03a: Cancer Flashcards

(61 cards)

1
Q

Cell cycle: which checkpoint is that of “no return”?

A

G1/S

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

(X) cell cycle phase: cell synthesizes all of the proteins

necessary for mitosis.

A

X = G2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

RTKs are bound by (X) and activate downstream signaling pathways.

A

X = growth factors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Cancer signaling: Elevated levels of Cyclin D (activate/inhibit) (X), which then do what?

A

Activate;
X = Cdk4/6 (cyclin-dep kinases)

Phosphorylate Rb, which then releases the E2F TFs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

30% of all cancers have which mutated oncogene?

A

Ras

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

T/F: Cyclins are oncogenes.

A

True

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

T/F: Rb is an oncogene.

A

False - tumor suppressor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

PTEN is a PI3K (stimulator/inhibitor). Which of these is an oncogene?

A

Inhibitor;

PI3K (oncogene)

and PTEN is tumor suppressor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

T/F: AKT and mTOR are both oncogenes.

A

True

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

List endogenous factors that cause DNA damage/mutations.

A
  1. ROS (by metabolic products)

2. DNA replication

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

T/F: Only about 5% of all cancer driving mutations arise from normal mutation rates.

A

False - 66%!!!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Why do BRCA1/2 mutations predispose women to breast/ovarian cancers?

A

BRCA1/2 are important in DNA double strand break repair; inherited mutations in these lead to cancer predisposition

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Aneuploidy refers to (X) chromosomes and occurs as a result of (Y) process.

A
X = abnormal (number/structure)
Y = defects in mitosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

T/F: Normal cells mis-segregate one chromosome in every 100 divisions.

A

True

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

EGFR inhibitors target which special function of tumor cells?

A

Sustained proliferative signaling

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Although many EGFR inhibitors are in trial, they’re all failing due to:

A

Developed resistance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Cyclin-dep kinase inhibitors target which special function of tumor cells?

A

Evading growth suppressors (ex: p53, Rb)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Why do Cyclin-dep kinase inhibitors fail as drugs?

A

Hard to target

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

T/F: Immunocompromised patients show higher tumor rates.

A

True - immune system detects and eliminates tumor cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Aspirin (increases/decreases) risk of (X) cancer by 40%. Why?

A

Decreases
X = colon

Reduces inflammation (release of ROS and Cytokines)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

VEGF signaling inhibitors target which special function of tumor cells?

A

Inducing angiogenesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

ITP: Most cases involve Ig(X) autoantibodies that target (Y).

A
X = G
Y = platelet membrane glycoproteins IIb-IIIa
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

TTP and HUS: excessive (activation/inhibition) of platelets, which then do what?

A

Activation

deposit as thrombi in small blood vessel (causing microangiopathic hemolytic anemia)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Two major mechanisms that trigger DIC:

A
  1. Release of procoagulants (esp tissue factor) into circulation
  2. Widespread endothelial damage
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
One mediator of endothelial injury, implicated in DIC occurring with sepsis, is (X). It induces endothelial cells to express (Y) on their cell surfaces and to decrease the expression of (Z).
``` X = TNF Y = tissue factor Z = thrombomodulin ```
26
Among lymphoid cells, potentially oncogenic mutations occur most frequently in (X) cells during (Y) process.
``` X = germinal center B Y = antibody diversification ```
27
Which 3 lymphotropic viruses have been implicated as causative agents in particular lymphomas?
1. HTLV-1 (human T cell lymphoma virus) 2. Epstein-Barr virus (EBV) 3. Kaposi sarcoma herpesvirus/human herpesvirus-8 (KSHV/HHV-8)
28
T/F: radiation therapy and certain forms of chemotherapy increase the risk of subsequent myeloid and lymphoid neoplasms.
True - mutagenic effects of ionizing radiation and chemotherapeutic drugs on hematolymphoid progenitor cells
29
Virtually all Hodgkin's and (X) portion of non-Hodgkin's lymphomas present with enlarged (tender/non-tender) lymph nodes.
X = 2/3 Non-tender
30
Most common plasma cell neoplasm:
multiple myeloma
31
Lymphoid neoplasms are sorted into which 5 broad categories (according to the WHO scheme)?
1. Premature B cell neoplasms 2. Peripheral (mature) B cell neoplasms 3. Premature T cell neoplasms 4. Peripheral (mature) T and NK cell neoplasms 5. Hodgkin lymphoma
32
T/F: Lymphoid neoplasia can be diagnosed from the clinical features/Hx, PE, and CBC.
False - histologic examination of lymph nodes or other involved tissues is required for diagnosis
33
(Hodgkin/non-hodgkin) lymphoma spreads in an orderly fashion.
Hodgkin
34
(X) is the most common cancer of children. Which cell type(s) involved?
X = ALL (Acute lymphoblastic leukemia/lymphoma) ``` Immature (pre-) B (85%) Or immature (pre-) T ```
35
Mutations involved in ALL disturb (X) process of lymphoid precursors, thus arresting (Y) and inducing (Z) processes.
``` X = differentiation Y = maturation Z = self-renewal (stem cell-like phenotype) ```
36
T/F: Single mutations are not sufficient to produce ALL.
True - need drive for cell growth (most commonly increased Tyr kinase/Ras activity)
37
Majority (95%) of ALL cases have immuno-staining positive for (X), expressed only in (Y) cells.
``` X = TdT (terminal deoxyNT transferase) Y = pre-B and pre-T lymphoblasts ```
38
ALL: positive immuno-staining for which markers would make you think this was a "late" pre-T cell tumor?
CD1-8 | CD3, 4, 8 negative in more immature T cell tumors
39
ALL: positive immuno-staining for CD 19, 20, and cytoplasmic IgM heavy chain would make you think this was (early/late) pre-(B/T) cell. Would CD10 be expressed too?
Late pre-B Yes - absent in very immature pre-B cells
40
Sx of ALL reflect (hyperactive/depressed) bone marrow function.
Depressed (anemia, neutropenia, thombocytopenia)
41
T/F: With aggressive chemotherapy about 95% of children and adults with ALL obtain a complete remission; 85% are cured.
False - numbers true for children, but adults have only 40% cure rate
42
T/F: ALL is the leading cause of cancer deaths in children
True
43
Most common leukemia of adults in the Western world
CLL (Chronic lymphocytic leukemia)
44
Seeing "proliferation centers" on lymph node biopsy is pathognomonic for:
CLL/SLL
45
Overall median survival for patients diagnosed with CLL
4-6y
46
Lymph node biopsy showing nodular aggregates of lymphoma cells. Which disease? Which cells did the cancer arise from?
Follicular lymphoma; Germinal center B cells
47
Follicular lymphoma strongly associated with chromosomal translocations involving:
BCL2 (expressed in over 90% of cases)
48
T/F: Normal follicular B cells are BCL2 positive.
False
49
Follicular lymphoma: (painful/painless) lymphadenopathy with (frequent/rare) involvement of extranodal sites.
Painless; rare
50
Therapy for follicular lymphoma typically involves:
Palliative (survival not improved by aggressive therapy); | Low dose chemo/immuno-Rx to treat symptoms
51
T/F: Histo transformation to other B cell lymphomas is rare in follicular lymphoma.
False - up to 50%
52
Most common form of non-hodgkin lymphoma:
Diffuse large B cell lymphoma
53
DLBCLs (Diffuse large B cell lymphomas) contain various translocations that have which common breakpoint?
BCL6
54
What are the remission and cure rates for DLBCLs?
60-80% complete remission and 50% cured
55
All forms of Burkitt lymphoma are highly associated with translocation of (X) gene on chromosome (Y). This leads to (increased/decreased) (X) protein levels.
``` X = MYC Y = 8 ``` Increased
56
(X) lymphoma is the fastest growing human tumor. Why does it grow so fast?
X = Burkitt Increase MYC expression increases aerobic glycolysis (Warburg effect); more biosynthesis (NT, lipids, proteins)
57
(X) lymphoma: "starry sky" pattern on tumor biopsy.
X = Burkitt
58
(X) lymphoma often presents as a mass involving the mandible.
X = ENDEMIC (not sporadic) Burkitt
59
Peripheral smear: Many Auer rods in (X) precursor cell is diagnostic of:
X = promyelocyte | APML (Acute promyelocyte Leukemia)
60
If you suspect APML (Acute promyelocyte Leukemia) in patient based on peripheral blood smear, what's the next step?
TREAT! (All-trans retinoic acid - ATRA) even before marrow biopsy
61
(X)% of patients with APML will die before/shortly after diagnosis due to:
X = 25 Bleeding (CNS, lungs, GI)