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Foundations2 > Cancer > Flashcards

Cancer Flashcards

0
Q

Squamous metaplastic cells? what kind of cancer does this lead to?

A

Endocervical, airway, urothelium
glandular/columnar –> squamous
Squamous cell carcinoma

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1
Q

Glandular metaplastic cells? what kind of cancer does this lead to?

A

Barrett’s esophagitis (squamous –> columnar, goblet)

Adenocarcinoma

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2
Q

Normal squamous epithelium?

A

skin, oral cavity, cervix

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3
Q

Normal glandular epithlium?

A

Endocrine/exocrine, resp tract, GI tract/system, prostate/ovaries/uterus/breast

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4
Q

How to characterize severity of dysplasia?

A

low–> high grade depending on thickness of epithelial invasion

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5
Q

What is carcinoma in situ?

A

full thickness dysplasia (has not yet invaded BM)

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6
Q

3 types of epithelial neoplasms

A

polyp- protrusion; sessile v pedunculated (mushroom)
papillary- fingers w fibrovascular core (ex. warts)
cystic- fluid filled; multilocular and unilocular

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7
Q

Unique path features of squamous cell carcinoma

A
  • intercelllular bridges

- keratinization (wholres, pearls, dyskeratotic; keratin antibody 5,6 will stain brown)

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8
Q

Unique path features of adenocarcinoma?

A

Variable patterns depending on differentiation
Good differentiation- acinar, glandular
Poor differentiation- nests, sheets, trabecular, signet ring, cords

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9
Q

What is a sarcoma?

A

mesenchymal tumor

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10
Q

Cancer of smooth muscle tissue? histo?

A

leiomyeosarcoma

cells no longer spindle shaped

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11
Q

Cancer of cartilage? histo?

A

chondrosarcoma

produces hyalin matrix; multiple cells per lacunae; pleomorphism

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12
Q

Leukemia v lymphoma?

A

Leukemia: bone marrow cells
Lymphoma: cells of lymphoid tiissue (anywhere, B and T cells)

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13
Q

Myeloma?

A

Type of lymphoma?

cancer of plasma B cells

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14
Q

Path of lymphomas?

A

Loss of germinal centers (germinal center is hypocrhomatic cookie)

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15
Q

Types of GOF mutation that –> cancer?

A
  1. point mutation
  2. copy number gain (amplification); detect via FISH
  3. chromosomal rearrangementf: regulatory region next to coding region for growth
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16
Q

Examples of copy number gain –> cancer?

A

MYCN gene (TF): often amplified in neuroblastomas (common in kids) (requries more aggressive treatment)

HER2 amplification (EGF receptor 2) –> worse prognosis but herceptin is target

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17
Q

MYCN gene mutation role in cancer?

A

MYCN codes for TF; often amplified in neuroblastomas

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18
Q

Herceptin?

A

Targets EGF receptor 2 which is amplified in HER2 amplification mutations –> better prognosis

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19
Q

Example of chromosomal rearrangement –> cancer?

A

Leukemias:

  1. Chronic myeloid leukemia (CML)- philly chromosome t9,22 (9 codes for ABL tyrosine kinase; 22 is regulatory) –> 3 different leukemias depending on length
  2. Burkitt’s lymphoma -cmyc related
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20
Q

RET gene in cancer

A

GOF –> increase express receptor tyrosine kianse –> kinase signal cascade
–> multiple endocrine neoplasia type 2 (MEN2)

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21
Q

MEN2 clinical features

A

MTC (medullary thyroid carcinoma)
pheochromocytoma- neuroendocrine tumor
hyperparathyroidism (HPT)

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22
Q

MEN2A v MEN2B

A

MEN2A- GOF in extracellular domain (disulfiide bond) –> constitutive activation

MEN2B- GOF in intracellular domain –> consitiitutive activation; earlier onset with developmental abnormalities

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23
Q

Familial MTC

A

medullary thyroid carcinoma
from GOF in RET gene
thyroid produces calcitonin which counteracts PTH which inhibits Ca2+ absorption to intestins and bones (secreted to urine)

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24
Q

What treatment for RET gene GOF?

A

early thyroidectomy to prevent MTC

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25
Q

Mode of inheritance for LOF in tumor suppressor gene?

A

Autosomal dominant, but two hit theory

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26
Q

Retinoblastoma genetics?

A

LOF gene

–> bilateral, multifocal tumors with earlier onset; also higher risk for secondary tumors later in life

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27
Q

Synchronous v metachronous tumors?

A

Synchronous- simultaneous multiple tumors in same tissue

Metachronous- tumors at different times in same tissue

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28
Q

FAP

  • clinical features
  • Risk
  • Genetics
A
  • 1000s of polyps in colon in adolescence
  • 100% cancer by 39
  • LOF in APC gene (normally antogonist of wnt pathway with binds beta catenin transcription activator)
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29
Q

Subtypes of FAP

  • clinical features
  • genetics
A
  1. attenuated FAP: 10-100 polyps; 40% have monoallelic APC mutaiton (dominant pedigree)
  2. MUTYH associated polypsis (MAP): 10-100polyps; not knudson (recessive); base excision repair
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30
Q

Lynch syndrome affected genes

A 
HNPCC
MSH2 (50%)
MLH1 (20%)
MSH6 (15%)
PMS2 (15%)
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31
Q

Lynch syndrome proteins?

A

MSH2/MSH6, MLH1/PMS2
Mismatch repair
MMR gene test to diagnose (cheap)

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32
Q

Lynch syndrome clinical features

A

80% risk for colorectal cancer
~15 adenamatous polyps
early onset colorectal cancer
other common cancers

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33
Q

Lynch syndrome inheritance?

A

Autosomal dominant (heterodimer) (knudson?)

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34
Q

Li-Fraumeni

  • clinical features
  • genetics
A

-100% risk for breast CA, 90% of some cancer type by 70
4Bs: breast, bone, blood, brain
-germline TP53 LOF; knudson dominant

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35
Q

TP53 gene mutation: role in cancer

A

seen in 50% of cancers
environmental factors often –> point mutations here
(ex. aflatoxin B1 in mold –> sporadic liver CA)
Li-fraumeni

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36
Q

HBOC syndrome

-genetics

A

germline LOF mutation in BRCA1/2
DNA break repair
Knudson dominant

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37
Q

Fanconi anemia

  • genetics
  • clinical features
A
  • biallelic LOF in FANCD1 (FANCD1=BRCA2) (9 subunits, one must be in subunit A)
  • short stature, malformation in radial arm, bone marrow failure by 15
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38
Q

Ataxia telangiesctasia:

  • genetics
  • clinical features
A
  • bialllelic LOF in ATM protein (which signals BRCA1/2); detects ds breaks
  • increased risk for blood cancers
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39
Q

3 steps of carcinogenesis

A
  1. initiation
  2. promotion
  3. progression
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40
Q

Endogenous intiators of carcinogenesis?

A

Depurination (kick out A or G)
Damination (C–> U)
ROS

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41
Q

Exogenous initiators of carcinogenesis?

A
  1. alkylating agents
  2. UV radiation
  3. Viral infection
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42
Q

Examples of alkylating agent initiators? (3)

A

polycyclic hydrocarbons, nitrosamines (in dyes), aflatoxin (–> TP53 mutation–> liver cancer)

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43
Q

2 types of UV radiation and mechanism of UV radiation for both

A
  1. UVB–> DNA photoadducts (CC–>TT) –> apoptosis dysregulation (via inact p53, act EGFR/COX2)
  2. UVA–> oxidative reaction
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44
Q

Xeroderma pigmentosa

A

disorder of DNA nT excision repair

sensitivity to UVB

45
Q

HPV virus types (3)

A 
Benign (warts only) 
Low risk (dysplasia): 6, 11
High risk (85% squamous carcinoma): 16, 18
46
Q

Path features of HPV warts

A
  • papillary
  • hyperkeratinosis (keratin apical) with parakeratinosis (presence of nuclei in keratin)
  • Acanthosis (thickened epithelium)
  • Koilocytosis (nuclei in caves with thickened cytoplasmic ring)
47
Q

Gradient from normal to invasive SqCCA in cervical cancer (histo)

A

LSIL (CN-1): koilocytes present, mostly mature squamous cells (requires colposcopy to confirm, differentiate between CN2/3)
HSIL (CN-2): polarity present; no koilocytes
HSIL (CN-3): no polarity, no koilocytes
iSqCCA: invasion through stroma

48
Q

HPV screen (how frequently?)/diagnosis

A
  • Pap test w cytology- high specificity, low sensitivity; every 3yrs (21-29), cytology + HPV testing every 5yrs (30-65)
  • diagnosis with colposcopy
49
Q

Describe HPV (virus), including proteins it codes for

A 
non-envelop; dsDNA
spread by skin
40% of STDs
codes for E6 and E7 protein (E6 is lower risk)
(E6 inhibits p53; E7 inhibits p21)
50
Q

Describe the HPV vaccine

A

capsid with virus like particles (VLPs)
Quadrivalent (6, 11, 16, 18) vs bivalent
recommended before sex
dose 1, wait 2 months, dose 2, wait 4 months

51
Q

Epstein barr virus causes what cancer?

A

Burkitt’s lymphoma (proteins that upregulate c-myc) (predisppose to rearrangement)

52
Q

HepB causes what cancer? mechanism?

A

hepatocellular carcinoma

binds p53 and causes liver damage that promotes hyperpplasia

53
Q

HHV8 virus –> what cancer?

A

Kaposi’s sarcoma and lymphomas, HIV patients

54
Q

HTLV-1 virus –> what cancer?

A

leukemia
common in japan and carribbean
targets CD4 T cells

55
Q

Lab model of promoter?

A

TPA (phorbol ester)

56
Q

Promoters in breast and prostate cancer?

A

estrogen, testosterone

57
Q

What is progression?

A

second irreversile gene mutation that –> malignancy

58
Q

Describe steps of morphogenesis via inflammation

A

Initiation - ROS (will alter G so that it pairs with A or C)

Promotion- GFs, cytokines, PGE2

59
Q

3 ways of metastasis

A
  1. lymphatics- carcinomas
  2. blood vessels- sarcomas (will –> liver and lungs)
  3. Mesothelial surfaces- ovarian and GI carcinomas (inoperable)
60
Q

Prognosis for tumor contained in capsule?

A

probably benign

61
Q

Prognosis for expansile/pushing tumor?

A

benign (“balloon-llike”)

62
Q

Prognosis for infiltrative tumor?

A

Malignant

63
Q

Histo indicators of proliferation?

A

mitotic spindles
Ki67 stain shows proliferatin cells
more apoptotic cells with frgamented nuclei

64
Q

Tumor specific v tumor associated antigen?

A

specific- only expressed on cancer cells

associated- higher expression on cancer cells

65
Q

Cancer cells are usually killed by what immune cells? how?

A

NK cells via MIC

66
Q

Ways that cancer evades immune response (4)

A
  1. Downregulate MHC-1 (evades CD8 T cells)
  2. Downregulate tumor antigen (evade CD8 T cells)
  3. No costimulatory moleccule expression (B7) (no costim for APC activation)
  4. produce anti-inflammatoyr cytokines (ex. TGF beta: normally inhibits proliferation and lytic CD8 granules, activates Treg)
67
Q

Uses for monoclonal antibodies in cancer?

A
  1. recognize size and location of metastases
  2. Toxin conjugate (ex. Gemtuzumab- antiCD33 expressed on myeloid leukemia)
  3. Radionuclide conjugate (ex. Ibritumomab/tositumomab- targets CD20 for non-hodgkins lymphoma)
68
Q

Types of chemotherapy

A

CCS (cell cycle specific) and CCNS (cell cycle nonspecific)

69
Q

Antimetabolites?

A

CCS chemotherapy

targets enzymes of S phase

70
Q

MTX

A

Methotrexate
CCS chemotherapy
anti-metabolite:targets enzymes of S phase
reduces folic acid to folate –> shut down DNA/RNA synthesis (cant make purine or thymidine)

71
Q

5-fluoruracil

A

CCS chemotherapy
anti-metabolite:targets enzymes of S phase
pyrimidine analogue

72
Q

Cytosine arabinoside

A

CCS chemotherapy
anti-metabolite:targets enzymes of S phase
cytidine analogue

73
Q

Mercaptopurine, thioguanine

A

CCS chemotherapy
anti-metabolite:targets enzymes of S phase
purine analogue

74
Q

Vinca alkaloids

A 
CCS chemotherapy
destabilizes microtubules (M phase)
75
Q

Vincristine

A

CCS chemotherapy
Vinca alkaloid: destabilizes microtubules (M phase)
binds free tubulin (aggregates) –> depolym of microtubules
effective for childhood leukemia
madagascar flower

76
Q

What chemotherapy option is effective for childhood leukemia?

A

Vincristine

77
Q

Taxanes

A 
CCS chemotherapy
hyperstabilizes microtubules (M phase)
78
Q

Paclitazel

A

CCS chemotherapy
Taxane: destabilizes microtubules (M phase)
from tree bark

79
Q

Epipodyphylotoxins

A

CCS chemotherapy
inhibits topoisomerase II (G2)
forms complex between DNA/isomerase/drug –> inactivation

80
Q

Etoposide (VP150)

A

CCS chemotherapy
Epipodophylotoxin- inhibits topoisomerase II (G2)
forms complex between DNA/isomerase/drug –> inactivation

81
Q

Teniposide

A

CCS chemotherapy
Epipodophylotoxin-inhibits topoisomerase II (G2)
forms complex between DNA/isomerase/drug –> inactivation

82
Q

Campothecin

A

inhibits topoisomerase I (G1? or 2?)

normallly TOPOI reversibly breaks ss DNA to relieve strain

83
Q

Types of CCNS agents? (3)

A

Antibiotics
Alkylating agents
Platinum coordination complexes

84
Q

Anthracyclins

  • mechanism
  • risks
A

CCNS
antibiotic
inserts to DNA –> ss/ds breaks
can only take lifetime max b/c cardiomyopathy risk

85
Q

Bleomycins

  • mechanism
  • risks
A

CCNS
antibiotic
glycopeptide that induces DNA fragmentation–> accum in G2
not immunosuppresive (often paired with other drugs)

86
Q

Nitrogen mustards

example and mechanism

A

CCNS
Alkylating agent
ex. is mechlorethamine: covalent bind guanine
crosslinking

87
Q

Nitrosureas

-mechanism

A

CCNS
alkylating agent
covalent binding to DNA

88
Q

Platinum coordination complex mechanism

A

reacts with DNA –> inter/intrastrand crosslinking

89
Q

Nuclear hormone receptor therapy:

-examples and mechanisms

A

Molecularly targeted therapy
Acts at receptor –> TF in nucleus
SERM- (selective estrogen receptor modulator)- breast cancer, ER antagonist (ex. Tamoxifen)
SARM- (androgen) (ex. bicalutamide)

90
Q

Kinase targeting

-example? problem with the drug?

A

Molecularly targeted therapy

  • Gleevac: inhibits ABL kinase of philly chromosome rearrangmenet –> cell apoptosis
  • relapse due to cancer mutation
91
Q

Bicalutamide?

A

SARM- androgen receptor modulator

nuclear homrone receptor therapy

92
Q

Molecularly targeted therapy: targets?

A

hormone receptor
kinase
angiogenesis
proteasome blocking

93
Q

Targeting angiogeneis for cancer:

Pathway to target?

A

Molecularly targeted therapy
hypoxia –> HIF release (TF) –> express VEGF and FGF
-target VEGF or VEGFR

94
Q

Bevacizumab (Avastin)

A

Molecularly targeted therapy
Angiogenesis target
VEGF antibody

95
Q

Sunitinib (Sutent)

A

Molecularly targeted therapy
Angiogenesis inhibitor
VEGFR kinase inhibitor (small molecule)

96
Q

Sorafinib (Nexavar)

A

Molecularly targeted therapy
Angiogenesis inhibitor
VEGFR/Raf kinase inhibitor (smalll molecule)

97
Q

drugs “-mab”?

A

antibody

98
Q

drugs “-nib”?

A

kinase inhibitor

99
Q

3 ways vaccines can work against cancer?

A

Preventative (HPV)
Therapeutic
Activate immune system

100
Q

Provenge

A

therapeutic use of vaccines
prostate CA
harvest APC, load prostate specific antigen, reinfuse into APC

101
Q

Ipilimumab (Yervoy)

A

Antibody that activates immune system against cancer
targets CTLA-4 with antibodies, potentiates T cell activity
used for melanoma

102
Q

Uses of biomarkers? (6)

A

risk assess, screen, diagnose, prognose, predict, monitor

103
Q

Requirements for functional biomarker?

A

benefit > risk
reproducible
valid (specific and sensitive)

104
Q

ER/PR biomarker?

A

immunohistochemistry
breast CA
predicts homrone therapy efficacy

105
Q

HER2/NEU biomarker

A

immunohistochemistry or FISH
breast CA
predicts resonsee to perceptin (blocks EGF binding)

106
Q

Gefitinib

A

blocks EGFR

presence of EGFR predicts response drug; lung cancer

107
Q

KRAS biomarker?

A

predict KRAS blocker response.

mutation in KRAS (sometimes in colorectal CA) –> no response to EGFR inhibiting

108
Q

High grade cancer histo?

A

higher grade - mitotic figures, nucleoli, pleomorphism

109
Q

Staging criteria?

A

TNM- tumor extent, nodal metastasis, metastasis distant

M1 = stage 4

Foundations2 (17 decks)

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