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Cancer Flashcards

1
Q

Chondro-

A

cartilage

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2
Q

Leiomyo-

A

smooth muscle

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3
Q

Rhabdomyo-

A

Skeletal muscle

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4
Q

seminoma

A

germ cell (testicular)

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5
Q

teratoma

A

germ cell (multiple layers)

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6
Q

Contrast gross pathology, histopathology, and cytopathology

A

gross - findings from naked eye examination of specimens
histopathology - findings from microscopic examination of stained tissue
cytopathology - findings from the microscopic examination of individual cells or groups of cells

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7
Q

Define molecular pathology

A

findings from the examination of the DNA/RNA of specimens

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8
Q

Contrast general gross characteristics of benign and malignant tumors.

A

Benign - smooth, well circumscribed border
sometimes are encapsulated by fibers

Malignant - irregular, diffuse and invasive borders

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9
Q

What are some key microscopic features of malignant tumors?

A

Nuclear irregularities, such as:

  • Irregular contours
  • Increased size (high nucleus to cytoplasm ratio)
  • Large and/or multiple nucleoli
  • Open chromatin or hyperchromasia (dark from abundance of chromatin)
  • Areas of necrosis (lack of blood supply)
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10
Q

What characteristics factor into tumor grading?

A

low-grade: well-differentiated cells (look like cell of origin)
High-grade: poorly differentiated (looks less like cell of origin) or undifferentiated (anaplastic)

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11
Q

What are three avenues for metastasis?

A

Hematogenously - blood vessels
Lymphatic - lymph (can invade nerves)
Transcoelemic - through body cavities

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12
Q

What are paraneoplastic syndomes and list a few common examples

A

Distant affects of malignant tumors
Cachexia (wasting)
Hypercalcemia (abundance of calcium)
Polycethemia (abnormally high Hbg)

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13
Q

adeno-

A

glands

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14
Q

Stage

A

T: Tumor Size/Extent
N: Nodal
M: Metastasis

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15
Q

Oncogenes

A

“Accelerators”
Normal genes that when mutated accelerate cell proliferation
- Amplification, alters transcription factors, promoter demethylation, miRNA overexpression

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16
Q

KRAS

A

Common in colon cancer

GTPase, mutations can result in inappropriate activation (oncogene)

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17
Q

HER2

A

Common in breast cancer
Amplification of activity leads to increased signalling for cell proliferation (oncogene)
receptive to Herceptin

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18
Q

Tumor Supressor Gene

A

“Brakes”
Genes that when mutated to be less active can lead to cancer
- Deletion, Alters transcription factos , promoter methylation, miRNA underexpression

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19
Q

RB

A

(Retinoblastoma) Tumor Suppressor Gene

Inactivating mutation doesn’t allow for Rb to inhibit the cell cycle

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20
Q

TP53

A

Tumor Suppressor

Deletion -> No protein, affected restriction point in cell cycle

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21
Q

Hallmark 1

A

Cancer Cells avoid Apoptosis
Overexpression of BCL2
Inhibits mitochondrial response to damage and lack of growth signals

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22
Q

Hallmark 2

A

Cancer cells use growth signaling pathways (autocrine)

Amplification of HER2 growth factor signalling, results in active GTPase

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23
Q

Hallmark 3

A

Cancer cells escape tumor suppression

Mutations that result in hyperphosphorylation of Rb (no inhibition of transcription factors) can cause cancer

24
Q

Hallmark 4

A

Tumors grow their own blood supply

Vascular endothelial growth factor (VEGF) induce blood vessel formation

25
Q

Hallmark 5

A

Cancer cells divide without end

Mutations for high telomerase activity

26
Q

Hallmark 6

A 
Cancer cells invade and spread
Loss of E-Cadherins allow cancer cells to break apart from each other
Matrix Metalloproteinases (MMP) breakdown of basement membrane
27
Q

Chronic Myelogenous Leukemia (CML)

A
  • BCR-ABL gene, balance 9:22 translocation (fusion gene)
  • codes a tyrosine kinase that is always on
  • Treated with imatinib (tyrosine kinase inhibitor)
28
Q

What Chemicals can cause cancer?

A
  1. Aflatoxin: reactive metabolite causing DNA damage (Hepatocellular carcinoma)
  2. Asbestos: (mesothelioma)
  3. Cigarrette Smoke: (3,4-benzyprene) reactive metabolite, obviously lung cancer
  4. Radiation (ionizing): mutations, genome level breakage (leukemia and thyroid)
  5. Sunlight (UV light): T-T dimers (carcinoma&melanomas)
29
Q

Human Papillomavirus (HPV)

A
  • VIruses can cause cancer
  • sex transmitted,
  • HPV proteins E6 binds p53
  • E7 binds Rb

Also Human-Herpes Virus 8 (HHV-8)
Epstein-Barr Virus (EBV)
Hepatitis B (HBV) and Hepatitis C (HCV)

30
Q

Adeno-Carcinoma Sequence

A

-Colorectal Carcinoma development
Normal Epithelium –(APC)–> Adenoma –
–(KRAS)–>–(Tp53)–> Carcinoma

31
Q

Familial Adenomas Polyposis (FAP)

A

Defects in mismatch repair genes leading to colonic adenocarcinoma

  • colon carpeted w/ polyps
  • auto dominant 100% chance after 50 years
32
Q

Hereditary NonPolyposis

A
  • Colon Cancer from a germline mutation of mismatch repair genes
  • Rare Auto dominant (Mutations of MLH1, MSH2, MSH6, PMS2)
    Unlike FAP, characterized by just a few polyps
33
Q

Li-Fraumeni Syndrome

A

Mutation of p53

34
Q

Neurofibromatosis

A

Mutation of NF1

35
Q

BRAF

A

Mutation->melanoma - Downstream of KRAS
Cell Surface receptor -> Ras -> BRAF -> Cell Proliferation
BRAF Kinase Inhibitor (medication)

36
Q

MircoRNAs

A
  • Don’t code for anything (down regulate gene expression)
  • Can be tissue specific
  • Form RISC complex on mRNA which suppresses translation
  • Can act as oncogenes and tumor supressors
37
Q

Cancer drugs that target cell cycle machinery

A

Antimetabolites, microtubule targeting drugs, topoisomerase II inhibitors

38
Q

Methotrexate

A

folic acid analog, inhibits dihydrofolate reductase
decreased Met synthesis
slow DNA/RNA/protein synthesis

39
Q

Metcaptopurine

A

Thiopurine prodrug, needs activation

induces mutations and inhibits de novo purine synth.

40
Q

Fluoruracil

A

inhibits thymidylate synthetase

dUMP–X–>dTMP

41
Q

Cytarabine

A

cytosine analog

blocks DNA/RNA polymerases

42
Q

Gemcitabine

A

cytosine analog

blocks DNA synth.

43
Q

Vinca alkaloids

A

bind tubulin, inhibit spindle formation

eg. Vinblastine / Vincristine

44
Q

Taxoids

A

induce polymerization of microtubes
arrest cell cycle

eg. Taxol/Paclitaxel

45
Q

Epipodophyllotoxins

A

dsDNA breaks

eg. Etoposide

46
Q

Alkylating agents

A

irreversible changes in DNA (cross-linking)
has unwanted effects, also alters RNA and proteins

eg. Cyclophosphamide (nitrogen mustard)

47
Q

Antitumor antibiotics

A

intercalate into DNA, inhibit transcription

eg. Doxorubicin / adriamycin

48
Q

Camptothecins

A

bind to DNA topoisomerase I
ssDNA breaks

eg. Irinotecan, topotecan

49
Q

Platinum compounds

A

induce DNA crosslinks

eg. Cisplatin / Carboplatin

50
Q

Tamoxifen

A

anti-estrogen

used for breast cancer

51
Q

Enzalutamide

A

anti-androgen

used for prostate cancer

52
Q

Lentrozole

A

prevents estrogen receptor activation

testosterone –X–> estradiol

53
Q

Abiraterone

A

inhibits androgen synthesis

54
Q

Combination chemotherapy

A

Cycle chemo. drugs 2-4 weeks
Benefits:
-Have different mech’s of action/resistance
-Side affects often wear off by week 4

55
Q

Log-kill hypothesis

A

drug kills a constant function of cells
drugs must be given frequently but not too frequently
-too often = sever illness
-too little = cancer growth>death

MCS (9 decks)

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