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SMP > cancer > Flashcards

cancer Flashcards

1
Q

cellular processes that must be altered for cancer

A
  1. evade apoptosis,
  2. insensitivity to antigrowth signals,
  3. self-sufficient growth signals,
  4. sustained angiogenesis,
  5. tissue invasion/metastasis,
  6. limitless replicative potential
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2
Q

oncogene

A 
dominant behavior (only 1 mutation needed)
= gain of function --> remove regulatory signals to control activity
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3
Q

tumor suppressor gene

A

normal gene,
when mutated in recessive fashion (loss of function)
lose ability to …

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4
Q

warburg effect

A

cancer cells proven to have abnormally high rate of aerobic glycolysis
(use LOTS of glucose, release lots of lactate)
*in almost ALL cancer cells
–> enables use of PET scan to find tumors/cancerous cells

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5
Q

isozyme (change) in bifunctional enzyme

A

PFKBP3 in cancer cells HIGHLY favors kinase activity
–> makes mostly fructose-2,6-biphosphate
(promotes glycolysis, esp. in hypoxic environment)

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6
Q

18F-2-fluorodeoxyglucose

A

radioactive chemical used in PET scanning for finding tumors,
converted in body to 18F-2-fluorglucose-6-phosphate (= glucose analog)
(see Warburg Effect)

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7
Q

PET scan

A

Positron emission tomography,
scan using radioactive glucose analog (18F-2-fluorodeoxyglucose) to image tumors
* basis: Warburg Effect (abnormally high glucose use in cancer cells)
** not useful for imaging bladder or kidney bc = excreted by urine, so always visualized there…

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8
Q

WHY aerobic glycolysis in cancer cells (vs. oxidative phosphorylation)?

A

more than ATP, need NADPH for AA and nucleotide synthesis!

–> ox. phosphorylation yields more ATP,
but glycolysis yields ATP and NADPH

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9
Q

Isozymes for metabolism, altered in cancer cells

A
  1. Glut1–> Glut4 (cancer)
  2. hexokinase1 –> hexokinase2
  3. PFKFB2 –> PFKFB3
  4. pyruvate kinase M1 –> pyruvate kinase M2
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10
Q

Isozyme

A

isoform of an enzyme,
for unique functions/needs.
can be normal, but many swapped in cancer cells

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11
Q

characteristics of Hexokinase2 (compared to HK1)

A

(HK2 = isozyme in cancer)
lower Km
higher ATP affinity
prevents apoptosis (unknown mechanism)

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12
Q

characteristics of PFKFB3 (vs. PFKFB2)

A

(PFKFB3 = cancer isozyme)

  • strong preference for kinase activity
  • –> promotes fructose-2,6-biphosphate as product;
  • promotes glycolysis (*inducible in hypoxic conditions)
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13
Q

p53

A

a transcription factor, induced by DNA damage.

action: maintain DNA integrity OR induce apoptosis (if too much damage)
target: TIGAR (inhibit glycolysis by lowering fructose-2,6-biphsophate)

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14
Q

TIGAR

A

gene encoding Phosphofructokinase (“bifunctional enzyme”) w/ ONLY biphosphatase domain.
–> lowers conc. frustose-2,6-biphosphate
—> INhibit glycolysis
(*activated by p53 trans. factor)

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15
Q

cancer cells have high need for glutamine bc…?

A

need glutamine for purine and pyrimidine synth,
(= nitrogen donor)
–> so high need for rapidly proliferating cell(s)

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16
Q

Myc (oncogene) activates…

A
  1. Glut1
  2. Hexokinase 2
  3. Pyruvate Kinase M2
  4. lactate dehydrogenase
  5. glutamine transporter
    (all promote glycolysis)
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17
Q

Src enzyme/pathway

A 
signal cascade enzyme activated by RTKs and cytokine Rs, 
promotes invasion (by cancer cells)
-- incr. cell motility
-- decr. adhesion
-- incr. cell survival
18
Q

Herceptin

A

HER2neu receptor antibody

  • -> RTK antagonist.
  • used for breast cancer chemotherapy
19
Q

Gatekeeper Tumor suppressor gene

A

Controls cell growth by regulating checkpoints
or promote cell death

*LOH => cancer, ie: Rb

20
Q

Caretaker tumor suppressor genes

A

guardians of cell genome,
protect against damage and mutations each day

  • LOH => cancer,
    ie: BRCA1
21
Q

Retinoblastoma (hereditary characteristics)

A

mutation in RB (gatekeeper) gene,
* requires 2 mutations to get tumor, BUT don’t have to be the same mutation.
very early onset, bilateral in hereditary cases

22
Q

tumor burden

A

When a cancerous tumor interferes with normal body and cell functioning,
ie: crowding out healthy cells

23
Q

3 categories of cancer (regarding genetics)

A
  1. Sporadic - no germline mutation, no family pattern
  2. Familial - family pattern, but no IDed germline mutation
  3. Hereditary - germline mutation (AD inherited)
24
Q

sequential nature of mutations

A

typically have multiple mutations in a single cell (do change behavior), before become malignant.
* critical step = when becomes malignant.

25
Q

sporadic cancer

A

no germline mutation, no family history.

  • many mutations that build up over years,
    • late age onset
26
Q

familial cancer

A

significantly high prevalence of a cancer within a family,
but no specific germline mutation.
no genetic testing for this

– can be varied forms of a cancer

27
Q

Rules of hereditary cancer

A

AD inheritance, specific germline mutation;
usually early onset and bilateral (ie: both breasts).
- if tumor suppressor, need 2nd hit mutation to get cancer.

28
Q

leukocoria

A

condition where retina of person (usually child) appears white (not red) when flashed with light.
indicates abnormal retina,
** tied to retinoblastomas**

29
Q

Hereditary Retinoblastoma

A

germline mutation in RB gene (gatekeeper –> uncontrolled prolif), BUT need 2nd mutation to have disease;
=> tumors in retina, often multiple and bilateral,
very early onset (sometimes before birth!)

30
Q

Cancer 2 hit theory

A

Rule: need 2 mutations (both alleles) to get cancer.
easier/earlier in inherited cancers bc:
inherit 1 mutation in germline,
–> only need second mutation to become malignant.

31
Q

2 types of inherited colon cancer

A
  1. FAP (familial adenomatous poliposis) – APC mutation

2. Lynch Syndrome (HNPCC) – 4 muts possible (MLH-1 or 2, PMS2, MSH-6) –> all mismatch repair genes

32
Q

FAP (familial adenomatous polyposis)

A

AD, inherited cause of colon cancer –> APC gene mut.
–> 1000s of polyps (but variable), become cancerous if not removed early;
Early onset (in teens)
* can be mosaic;

33
Q

Lynch Syndrome

aka: HNPCC (hereditary non-polyposis colon cancer)

A

mutation in mismatch repair genes (MLH1&2, PMS2, MSH6).
early onset colon and endometrial cancers (avg age = 43)
—- also gastric, skin, urinary cancers! *more aggressive cancer

Dx tests: microsatellite instability and Immunohistochemistry

34
Q

Microsatellite instability

A

characteristic of Lynch Syndrome tumors,
DNA slippage in short repeats not repaired (bc mut = mismatch gene)
–> show diff. microsatellite sizes when run on gel

35
Q

Li Fraumeni Syndrome

A

inherited mutation in p53 gene.

high incidence of early onset cancers…
ie: breast, adrenocortical, brain, and soft tissue cancers, etc.

36
Q

hereditary breast cancer

A

mutation in BRCA1 (DNA repair) or 2 (double strand break repair),
increased risk of breast and ovarian cancer.

  • esp. in Ashkenazi jewish women
    (CAN also occur in men)
37
Q

clonal abnormality

A

when 2 or more cells have the same chromosomal abnormality

– characteristic of cancer

38
Q

cytogenetic characteristics of cancer

A
  1. acquired chromosomal abnormality
  2. abnormality is clonal (in more than 1 cell)
  3. abnormality limited to malignant tissue
39
Q

t(9;22) chromosome abnormality

A 
get novel (chimeric) gene with altered tyrosine kinase activity,
--> chronic myelogenous leukemia ("CML").

cytogenetic analysis:
karyotype – see Philadelphia chromosome (der. 22) and altered 9

40
Q

Concerns about cancer treatment and stem cells

A

cancer stem cells are resistant to treatments,
so may select out for more aggressive cancer to return!
why?
- do NOT replicate rapidly (not targeted by chemo/rad.)
- resistant to drugs (pump out via ABC transporters!)

SMP (8 decks)

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