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POD 3 > Onc > Flashcards

Onc Flashcards

1
Q

What are the characteristics of neoplasia?

A

abnormal collection of new cells with autonomous/unregulated proliferation
clonal population-same initial genetic changes

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2
Q

What is the definition of a tumor?

A

swelling

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3
Q

How does a malignant tumor differ from a benign tumor?

A

malignant-can invade, destroy adjacent structures and/or metastasize
benign-bland appearance, localized

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4
Q

What is a pseudotumor?

A

non-neoplastic tumor (swelling from inflammation)

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5
Q

What is scirrhous?

A

dense desmoplasia making a tumor rock hard

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6
Q

What are violations of the -oma/benign naming scheme?

A 
leukemia-malignant
plasmacytoma/multiple myeloma-malignant
melanoma-malignant
glioma/glioblastoma-malignant (meningioma is benign)
mesothelioma
hepatoma
seminoma/dysgerminoma
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7
Q

What is characteristic for a true papillary structure?

A

has a central blood vessel

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8
Q

What is a mixed tumor?

A

single clone with different lines of differentiation
mixed tumor of salivary gland-pleomorphic adenoma
uterine tumor-3MT carcinosarcoma

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9
Q

What is the difference between desmoplasia and neoplasia?

A

normal cells reacting to a neoplasm (do not contain the mutations that the neoplasm does)

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10
Q

What is the difference between a mature and immature teratoma?

A

teratoma-cells of more than 1 germ cell layer (totipotential cells)-usually found in ovary or testicle
mature-mature elements
immature-immature elements, particularly immature neural cells, aggressive

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11
Q

What is a dermoid cyst?

A

tumor of ovary

lined with skin and skin appendages; may have hair, teeth

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12
Q

What is a hamartoma?

A

right cells for the right place but in wrong arrangement

benign, clonal proliferation

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13
Q

What is a choristoma?

A

wrong cells in the wrong place but in the right arrangement

ex-gastric heteropia of the esophagus

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14
Q

What is differentiation?

A

determines the grade
well-1 (trouble calling it cancer)
moderate-2 (no trouble calling it a specific kind)
poorly differentiated-3 (trouble figuring out kind of cancer)

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15
Q

What is anaplasia? What are the hallmarks of anaplasia?

A 
lack of differentiation
pleomorphism
hyperchromasia-darker nuclei
incrased nuclear:cytoplasmic ratio
large nucleoli 
atypical mitoses 
loss of polarity-nucleus away from lumen in colon
tumor giant cells
necrosis-outgrow blood supply
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16
Q

What does differentiation reveal about cell function?

A

well differentiated may maintain normal function
endocrine-secrete hormones
squamous-make carcinoma
less differentiated can also secrete hormones but they are frequently hormones not found in normal tissue ex AFP from hepatocellular carcinoma

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17
Q

What is metaplasia?

A

replacement of one normal cell type with a different normal cell type
ex. smokers keratin for protection, Barretts Esophagus

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18
Q

What is dysplasia?

A

neoplastic replacement of normal cells by abnormal cells-starting march to cancer
pleomorphism
loss of polarity
mitotic figures

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19
Q

What is carcinoma in situ?

A

severe dysplasia with marked pleomorphism
full thickness changes in epithelium but no invasion of basement membrane
when invasion of basement membrane-invasive

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20
Q

What is the tumor stage?

A 
more pathologic/prognostic than grade
TNM system
T-size and extent of invasion
N-number and location of involved lymph nodes
M-metastasis
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21
Q

What limits the rate of growth?

A

doubling time

growth fraction-what fraction of cells is replicative

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22
Q

Why does rate of growth correlate to differentiation?

A

well differentiated cells take more time to grow

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23
Q

What influences rate of growth?

A

hormone-leiomyoma grows with high estrogen stimulation

blood supply

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24
Q

How do cancer stem cells differ from normal stem cells?

A

In normal-divide asymmetrically (daughter cell with limited proliferative capacity)
cancer-has immortality, arise from normal tissue stem cells

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25
Q

Why are cancer stem cells resistant to conventional therapy?

A

low rate of cell division
multiple drug resistance
tumor initiating cells may remain-cause more cancer

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26
Q

What is the Warburg effect?

A

tumors lack oxygen dependent ATP generation
“glucose hunger”
build up of Kreb cycle intermediates-catabolic building for new daughter cells
PET measures 18F-flurodeoxyglucose uptake

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27
Q

How can a cancer cell avoid apoptosis?

A 
decrease CD95 (Fas)-->extrinsic pathway
FLIP expression to inhibit death complex
decrease p53
loss of APAF-1 (normally decreases caspase activation)
increased Bcl-2
increased IAPs (block caspase 9)
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28
Q

What are tumor suppressor genes?

A

genes that reduce genomic instability

slow cell growth (cancer wants to inactivate these)

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29
Q

What are oncogenes?

A

genes that increase genomic instability

promote cell growth (cancer wants to activate these)

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30
Q

How can you test for tumor suppressor mutations?

A

PCR for microsatellite instability-mutations hint at genomic instability

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31
Q

What is the two hit hypothesis?

A

need to mutations for tumor suppressors to be inactivated

mutations that activate tumor suppressors do not help cancer

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32
Q

How many mutations are necessary for oncogenes?

A

only one mutation needs to be activated for cancer cell to benefit
mutations that inactivate oncogenes do not help cancer

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33
Q

Why is there an increase in p53 in cancer?

A

mutant p53 when cell is under stress makes more inactive p53

creates a functional but not quantitative deficiency

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34
Q

How does HPV interact with tumor suppressors?

A

E6 binds to p53 and promotes degradation

E7 binds and inactivates Rb

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35
Q

What is Li-Fraumeni syndrome?

A

inherited p53 mutation
another somatic mutation
leads to multiple tumors at a young age
predisposed to various sarcomas and carcinomas

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36
Q

What is the APC/beta catenin pathway?

A

APC-tumor suppressor

down regulates growth promoting signal of beta-catenin

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37
Q

How many mutations are necessary within the APC/beta catenin pathway for cancer progression?

A

APC-2
Beta catenin-1
E-cadherin (functional APC can still handle this unless WNT is activated and blocks APC)
WNT-1 (works as an oncogene)

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38
Q

What is INK4a/ARF associated with?

A

familial melanoma

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39
Q

What is TGF-beta associated with?

A

pancreas

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40
Q

What is PTEN associated with?

A

Cowden syndrome (breast carcinomas)

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41
Q

What is NF1/NF2 associated with?

A

neurofibromatosis

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42
Q

What is VHL associated with?

A

von Hippel-Lindau syndrome

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43
Q

What is WT1/WT2 associated with?

A

Wilms tumor

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44
Q

What is PTCH associated with?

A

nevoid basal cell carcinoma syndrome

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45
Q

What does the RET gene cause?

A

cell survival in neuroendocrine cells

MEN2A and MEN2B

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46
Q

How can MEN2A and MEN2B be differentiated?

A

MEN2A-extracellular, thyroid, parathyroid, adrenal

MEN2B-intracellular, thyroid and adrenal

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47
Q

What mutation is responsible for gastrointestinal stromal tumor?

A

C-kit

treat with Imatinib

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48
Q

What translocation is seen in chronic myelomonocytic leukemia?

A

t (5;12)

PDGFR fused with TEL transcription factor (active without stimulus)

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49
Q

What translocation is seen in the Philadelphia chromosome? What gene product is seen and what does it cause?

A 
t (9;22)
BCR-ABL fusion gene
M-CML and ALL
m-ALL
can be treated with imatinib mesylate
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50
Q

What happens to growth receptors in cancer cells? What is an example?

A

upregulated receptors
Her2/neu overexpressed in breast cancers
treat with Trastuzumab

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51
Q

Where is EGFR activated?

A 
activated in carcinomas
lung and colon
upregulated in some glioblastomas 
treat with erlotinib, cetuximab (glio)
only works if activating mutations further down the chain are not present
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52
Q

Where are KRAS, NRAS, and HRAS mutations seen?

A

KRAS-common in GI and pancreatic tumors (codon 12, 13)

NRAS, HRAS-more common in thyroid neoplasms (codon 61)

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53
Q

Where are BRAF mutations seen?

A

V600E mutation
common in thyroid, melanoma, colon
can be targeted in metastatic melanoma

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54
Q

Where are PI3KCA mutations seen?

A

associated with breast, lung, colon, gynecologic cancers

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55
Q

How do tumors kill?

A 
Cachexia/wasting
hormones or paraneoplastic syndromes
infarction
bleeding
infection
bad location
invasion and metastasis
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56
Q

What causes cachexia?

A

increased BMR

probably due to cytokines

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57
Q

What is the difference between hormone secretion and paraneoplastic syndromes?

A

hormone-release hormones produced by tissue type

paraneoplastic-molecules not normally made by the tumor tissue creating symptoms

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58
Q

What cancers are associated with Cushing syndrome?

A

lung small cell
pancreatic
neural tumors

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59
Q

What cancers are associated with SIADH?

A

lung small cell

intracranial neoplasms

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60
Q

What cancers are associated with hypercalcemia?

A

lung squamous cell
breast
renal
adult T cell leuk/lymph

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61
Q

What is carcinoid syndrome?

A

elevated serotonin and bradykinin

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62
Q

What cancers are associated with polycythemia?

A

gastric
renal
cerebellar hemangioma
hepatocellular ca

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63
Q

What is hypertrophic osteroarthropathy?

A

seen in bronchogenic carcinoma

clubbing of digits (also seen in liver disease, diffuse lung disease, congenital heart disease)

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64
Q

What is associated with migratory thrombophlebitis?

A

lung and pancreas cancer

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65
Q

What is associated with DIC?

A

acute promyelocytic leukemia

prostate cancer

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66
Q

What is nonbacterial thrombotic endocarditis?

A

sterile fibrin vegetations on valve leaflets

seen in non-neoplastic causes like rheumatic fever and lupus

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67
Q

What cancer is the most thrombogenic?

A

mucinous adenocarcinoma

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68
Q

What are examples of bleeding seen in cancer?

A

melena-coln cancer eroded by fecal flow

hematuria in bladder cancer

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69
Q

What is an example of a metastasis that seeds the body cavities?

A

pseudomyxoma peritonei-from mucous secreting appendix carcinoma

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70
Q

What is the sentinel lymph node?

A

first node in a regional lymphatic basin receiving lymph flow from tumor

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71
Q

What is a skip metastasis?

A

lymph node metastasis beyond first line lymph nodes due to anastomoses of lymphatics

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72
Q

What is hematogenous spread? What are examples?

A

veins are more easily penetrated than arteries
tend to rest in first capillary bed encountered
portal vein-liver metastases in colon cancer
veins-lung metastasis
paravertebral venous plexus-prostate and thyroid vertebral metastasis

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73
Q

What is tumor emboli homing? What are examples?

A

Organ tropism for metastaiss
breast-bone
lung-adrenal gland and brain
neuroblastoma-liver and bones

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74
Q

What cancers are most known for dormancy?

A

breast and melanoma

prolonged survival of micrometastases without progression

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75
Q

What does a tumor secrete to make metastatic site habitable?

A

cytokines
growth factors
ECM molecules

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76
Q

What are the universal properties of cancer?

A

uncontrolled proliferation-autocrine growth stimulation and do not exhibit contact inhibition
immortalization
protection from antiproliferative signaling
protection from apoptosis

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77
Q

What are the properties of solid tumors?

A

angiogenesis

invasion and metastasis

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78
Q

What are the emerging properties of tumors?

A

deregulation of cellular energetics

evasion of immune system

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79
Q

What are enabling properties of tumors?

A

genome instability and mutation

tumor-promoting inflammation

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80
Q

How can clonal relationships be established in cancer?

A

same G6PD

mixture of different A/B isotypes are not 1:1

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81
Q

What are the results of gain of function mutations in oncogenes?

A 
sustained cellular proliferation
advancement of cell cycle progression
decreased requirement of growth factors
promotion of metastasis
protection from apoptosis
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82
Q

How are proto-oncogenes converted?

A

gain of function-increased expression or loss of regulation
viral mechanisms or mutational mechanisms
-deletion or point mutation
-gene amplification
-overexpression (novel promoter)
-novel product (new coding region)

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83
Q

What disorders are associated with defects in Rb?

A

retinoblastoma

sporadic-small cell lung carcinoma

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84
Q

What disorders are associated with p53 mutations?

A

Li-Fraumeni

sporadic-lung and breast cancer

85
Q

What disorders are associated with BRCA1?

A

familial breast cancer due to mutated ds break repair

sporadic-breast and ovarian cancer

86
Q

What disorders are associated with NF1?

A

neurofibromatosis due to mutated GTPase activator

87
Q

What are the differences between familial and sporadic retinoblastoma?

A

familal-multiple tumors, early onset, bilateral

sporadic-single unilateral tumor, late onset

88
Q

What is LOH? How can it occur

A 
loss of heterozygosity is loss of one allele
discoverd by RFLP
-local events
-somatic recombination
-loss and duplication
-chromosome loss
89
Q

What is FAP?

A

familial adenomatous polyposis due to mutation in APC
presents with rectal bleeding
attenuated (100 polyps) or fulminant (100-1000 polyps)

90
Q

What genes are associated with hereditary nonpolyposis colorectal cancer syndrome?

A

MLH1, MSH2, MSH6, or PMS2

91
Q

What is chromosomal instability?

A

increased mutability to a cancer

translocations can be defining or diagnostic markers

92
Q

What causes chromosomal instability?

A

mutations in nucleotide metabolism, DNA replication, chromosome segregation
telomere attrition
aneuploidy
hypomethylation
ds breaks
cellular stress-hypoxia, pH, high osmolarity
VDJ recombination therapies

93
Q

How do epigenetics influence cancer?

A

gene silencing of tumor suppressors by hypermethylation
activation of oncogenes by hypomethylation
genomic instability
reversible changes

94
Q

What epigenetic factors can contribute to cancer progression?

A

reactivation of retrosposons and elimination of methylation borders secondary to hypomethylation
Alu elements harbor 33% of CpG
strongest risk of hypomethylation is age

95
Q

How do epigenetics influence therapy?

A

epigenetic alterations may be driving drug resistance
decitabine
HDAC inhibitors have been developed

96
Q

What is the relationship between IDH1 and glioblastoma?

A

90% of IDH1 mutations are R132H in glioblastoma
epigenetically driven responds poorly to surgery
(most of secondary glioblastomas are IDH1 mutant)

97
Q

What is the difference between a carcinogen and mutagen?

A

carcinogen-agent that induces cancer (most are mutagens)

mutagen-raises the frequency of mutation above the spontaneous rate

98
Q

What is remission?

A

cancer not detectable by the most sensitive measures

99
Q

What is cure?

A

zero cancer cells present

100
Q

What is first line therapy?

A

first treatment for a disease

101
Q

What is used for Hodgkin’s disease?

A

MOPP, ABVD

102
Q

What is used for non-Hodgkin’s disease?

A

CHOP

103
Q

What is used for breast cancer?

A

CMF, CAF

104
Q

What is used for small cell lung cancer?

A

PACE

105
Q

What is used for germ line cancer?

A

VIP

106
Q

What is used for cervical cancer?

A

BIP

107
Q

What is used for lymphomas?

A

M-BACOD

108
Q

What is for ovarian cancer?

A

BEP

109
Q

What is used for pheochromocytoma?

A

CVD

110
Q

What is used for testicular cancer?

A

PEB

111
Q

What drugs are M phase specific?

A

vincristine, vinblastine, paclitaxel

112
Q

What drugs are S phase specific?

A

cytosine arabinoside

hydroxyurea

113
Q

What are the problems with cancer chemotherapy?

A

dose-limiting toxicities
resistance
multidrug glycoprotein pumps
second cancers-leukemia and lymphoma

114
Q

What are the characteristics of alyklating agents?

A

cross linking DNA-blocks DNA replication and transcription
cytotoxic-proliferative dependent, mainly affect G1 and S
resistance-decreased permeability or uptake, increased nucleophiles or repiar
toxicity-decreased bone marrow, nausea, fetal death

115
Q

Which drug resembles phenylamine?

A

melphalon

116
Q

What is the MOA of alkylating agents?

A

reaction with N7 of guanine in DNA

needs both strands for cross-linking to occur

117
Q

What are the unique characteristics of cylcosphamide?

A

must be activated by p450, causes hemorrhagic cystitis and SIADH

118
Q

What is the toxicity caused by chlorambucil?

A

hepatotoxicity

119
Q

What can be given to decrease the hemorrhagic cystitis?

A

MESNA (byproduct acrolein is responsible for the adverse reaction)
MESNA reacts and detoxes

120
Q

What is a unique toxicity of busulfan?

A

pulmonary fibrosis and hyperpigmented skin

121
Q

What are carmustine, lomustine, semustine, streptozocin used to treat?

A

first line of therapy for brain tumors

122
Q

What should be avoided when giving procarbazine?

A

MAOI and alcohol

123
Q

What is the MOA of dacarbazine and temozolamide?

A

methylates DNA and RNA

124
Q

What is the MOA for platinum containing drugs?

A

binds to guanine and forms intrastrand crosslinks

also binds to protein

125
Q

What are the toxicities associated with cisplatin?

A

nephrotoxicity-give forced diuresis
avoid if renal clearance is below 60
ototoxicity
peripheral neuropathy

126
Q

What is the MOA for anthracyclines?

A

tight bindign between base pairs in DNA
blocks activity of topo II
inhibition of DNA repair
cause histone eviction from open chromatin

127
Q

What is a unique toxicity of antracyclines, particularly doxorubicin?

A

cardiotoxicity (can be prevented by dexrazoxane)

128
Q

What is the MOA for mitoxantrone?

A

produce double stranded breaks through complexes but does not produce free radicals
lowers liklihood of cardiotoxicty

129
Q

What drugs are a derivative of podophyllotoxin? What is the MOA?

A

epipodophyllotoxins (etoposide and tenopside)
form a complex with DNA topo II
kills in S and G2

130
Q

What is the MOA for camptothecin analogs?

A

captothecin, topetecan, irinotecan inhibit topo I

act in S phase

131
Q

What is unique about irinotecan?

A

prodrug activated in tissue by carboxyesterases (high in carcinoma)

132
Q

What are bleomycins and when are they active?

A

combination of structurally related antibiotics

active in G2 phase

133
Q

What are the unique toxicities associated with bleomycins?

A

pulmonary fibrosis and pneumonitis
cutaneous reactions
low grade fever
minimal BM suppression

134
Q

What is the mechanism of action for dactinomycin?

A

interaction of peptide loops of dactinomycin at purine-pyrimidine (dG-dC) base pairs and intercalate to prevent DNA transcription

135
Q

What are the toxicities associated with dactinomycin?

A

oral and GI ulceration

stomatitis

136
Q

What is the MOA of folic acid analogs?

A

MTX inhibits dihydrofolate reductase to block biosyntehsis of thymidylate and purines-decreases DNA synthesis
pemetrexed also directly inhibits thymidylate synthase
S phase specific

137
Q

What does pemetrexed inhibit?

A

tymidylate synthase, GAR formyltransferase, AICAR formyltransferase

138
Q

What are the unique toxicities associated with methotrexate and pemetrexed?

A

oral and GI ulceration; hepatotoxicity; pulmonary toxicity

139
Q

What is leucovorin?

A

minimizes the toxic effects of folate depletion

given 24-36 hours after MTX (bypass block without minimizing anti-tumor activity)

140
Q

What is the MOA of 5-flurouracil?

A

decrease DNA synthesis by inhibition of thymidylate synthase, incorporation into DNA
G1 and S phase

141
Q

What are the toxicities associated with 5FU?

A

oral and GI ulceration

142
Q

What is the MOA for cytarbine?

A

S phase

inhibits polymerase alpha

143
Q

What is the MOA for mercaptopurine?

A

S phase

inhibits synthesis of adenine and guanine by blocking conversion of inosinate to purine precursors

144
Q

What are adenosine deaminase inhibitors?

A

pentostatin, cladribine, fludarabine

inhibits ADA leading to buildup of adenosine and deoxyadenosine nucleotides

145
Q

What are the vinca alkaloids?

A

vincristine, vinblastine, vinorelbine

146
Q

What are the yew alkaloids?

A

paclitaxel, docetaxel

147
Q

What is the MOA for vincristine?

A

M phase

bind to soluble tubulin and blocks polymerization

148
Q

What is the MOA for paclitaxel?

A

M phase

prevents depolymerization

149
Q

What are the toxicities associated with vincristine?

A

alopecia, peripheral neuropathy, SIADH

150
Q

What are the toxicities associated with paclitaxel?

A

peripheral neuropathy

151
Q

What is the MOA of asparaginase?

A

depletion of L asparagine leads to inhibition of RNA and DNA synthesis

152
Q

What is mitotane?

A

similar to DDT
used for adrenocortical cancers
blocks hormone production of adrenal
steroid hormone pills must be given to minimize side effects

153
Q

What are interferons?

A

cytokines

INF-alpha slows G1 to S and S to G2

154
Q

What is prednisone?

A

anti-inflammatory used to cause apoptosis in leukemic cells

155
Q

What are progestins used for?

A

used in hormone responsive cancers expressing progesterone receptor

156
Q

What are antiestrogens (tamoxifen, toremefine) used for?

A

used in estrogen receptor positive breast cancer

157
Q

What is tamoxifen?

A

not a steroid, has activity against estrogen

158
Q

What are the anti-androgens (bicalutamide, flutamide, and nilutamide) used for?

A

blocks androgen growth

159
Q

What is the purpose of leuprolide?

A

luteinizing hormone releasing hormone agonist

combination leads to total androgen ablation

160
Q

What is bevaczimab used for?

A

blocks VEGF and prevents angiogenesis

161
Q

What is denusomab used for?

A

blocks RANK-RANKL in bone

162
Q

What is trastuzumab used for?

A

blocks Her2/neu

163
Q

What is gemtuzumab used for?

A

blocks CD33 on leukemia

164
Q

What is rituximab used for?

A

blocks CD20 on B cells

165
Q

What is alemtuzumab used for?

A

blocks CD52 on lymphocytes

166
Q

What drugs are CLTA4 antibodies?

A

ipilimumab and tremelimumab

cause colitis

167
Q

What drugs are PD1 antibodies?

A

nivolumab and pembrolizumab

cause colitis and skin rash

168
Q

What is the MOA for imatinib?

A

blocks Bcr-Abl kinase

169
Q

What is the MOA for erlotinib, gefitinib?

A

blocks EGFR

170
Q

What is the MOA for crizotinib?

A

blocks ALK-1 kinase

171
Q

What is the MOA for bortezomib?

A

blocks proteosomal degradation

172
Q

What is the MOA for sorafenib?

A

blocks B-raf kinase

173
Q

What drug binds to Bcl-2?

A

venetoclax

174
Q

What are some HDAC inhibitors?

A

vorinostat

romidepsin

175
Q

What is a PARP-1 inhibitor?

A

olaparib

176
Q

What is amirubicin?

A

anthracycline with reduced cardiotoxicity

177
Q

What is the MOA of fulvestrant?

A

ER blocker, partial estrogen activity

178
Q

What is abraxane?

A

nanoparticle for formulation of paclitaxel, chemophor free (decrease in hypersensitivity)

179
Q

What is picoplatin?

A

does not cause platinum resistance like other platinum containing drugs

180
Q

What is cytology used from?

A

fine needle aspirate
pap smear
body fluid

181
Q

What is immunochemistry useful for?

A

stain specific antigens in a cell

prognostic or predictive-Her2/neu presence

182
Q

Why is electron microscopy frequently not used?

A

special handling and fixation

outrageously expensive

183
Q

What is flow cytometry used for?

A

count individual cells and characterize cell antigens/DNA content
used for lymphomas and leukemias

184
Q

How can residual disease be detected?

A

FISH, PCR, RT-PCR

problem-low sensitivity and specificity when testing for tumor markers

185
Q

What is PSA?

A

prostate adenocarcinoma marker

186
Q

What is alpha FP?

A

hepatoma and seminoma marker

187
Q

What is HCG?

A

choriocarcinoma marker

188
Q

What is CEA?

A

colon cancer marker

189
Q

What is CA19.9?

A

marker for pancreatic cancer

190
Q

What is CA125?

A

marker for ovarian cancer

191
Q

What are some GWA genetic markers?

A

prostate-8q24

lung-15q25

192
Q

When is ALK inhibitor crizotinib most beneficial?

A

neuroblastoma with ALK mutations R1275Q or F11742

193
Q

What did ch14.18 target?

A

GD2 on surface of neuroblastoma

194
Q

What was ATRA added to treat?

A

APL, increased survival

195
Q

What is CART T?

A

T cells programmed against CD19 cells

196
Q

What are the most common cancers by incidence?

A

prostate/breast
lung
colorectal

197
Q

What are the most common cancers by death?

A

lung
bresast/prostate
colorectal

198
Q

Why have death rates declined?

A

improved detection and treatment

decreased smoking

199
Q

What does chronic inflammation do?

A

cellular damage created that can lead to cancer

non-hereditary predisposing condition

200
Q

What cancers are the immunodeficient susceptible to?

A

Lymphomas-diffuse large B cell lymphomas

Kaposi sarcoma

201
Q

What does UV exposure increase risk of?

A

cumulative-nonmelanoma skin cancer

intermittent but intense-melanoma

202
Q

What tissues are most sensitive to ionizing radiation?

A

directly fractures double helix
hematopoietic-leukemia
thyroid in young
breast, lung, salivary gland

203
Q

What is the difference between direct and indirect acting agents?

A

direct-no metabolic conversion needed, weak carcinogens (alkylating agents)
indirect-require metabolic conversion, enzymes matter (CYP1A1 increases lung cancer in smokers) (PCV, amides, nitrites)

204
Q

What are the major infection associated malignancies?

A

stomach-H pylori
cervical-HPV
liver-Hep B and C
Burkitts lymphoma and nasopharyngeal-EBV
Kaposi sarcoma and non-Hodgkin lymphoma-HIV/HHV8
bladder and colon-schistosomiasis
adult T cell leukemia/lymphoma-human T cell lymphotrophic virus type 1

205
Q

How do infections induce malignancies?

A 
immunosuppression
chronic inflammation
oxidative stress
DNA damage and mutation
cell injury 
cell division
206
Q

What is aflatoxin B associated with?

A

Hepatocellular carcinoma (when given a high protein diet)

207
Q

What are examples of primary prevention?

A 
decrease alcohol and tobacco use
decreased exposure to carcinogens
decreased exposure to radiation and excessive sunlight
access to clean water
safe sex
immunization and treatment of infections
208
Q

What are examples of secondary prevention?

A

mass population and selective cancer screening through IARC and SEER

POD 3 (4 decks)

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