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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
Why are cancer stem cells resistant to conventional therapy?
low rate of cell division multiple drug resistance tumor initiating cells may remain-cause more cancer
26
What is the Warburg effect?
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
27
How can a cancer cell avoid apoptosis?
``` 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) ```
28
What are tumor suppressor genes?
genes that reduce genomic instability | slow cell growth (cancer wants to inactivate these)
29
What are oncogenes?
genes that increase genomic instability | promote cell growth (cancer wants to activate these)
30
How can you test for tumor suppressor mutations?
PCR for microsatellite instability-mutations hint at genomic instability
31
What is the two hit hypothesis?
need to mutations for tumor suppressors to be inactivated | mutations that activate tumor suppressors do not help cancer
32
How many mutations are necessary for oncogenes?
only one mutation needs to be activated for cancer cell to benefit mutations that inactivate oncogenes do not help cancer
33
Why is there an increase in p53 in cancer?
mutant p53 when cell is under stress makes more inactive p53 | creates a functional but not quantitative deficiency
34
How does HPV interact with tumor suppressors?
E6 binds to p53 and promotes degradation | E7 binds and inactivates Rb
35
What is Li-Fraumeni syndrome?
inherited p53 mutation another somatic mutation leads to multiple tumors at a young age predisposed to various sarcomas and carcinomas
36
What is the APC/beta catenin pathway?
APC-tumor suppressor | down regulates growth promoting signal of beta-catenin
37
How many mutations are necessary within the APC/beta catenin pathway for cancer progression?
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)
38
What is INK4a/ARF associated with?
familial melanoma
39
What is TGF-beta associated with?
pancreas
40
What is PTEN associated with?
Cowden syndrome (breast carcinomas)
41
What is NF1/NF2 associated with?
neurofibromatosis
42
What is VHL associated with?
von Hippel-Lindau syndrome
43
What is WT1/WT2 associated with?
Wilms tumor
44
What is PTCH associated with?
nevoid basal cell carcinoma syndrome
45
What does the RET gene cause?
cell survival in neuroendocrine cells | MEN2A and MEN2B
46
How can MEN2A and MEN2B be differentiated?
MEN2A-extracellular, thyroid, parathyroid, adrenal | MEN2B-intracellular, thyroid and adrenal
47
What mutation is responsible for gastrointestinal stromal tumor?
C-kit | treat with Imatinib
48
What translocation is seen in chronic myelomonocytic leukemia?
t (5;12) | PDGFR fused with TEL transcription factor (active without stimulus)
49
What translocation is seen in the Philadelphia chromosome? What gene product is seen and what does it cause?
``` t (9;22) BCR-ABL fusion gene M-CML and ALL m-ALL can be treated with imatinib mesylate ```
50
What happens to growth receptors in cancer cells? What is an example?
upregulated receptors Her2/neu overexpressed in breast cancers treat with Trastuzumab
51
Where is EGFR activated?
``` 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 ```
52
Where are KRAS, NRAS, and HRAS mutations seen?
KRAS-common in GI and pancreatic tumors (codon 12, 13) | NRAS, HRAS-more common in thyroid neoplasms (codon 61)
53
Where are BRAF mutations seen?
V600E mutation common in thyroid, melanoma, colon can be targeted in metastatic melanoma
54
Where are PI3KCA mutations seen?
associated with breast, lung, colon, gynecologic cancers
55
How do tumors kill?
``` Cachexia/wasting hormones or paraneoplastic syndromes infarction bleeding infection bad location invasion and metastasis ```
56
What causes cachexia?
increased BMR | probably due to cytokines
57
What is the difference between hormone secretion and paraneoplastic syndromes?
hormone-release hormones produced by tissue type | paraneoplastic-molecules not normally made by the tumor tissue creating symptoms
58
What cancers are associated with Cushing syndrome?
lung small cell pancreatic neural tumors
59
What cancers are associated with SIADH?
lung small cell | intracranial neoplasms
60
What cancers are associated with hypercalcemia?
lung squamous cell breast renal adult T cell leuk/lymph
61
What is carcinoid syndrome?
elevated serotonin and bradykinin
62
What cancers are associated with polycythemia?
gastric renal cerebellar hemangioma hepatocellular ca
63
What is hypertrophic osteroarthropathy?
seen in bronchogenic carcinoma | clubbing of digits (also seen in liver disease, diffuse lung disease, congenital heart disease)
64
What is associated with migratory thrombophlebitis?
lung and pancreas cancer
65
What is associated with DIC?
acute promyelocytic leukemia | prostate cancer
66
What is nonbacterial thrombotic endocarditis?
sterile fibrin vegetations on valve leaflets | seen in non-neoplastic causes like rheumatic fever and lupus
67
What cancer is the most thrombogenic?
mucinous adenocarcinoma
68
What are examples of bleeding seen in cancer?
melena-coln cancer eroded by fecal flow | hematuria in bladder cancer
69
What is an example of a metastasis that seeds the body cavities?
pseudomyxoma peritonei-from mucous secreting appendix carcinoma
70
What is the sentinel lymph node?
first node in a regional lymphatic basin receiving lymph flow from tumor
71
What is a skip metastasis?
lymph node metastasis beyond first line lymph nodes due to anastomoses of lymphatics
72
What is hematogenous spread? What are examples?
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
73
What is tumor emboli homing? What are examples?
Organ tropism for metastaiss breast-bone lung-adrenal gland and brain neuroblastoma-liver and bones
74
What cancers are most known for dormancy?
breast and melanoma | prolonged survival of micrometastases without progression
75
What does a tumor secrete to make metastatic site habitable?
cytokines growth factors ECM molecules
76
What are the universal properties of cancer?
uncontrolled proliferation-autocrine growth stimulation and do not exhibit contact inhibition immortalization protection from antiproliferative signaling protection from apoptosis
77
What are the properties of solid tumors?
angiogenesis | invasion and metastasis
78
What are the emerging properties of tumors?
deregulation of cellular energetics | evasion of immune system
79
What are enabling properties of tumors?
genome instability and mutation | tumor-promoting inflammation
80
How can clonal relationships be established in cancer?
same G6PD | mixture of different A/B isotypes are not 1:1
81
What are the results of gain of function mutations in oncogenes?
``` sustained cellular proliferation advancement of cell cycle progression decreased requirement of growth factors promotion of metastasis protection from apoptosis ```
82
How are proto-oncogenes converted?
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)
83
What disorders are associated with defects in Rb?
retinoblastoma | sporadic-small cell lung carcinoma
84
What disorders are associated with p53 mutations?
Li-Fraumeni | sporadic-lung and breast cancer
85
What disorders are associated with BRCA1?
familial breast cancer due to mutated ds break repair | sporadic-breast and ovarian cancer
86
What disorders are associated with NF1?
neurofibromatosis due to mutated GTPase activator
87
What are the differences between familial and sporadic retinoblastoma?
familal-multiple tumors, early onset, bilateral | sporadic-single unilateral tumor, late onset
88
What is LOH? How can it occur
``` loss of heterozygosity is loss of one allele discoverd by RFLP -local events -somatic recombination -loss and duplication -chromosome loss ```
89
What is FAP?
familial adenomatous polyposis due to mutation in APC presents with rectal bleeding attenuated (100 polyps) or fulminant (100-1000 polyps)
90
What genes are associated with hereditary nonpolyposis colorectal cancer syndrome?
MLH1, MSH2, MSH6, or PMS2
91
What is chromosomal instability?
increased mutability to a cancer | translocations can be defining or diagnostic markers
92
What causes chromosomal instability?
mutations in nucleotide metabolism, DNA replication, chromosome segregation telomere attrition aneuploidy hypomethylation ds breaks cellular stress-hypoxia, pH, high osmolarity VDJ recombination therapies
93
How do epigenetics influence cancer?
gene silencing of tumor suppressors by hypermethylation activation of oncogenes by hypomethylation genomic instability reversible changes
94
What epigenetic factors can contribute to cancer progression?
reactivation of retrosposons and elimination of methylation borders secondary to hypomethylation Alu elements harbor 33% of CpG strongest risk of hypomethylation is age
95
How do epigenetics influence therapy?
epigenetic alterations may be driving drug resistance decitabine HDAC inhibitors have been developed
96
What is the relationship between IDH1 and glioblastoma?
90% of IDH1 mutations are R132H in glioblastoma epigenetically driven responds poorly to surgery (most of secondary glioblastomas are IDH1 mutant)
97
What is the difference between a carcinogen and mutagen?
carcinogen-agent that induces cancer (most are mutagens) | mutagen-raises the frequency of mutation above the spontaneous rate
98
What is remission?
cancer not detectable by the most sensitive measures
99
What is cure?
zero cancer cells present
100
What is first line therapy?
first treatment for a disease
101
What is used for Hodgkin's disease?
MOPP, ABVD
102
What is used for non-Hodgkin's disease?
CHOP
103
What is used for breast cancer?
CMF, CAF
104
What is used for small cell lung cancer?
PACE
105
What is used for germ line cancer?
VIP
106
What is used for cervical cancer?
BIP
107
What is used for lymphomas?
M-BACOD
108
What is for ovarian cancer?
BEP
109
What is used for pheochromocytoma?
CVD
110
What is used for testicular cancer?
PEB
111
What drugs are M phase specific?
vincristine, vinblastine, paclitaxel
112
What drugs are S phase specific?
cytosine arabinoside | hydroxyurea
113
What are the problems with cancer chemotherapy?
dose-limiting toxicities resistance multidrug glycoprotein pumps second cancers-leukemia and lymphoma
114
What are the characteristics of alyklating agents?
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
Which drug resembles phenylamine?
melphalon
116
What is the MOA of alkylating agents?
reaction with N7 of guanine in DNA | needs both strands for cross-linking to occur
117
What are the unique characteristics of cylcosphamide?
must be activated by p450, causes hemorrhagic cystitis and SIADH
118
What is the toxicity caused by chlorambucil?
hepatotoxicity
119
What can be given to decrease the hemorrhagic cystitis?
MESNA (byproduct acrolein is responsible for the adverse reaction) MESNA reacts and detoxes
120
What is a unique toxicity of busulfan?
pulmonary fibrosis and hyperpigmented skin
121
What are carmustine, lomustine, semustine, streptozocin used to treat?
first line of therapy for brain tumors
122
What should be avoided when giving procarbazine?
MAOI and alcohol
123
What is the MOA of dacarbazine and temozolamide?
methylates DNA and RNA
124
What is the MOA for platinum containing drugs?
binds to guanine and forms intrastrand crosslinks | also binds to protein
125
What are the toxicities associated with cisplatin?
nephrotoxicity-give forced diuresis avoid if renal clearance is below 60 ototoxicity peripheral neuropathy
126
What is the MOA for anthracyclines?
tight bindign between base pairs in DNA blocks activity of topo II inhibition of DNA repair cause histone eviction from open chromatin
127
What is a unique toxicity of antracyclines, particularly doxorubicin?
cardiotoxicity (can be prevented by dexrazoxane)
128
What is the MOA for mitoxantrone?
produce double stranded breaks through complexes but does not produce free radicals lowers liklihood of cardiotoxicty
129
What drugs are a derivative of podophyllotoxin? What is the MOA?
epipodophyllotoxins (etoposide and tenopside) form a complex with DNA topo II kills in S and G2
130
What is the MOA for camptothecin analogs?
captothecin, topetecan, irinotecan inhibit topo I | act in S phase
131
What is unique about irinotecan?
prodrug activated in tissue by carboxyesterases (high in carcinoma)
132
What are bleomycins and when are they active?
combination of structurally related antibiotics | active in G2 phase
133
What are the unique toxicities associated with bleomycins?
pulmonary fibrosis and pneumonitis cutaneous reactions low grade fever minimal BM suppression
134
What is the mechanism of action for dactinomycin?
interaction of peptide loops of dactinomycin at purine-pyrimidine (dG-dC) base pairs and intercalate to prevent DNA transcription
135
What are the toxicities associated with dactinomycin?
oral and GI ulceration | stomatitis
136
What is the MOA of folic acid analogs?
MTX inhibits dihydrofolate reductase to block biosyntehsis of thymidylate and purines-decreases DNA synthesis pemetrexed also directly inhibits thymidylate synthase S phase specific
137
What does pemetrexed inhibit?
tymidylate synthase, GAR formyltransferase, AICAR formyltransferase
138
What are the unique toxicities associated with methotrexate and pemetrexed?
oral and GI ulceration; hepatotoxicity; pulmonary toxicity
139
What is leucovorin?
minimizes the toxic effects of folate depletion | given 24-36 hours after MTX (bypass block without minimizing anti-tumor activity)
140
What is the MOA of 5-flurouracil?
decrease DNA synthesis by inhibition of thymidylate synthase, incorporation into DNA G1 and S phase
141
What are the toxicities associated with 5FU?
oral and GI ulceration
142
What is the MOA for cytarbine?
S phase | inhibits polymerase alpha
143
What is the MOA for mercaptopurine?
S phase | inhibits synthesis of adenine and guanine by blocking conversion of inosinate to purine precursors
144
What are adenosine deaminase inhibitors?
pentostatin, cladribine, fludarabine | inhibits ADA leading to buildup of adenosine and deoxyadenosine nucleotides
145
What are the vinca alkaloids?
vincristine, vinblastine, vinorelbine
146
What are the yew alkaloids?
paclitaxel, docetaxel
147
What is the MOA for vincristine?
M phase | bind to soluble tubulin and blocks polymerization
148
What is the MOA for paclitaxel?
M phase | prevents depolymerization
149
What are the toxicities associated with vincristine?
alopecia, peripheral neuropathy, SIADH
150
What are the toxicities associated with paclitaxel?
peripheral neuropathy
151
What is the MOA of asparaginase?
depletion of L asparagine leads to inhibition of RNA and DNA synthesis
152
What is mitotane?
similar to DDT used for adrenocortical cancers blocks hormone production of adrenal steroid hormone pills must be given to minimize side effects
153
What are interferons?
cytokines | INF-alpha slows G1 to S and S to G2
154
What is prednisone?
anti-inflammatory used to cause apoptosis in leukemic cells
155
What are progestins used for?
used in hormone responsive cancers expressing progesterone receptor
156
What are antiestrogens (tamoxifen, toremefine) used for?
used in estrogen receptor positive breast cancer
157
What is tamoxifen?
not a steroid, has activity against estrogen
158
What are the anti-androgens (bicalutamide, flutamide, and nilutamide) used for?
blocks androgen growth
159
What is the purpose of leuprolide?
luteinizing hormone releasing hormone agonist | combination leads to total androgen ablation
160
What is bevaczimab used for?
blocks VEGF and prevents angiogenesis
161
What is denusomab used for?
blocks RANK-RANKL in bone
162
What is trastuzumab used for?
blocks Her2/neu
163
What is gemtuzumab used for?
blocks CD33 on leukemia
164
What is rituximab used for?
blocks CD20 on B cells
165
What is alemtuzumab used for?
blocks CD52 on lymphocytes
166
What drugs are CLTA4 antibodies?
ipilimumab and tremelimumab | cause colitis
167
What drugs are PD1 antibodies?
nivolumab and pembrolizumab | cause colitis and skin rash
168
What is the MOA for imatinib?
blocks Bcr-Abl kinase
169
What is the MOA for erlotinib, gefitinib?
blocks EGFR
170
What is the MOA for crizotinib?
blocks ALK-1 kinase
171
What is the MOA for bortezomib?
blocks proteosomal degradation
172
What is the MOA for sorafenib?
blocks B-raf kinase
173
What drug binds to Bcl-2?
venetoclax
174
What are some HDAC inhibitors?
vorinostat | romidepsin
175
What is a PARP-1 inhibitor?
olaparib
176
What is amirubicin?
anthracycline with reduced cardiotoxicity
177
What is the MOA of fulvestrant?
ER blocker, partial estrogen activity
178
What is abraxane?
nanoparticle for formulation of paclitaxel, chemophor free (decrease in hypersensitivity)
179
What is picoplatin?
does not cause platinum resistance like other platinum containing drugs
180
What is cytology used from?
fine needle aspirate pap smear body fluid
181
What is immunochemistry useful for?
stain specific antigens in a cell | prognostic or predictive-Her2/neu presence
182
Why is electron microscopy frequently not used?
special handling and fixation | outrageously expensive
183
What is flow cytometry used for?
count individual cells and characterize cell antigens/DNA content used for lymphomas and leukemias
184
How can residual disease be detected?
FISH, PCR, RT-PCR | problem-low sensitivity and specificity when testing for tumor markers
185
What is PSA?
prostate adenocarcinoma marker
186
What is alpha FP?
hepatoma and seminoma marker
187
What is HCG?
choriocarcinoma marker
188
What is CEA?
colon cancer marker
189
What is CA19.9?
marker for pancreatic cancer
190
What is CA125?
marker for ovarian cancer
191
What are some GWA genetic markers?
prostate-8q24 | lung-15q25
192
When is ALK inhibitor crizotinib most beneficial?
neuroblastoma with ALK mutations R1275Q or F11742
193
What did ch14.18 target?
GD2 on surface of neuroblastoma
194
What was ATRA added to treat?
APL, increased survival
195
What is CART T?
T cells programmed against CD19 cells
196
What are the most common cancers by incidence?
prostate/breast lung colorectal
197
What are the most common cancers by death?
lung bresast/prostate colorectal
198
Why have death rates declined?
improved detection and treatment | decreased smoking
199
What does chronic inflammation do?
cellular damage created that can lead to cancer | non-hereditary predisposing condition
200
What cancers are the immunodeficient susceptible to?
Lymphomas-diffuse large B cell lymphomas | Kaposi sarcoma
201
What does UV exposure increase risk of?
cumulative-nonmelanoma skin cancer | intermittent but intense-melanoma
202
What tissues are most sensitive to ionizing radiation?
directly fractures double helix hematopoietic-leukemia thyroid in young breast, lung, salivary gland
203
What is the difference between direct and indirect acting agents?
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
What are the major infection associated malignancies?
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
How do infections induce malignancies?
``` immunosuppression chronic inflammation oxidative stress DNA damage and mutation cell injury cell division ```
206
What is aflatoxin B associated with?
Hepatocellular carcinoma (when given a high protein diet)
207
What are examples of primary prevention?
``` 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
What are examples of secondary prevention?
mass population and selective cancer screening through IARC and SEER

POD 3 (4 decks)

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