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PAS 511 Foundations in Clinical Medicine > Oncology > Flashcards

Oncology Flashcards

1
Q

What is neoplasia? What are the leading causes of death for men and women? What are the leading sites for cancer?

A

Abnormal and uncontrolled growth of cell
Site of Cancer cases- prostate, breast
Cancer death- lung for both

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2
Q

What are the risk factors for neoplasm?

A
  • Behavorial (smoking)
  • Geographic and environmental (japanese and stomach cancer) (UV,methotrexate, alocohol)
  • Age (>55 years, immuno-competence, increase accumulation of somatic mutations)
  • Genetic Predisposition to cancer (<10%)
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3
Q

What is hereditary retinoblastoma?

A

Inherited cancer risk
Hereditary- 1 abnormal allele increase 10,000 fold risk to develop retinoblastoma
Only takes 1 more spontaneous mutation
*cancers treated with radiation had increased frequency of cancers at different sites

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4
Q

What is Xeroderma pigmentosum?

A

Inherited cancer risk

defective DNA EXCISION repair leads to severe sun sensitivity= increased risk to develop skin malignancies

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5
Q

What is hereditary nonpolyposis colorectal cancer?

A

mutation in DNA MISMATCH repair gene= high risk of colon cancer (like Rb, born with one normal and one abnormal)

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6
Q

What is breast cancer susceptibility?

A

Inherited cancer risk
BRCA 1 & 2
risk increases from 12% to 60% if both are mutated- DNA REPAIR BY HOMOLOGOUS RECOMBINATION
also associated with age, increased cases in family

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7
Q

How does chronic inflammation lead to an increased risk for cancer?

A

Maladaptive IR and continuous tissue damage and repair LEADS to increased proliferation, inflammatory mediators LEADS to increased chances of mistakes and factors promoting angiogenesis, survival, and tissue remodeling

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8
Q

What is the nomenclature for benign v malignant tumors? What are the exceptions?

A

Benign: -oma
Malignant: sarcoma for mesenchymal AND carcinoma for epithelial
Exceptions: malignant lymphoma, melanoma, mesolithioma, seminoma

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9
Q

What is a teratoma?

A

Originate form totipotent cells. Usually more differentiated is benign and less is malignant

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10
Q

How can one distinguish between benign and malignant?

A

Differentiation v Anaplasia
Rate of growth
local invasion
metastasis

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11
Q

What is the rule of thumb for benign v malignant regarding differentiation?

A

Benign is well differentiation.

Malignant can be well differentiated, but undifferentiated is only malignant

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12
Q

What is anaplasia?

A

Anaplasia= lack of differentiation:
morphological changes
pleiomorphism,
abnormal nuclear morphology
mitosis bizzare/atypical configurations
loss of polarity (order is re-arranged, clumpy)

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13
Q

What is hyperplasia?

A

increased cell production- may be normal (pregnancy, lactation, puberty) or sign of cancer

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14
Q

What is metaplasia?

A

replacement of one cell type by another

ex: smoking causes normal columnar epithelial to change to squamous because it can withstand abuse of smoking better

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15
Q

What is dysplasia?

A

disordered growth, architecture and maturation

-increases number of immature cells

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16
Q

Describe carcinoma in situ.

A

Pre-invasive, severe dysplasia.

Treatment is generally effective due to confined localization.

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17
Q

What factors affect the growth rate of tumors?

A

doubling time (indicator of aggressiveness)
growth fraction/proliferative pool
rate at which cells die (apoptosis receptiveness)

18
Q

How do benign v malignant differ in terms of local invasion?

A

benign do not invade or metastasize and are often encapsulated
malignant progressively invade and destroy surrounding tissue and are poorly demarcated

19
Q

What is metastasis?

A

It requires:
-Invasion (detachment, proteolytic enzymes,
migration)
, -Dissemination (many threats include mechanical
sheer, apoptosis as a result of adhesion, innate
and adaptive IR)
uses lymphatics, body cavity,
-Colonization

20
Q

What does a tumor need in order to grow bigger than the diffusion rate?

A

angiogenesis to get nutrients “shipped” rather than just relying on diffusion

21
Q

What is the grading system of tumors?

A

takes into account the way the tumor looks and its growth pattern:
degree of differentiation, # of mitosis,
architectural features
*higher grade= more different than normal

22
Q

What is staging of cancer?

A

describes behavior based on size (T), number of lymph nodes involved (N), and presence or absence of blood borne mestastases (M)

23
Q

What are the 4 molecular bases of cancer?

A
  1. Proto-oncogenes- growth promotion
  2. Tumor suppressor genes- suppressor growth
  3. Regulator of cell death-apoptosis
  4. Regulator of DNA repair-alters ability to repair non-lethal DNA damage
24
Q

What differs between proto-onco gene and oncogene?

A

Proto-onco gene is normal, but if mutated can be a factor in cancer (where it would be considered an oncogene). They are self-sufficient in growth signals.

25
Q

How do proto-oncogenes promote cancer?

A

A. Growth factors- induce proliferation, paracrine switches to autocrin
B. Growth factor receptor-activated by being constitutively expressed. ERBB1 and 2.
C. Signal Transduction proteins- RAS usually activated when bound to GTP and RAS inactivated when bound to GDP. ABL1 encodes protein tyrosine kinase.
D. Nuclear Regulatory Proteins- Myc, myb, jun/fos, rel rapidly induced and initiates cell proliferation and high rate of cell division

26
Q

What type of mutation is involved in lymphomas?

A 
Translocation
Burkitt's: chromosome 8 to regulatory elements on B cell Ig heavy chaing
Mantel cell: cyclinD1 to IgH locus
Follicular: BCL2 to IgH locus
T cell acute LL: HOX11 into TCR locus
27
Q

What are the types of proto-onco genes?

A
  1. Growth factor
  2. Growth factor Receptor
  3. Signal Transduction proteins
  4. Transcription factors
28
Q

How do growth factors become onco genes?

A

induce proliferation by switching to autocrine

29
Q

What is an example of growth factor receptor proto-onco genes?

A

EGFR family such as ERBB1 and ERBB2

30
Q

What are examples of signal transduction proteins as proto-onco genes?

A
  1. Ras always bound to GTP= active form
  2. ABL1 encodes tyrosine kinase, phosphorylates tyrosine to activate differentiation, cell division, and cell adhesion.
  3. BCR-ABL1- translocation to BCR so it’s under the regulation of BCR and is constitutively expressed (CML): Tx using Gleevec to bind to ATP binding site and inhibit enzyme
31
Q

What are examples of transcription factors as proto-onco genes?

A
  1. Myc translocation in Burkitt’s lymphoma
  2. Mantel cell lymphoma: cyclinD1 to IgH locus
  3. Follicular lymphoma: BCL2 to IgH locus
  4. T cell ALL: HOX11 onto TCR locus
32
Q

What role do tumor suppressor genes play in leading to cancer?

A
  1. Retinoblastoma gene plays a role at G1/S checkpoint. When not phosphorylated, it is actively suppressing E2F from transcription, but when phosphorylated, is unbound so E2F transcribes gene
  2. p53: activated by stresses to activate DNA repair and arrest cell cycle until damage can be repaired. Initiates apoptosis if DNA cannot be repaired, also inhibits angiogenesis.
    LiFraumeni syndrome- inherited mutant p53 allele
  3. Beta catenin and contact inhibition: usually Bcatenin is bound but when contact inhibition is lost, it migrates to nucleus and acts as a transcription factor to induce proliferation.
33
Q

How are apoptotic proteins mutated in a way which leads to cancer?

A
  1. Bc12 family regulate mitochondria membrane integrity- balance of pro and anti-apoptotic normally but mutation shifts balance
    Pro-apoptotic- BAX and BAK form pores
    Anti-apoptotic- BCL2 and BCL-XL inhibit pore
    formation
    Tx: Genasense targets bcl2
  2. Follicular B cell lymphomas- carry translocation 3. BcL2 to IgH, which leads to B cells living longer, but progression is slow
34
Q

What os senescence? How does this process relate to cancer?

A

telomeres shorten so that there is a limited amount of divisions (60-70)
But cancer cells express telomerase to achieve unlimited replicative potential

35
Q

What is an example of a chemical carcinogen?

A

Aflotoxin B1 from mold Aspergillus grows in improperly stored grains and nuts. Leads to increase in hepatocellular carcinoma

36
Q

How is radiation a carcinogen?

A

UV- burns cause DNA damage that overwhelms nucleotide exicision repair pathway
Ionization- electromagnetic (x rays and gamma rays) and particulate (alpha/beta particles, protons, neutrons)

37
Q

Which viruses/bacteria are oncogenic?

A
  1. HPV- high risk for cervical cancer 16,18 and risk for genital warts 6,11
    Produced by virus are E6 and E7. E6 prevents p53 from apoptosis and E7 prevents Rb from stopping damaged cells from growing.
  2. Hepatitis A,B,C
  3. Heliobacter pylori- leads to ulcers
38
Q

How does the immune system help to fight against tumor growth?

A

Tumors contain Ag which IS recognizes as non-self

39
Q

What is cancer cachexia and why is it so dangerous?

A

TNF release from MO= fat mobilization and suppression of appetite. Limits chemotherapy dosage…1/3 cancer deaths due to this.

40
Q

What are the methods for getting a sample to test for cancer? What are the methods for analysis?

A

biopsy, needle aspiration, cytologic smears, bone marrow, body fluids/blood, frozen section
histology and cytology, immunohistochemistry (Ab staining), flow cytometry, and molecular diagnostics (uses DNA, RNA and proteins)

PAS 511 Foundations in Clinical Medicine (12 decks)

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