory activity of the tumors is referred to as ectopic hormone production

18
Q

hypercalcemia

A

MOST COMMON

osteolysis induced by cancer

19
Q

neuromyopathic paraneoplastic syndrome

A

peripheral neuropathies, cortical cerebellar degeneration, polymyopathy resembling polymyositis, myasthenic syndrome

20
Q

acanthosis nigricans

A

gray black patches of thickened hyperkeratotic skin w/ velvety appearance

21
Q

hypertrophic osteoarthropathy

A

perosteal new bone formation at distal end of long bones, metatarsals, metacarpals, proximal phalanges

22
Q

migratory thrombophlebitis

A

associated w/ deep seated cancers (pancreas and lung)

23
Q

disseminated intravascular coagulation

A

associated w/ promyelocytic leukemia and prostatic adenocarcinoma

24
Q

grading

A

cytologic
behavior and differentiation are related
pathologist

25
Q

staging

A

surgical
based on size of primary lesion, extent of spread to regional lymph nodes, presence or absence of blood borne metastases
clinical