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MCS > Cancer > Flashcards

Cancer Flashcards

(55 cards)

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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

Study These Flashcards
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

Study These Flashcards
A

Tumors grow their own blood supply

Vascular endothelial growth factor (VEGF) induce blood vessel formation

25
Hallmark 5
Cancer cells divide without end | Mutations for high telomerase activity
26
Hallmark 6
``` 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
Chronic Myelogenous Leukemia (CML)
- BCR-ABL gene, balance 9:22 translocation (fusion gene) - codes a tyrosine kinase that is always on - Treated with imatinib (tyrosine kinase inhibitor)
28
What Chemicals can cause cancer?
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
Human Papillomavirus (HPV)
- 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
Adeno-Carcinoma Sequence
-Colorectal Carcinoma development Normal Epithelium --(APC)--> Adenoma -- --(KRAS)-->--(Tp53)--> Carcinoma
31
Familial Adenomas Polyposis (FAP)
Defects in mismatch repair genes leading to colonic adenocarcinoma - colon carpeted w/ polyps - auto dominant 100% chance after 50 years
32
Hereditary NonPolyposis
- 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
Li-Fraumeni Syndrome
Mutation of p53
34
Neurofibromatosis
Mutation of NF1
35
BRAF
Mutation->melanoma - Downstream of KRAS Cell Surface receptor -> Ras -> BRAF -> Cell Proliferation BRAF Kinase Inhibitor (medication)
36
MircoRNAs
- 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
Cancer drugs that target cell cycle machinery
Antimetabolites, microtubule targeting drugs, topoisomerase II inhibitors
38
Methotrexate
folic acid analog, inhibits dihydrofolate reductase decreased Met synthesis slow DNA/RNA/protein synthesis
39
Metcaptopurine
Thiopurine prodrug, needs activation | induces mutations and inhibits de novo purine synth.
40
Fluoruracil
inhibits thymidylate synthetase | dUMP--X-->dTMP
41
Cytarabine
cytosine analog | blocks DNA/RNA polymerases
42
Gemcitabine
cytosine analog | blocks DNA synth.
43
Vinca alkaloids
bind tubulin, inhibit spindle formation eg. Vinblastine / Vincristine
44
Taxoids
induce polymerization of microtubes arrest cell cycle eg. Taxol/Paclitaxel
45
Epipodophyllotoxins
dsDNA breaks eg. Etoposide
46
Alkylating agents
irreversible changes in DNA (cross-linking) has unwanted effects, also alters RNA and proteins eg. Cyclophosphamide (nitrogen mustard)
47
Antitumor antibiotics
intercalate into DNA, inhibit transcription eg. Doxorubicin / adriamycin
48
Camptothecins
bind to DNA topoisomerase I ssDNA breaks eg. Irinotecan, topotecan
49
Platinum compounds
induce DNA crosslinks eg. Cisplatin / Carboplatin
50
Tamoxifen
anti-estrogen | used for breast cancer
51
Enzalutamide
anti-androgen | used for prostate cancer
52
Lentrozole
prevents estrogen receptor activation | testosterone --X--> estradiol
53
Abiraterone
inhibits androgen synthesis
54
Combination chemotherapy
Cycle chemo. drugs 2-4 weeks Benefits: -Have different mech's of action/resistance -Side affects often wear off by week 4
55
Log-kill hypothesis
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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