Cancer Flashcards

1
Q

What is the Warburg effect?

A

Cancer cells predominantly produce ATP/energy through glycolysis rather than the TCA cycle, even in the presence of oxygen

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

What is the process of tumor cell mobility?

A

(1) Extend lamellipod
(2) Stress fibers pull on the cell
(3) Tail end moves forward

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

What are the only three screening tests that increase longevity?

A

(1) Pap smears
(2) Mammograms
(3) Colorectal exams

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

What is the smallest size of tumor detectable on x-ray?

A

1 cm (1 billion cells, 30 divisions)

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

What are two categories of carcinomas and from what types of cells do they arise?

A

(1) Squamous cell carcinoma - cells of protective covering layers
(2) Adenocarcinomas - from cells lining ducts with secretory functions (glands)

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

From what types of cells do sarcomas arise?

A

Mesenchymal cells - bone, fat, blood vessels, muscle

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

What are three types of genes involved in cancer?

A

Proto-oncogenes
Tumor suppressors
Apoptosis regulator genes

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

How are oncogenes activated?

A

(1) Viral invasion - a provirus is inserted into vicinity of a proto-oncogene or a transduced proto-oncogene is mutated and inserted into the cell
(2) Genetic rearrangements - chromosomal translocations, gene amplification, somatic mutation

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

What is a gene amplified in 28% of primary breast carcinomas?

A

Her-2/neu - epidermal growth factor (EGF) receptor

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

How can HER-2 be treated?

A

Herceptin, an antibody against HER-2

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

How does RAS mutation cause cancer?

4

A

(1) Mutation in RAS inhibits (2) GTPase activating protein, (3) preventing cleavage of GTP and (4) leading to over-transduction of growth signal to nucleus

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

What is the cause of Burkitt Lymphoma?

A

t(8;14) involving IgH and c-MYC, leading to overexpression of c-MYC
c-MYC on C8
IgH on c14

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

What is the cause of chronic myelogenous leukemia (CML)?

A

t(9;22) involving ABL and BCR, leading to overexpression of ABL, a tyrosine kinase, and activation of growth factor signaling pathways
ABL on C9
BCR on C22

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are three tumor suppressor genes?

A

(1) p53
(2) BRCA1
(3) BAX

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

What are two cancers associated with BRCA1?

A

(1) Breast

(2) Ovarian

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

How does mutation of RF cause cancer?

A

(1) Normal RF binds E2F, preventing transition from G1 to S phase
(2) Normal RF is phosphorylated by cyclin-dependent kinase 4 (CDK4), leading to release of E2F
(3) Mutated RF leads to constitutively free E2F, so no regulation of trnasition from G1 to S phase

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

What mutated gene and protein are associated with hereditary nonpolyposis colorectal cancer (HNPPC)?

A

(1) MSH 2 gene

(2) DNA mismatch repair (MMR) protein

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

What are the two types of acute leukemia?

A

(1) Acute myeloid leukemia (AML)

2) Acute lymphoblastic leukemia (ALL

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

What are the two types of chronic leukemia?

A

(1) Chronic myeloid leukemia (CML)

2) Chronic lymphocytic leukemia (CLL

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

What defines acute leukemia?

A

(1) >20% blasts in bone marrow, which (2) crowd out hematopoiesis

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

What are the cellular characteristics of acute leukemia seen under microscope?

A

(1) Large immature cell
(2) Little cytoplasm
(3) Large or punched out nucleolus

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

What age groups to AML and ALL affect?

A

ALL - L for little, affects children

AML - M for middle age, affects adults 50+

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What are the cellular characteristics of acute myeloid leukemia seen under microscope?

A

Auer rods (aggregation of myeloperoxidase)

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

What are AML markers?

6

A

(1) MPO - myeloperoxidase
(2) CD13
(3) CD33
(4) CD117
(5) HLA-DR
(6) CD15

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What are monocytic markers of AML?

4

A

(1) CD64
(2) CD14
(3) CD11b
(4) CD11c

26
Q

Which cytogenetic risk group has the most favorable prognosis?

A

t(15;17) - produces PML-RAR in acute promyelocytic leukemia, arresting cells in promyelocyte stage
inv(16) and t(8;21) also good

27
Q

What is acute megakaryoblastic leukemia associated with?

A

Down syndrome, with acute megakaryoblastic leukemia arising before age 5

28
Q

What clinical presentation is associated with acute monocytic leukemia?

A

Gum infiltration

29
Q

What happens in tumor lysis syndrome and how is it treated?

6;4

A
(1) High cell turnover leading to (2) elevated uric acid, (3) renal failure, (4) increased K, (5) increased phosphate, and (6) decrease in calcium
Treatment by (1) IV hydration with NaHCO3, (2) allopurinol for prevention of hemolysis, (3) hemodialysis, and (4) Rasburicase to break down uric acid
30
Q

How is acute promyelocytic leukemia treated?

A

All-trans-retinoic acid (ATRA), which binds PML-RAR and causes blast maturation

31
Q

What other disease is acute lymphoblastic leukemia associated with?

A

Down syndrome over the age of 5

32
Q

Which B-ALL translocation is associated with a poor prognosis and seen in adults?

A

t(9;22) - Philadelphia chromosome

33
Q

Which cell surface markers are characteristic of B-ALL?

A

(1) CD10
(2) CD19
(3) CD20
(4) CD 22
(5) cytoplasmic Ig

34
Q

Which cell surface markers are characteristic of T-ALL?

A

CD2-8

35
Q

What clinical characteristics are associated with T-ALL?

A

Appearance of a Thymic mass in Teenagers

36
Q

What are the three phases of treatment for ALL?

A

(1) Induction (bring down counts) - Vincristine, Prednisone, Dauno
(2) Consolidation (eliminate remaining cancer cells) - Etoposide, Ara-C, methotrexate
(3) Continuation and maintenance

37
Q

What is the difference between acute leukemia and chronic leukemia?

A

(1) Acute leukemia is a proliferation of blasts

(2) Chronic leukemia is a neoplastic proliferation of mature circulating lymphocytes

38
Q

What are the four important types of chronic leukemia?

A

(1) Chronic lymphocytic leukemia (most important)
(2) Mantle cell leukemia
(3) Hairy cell leukemia
(4) Mycosis fungoides

39
Q

What is chronic lymphocytic leukemia?

A

Neoplastic proliferation of naive, mature B cells

40
Q

What is seen on a blood smear of chronic lymphoblastic leukemia?

A

Smudge cells, increased lymphocytes with low cytoplasm

41
Q

What cell surface markers are expressed on B cells in chronic lymphocytic leukemia?

A

CD5 and CD20

42
Q

What are three complications of CLL?

A

(1) Hypogammaglobulinemia
(2) Autoimmune hemolytic anemia
(3) Richter’s transformation to aggressive large cell lymphoma

43
Q

What is treatment for CLL?

A

(1) Rituximab - monoclonal antibody against CD20 (reducin mah B)
(2) Chemotherapy + rituximab

44
Q

What are four myeloproliferative disorders?

A

(1) Chronic myeloid leukemia (CML)
(2) Polycythemia vera
(3) Essential thrombocytopenia
(4) Myelofibrosis

45
Q

What are myeloproliferative disorders?

2

A

(1) Neoplastic proliferation of mature cells of myeloid lineage (2) occurring in late adulthood

46
Q

What are three complications of myeloproliferative disorders?

A

(1) Increased risk of hyperuricemia/gout
(2) Progression to bone marrow fibrosis from burnout
(3) Transformation to acute leukemia

47
Q

Which cells are increased in chronic myeloid leukemia?

A

(1) Granulocytes and precursors

(2) Basophils

48
Q

What is a common clinical manifestation of CML?

A

Splenomegaly, suggesting transformation to accelerated phase of disease (leading to acute leukemia)

49
Q

How can chronic myeloid leukemia be distinguished from a leukemoid reaction?

A

(1) Negative LAP
(2) Increased basophils
(3) t(9;22)

50
Q

What is treatment for CML?

A

Imatinib - a tyrosine kinase inhibitor

51
Q

What is the cause of chronic myeloid leukemia?

A

t(9;22) - Philadelphia chromosome

52
Q

Which cells are increased in polycythemia vera?

A

Mature myeloid cells, especially RBCs (also granulocytes and platelets)

53
Q

How does polycythemia vera present clinically?

4

A

(1) Blurry vision and headache
(2) Flushed face
(3) Itching, especially after bathing
(4) Increased risk of venous thrombosis (Budd Chiari syndrome - hepatic vein thrombosis)

54
Q

How can polycythemia vera be diagnosed?

3

A

(1) High RBC count
(2) Low EPO - high in reactive polycythemia
(3) JAK2 kinase mutation

55
Q

How is polycythemia vera treated?

A

(1) Phlebotomy - lowers hematocrit

(2) Hydroxyurea - decreases RBC mass and risk of thromosis

56
Q

What cells are increased in essential thrombocytosis?

A

Platelets and megakaryocytes

57
Q

What mutation is essential thrombocytosis associated with?

A

JAK2 kinase

58
Q

How is essential thrombocytosis treated?

2

A

(1) Aspirin

(2) Hydroxyurea

59
Q

What is myelofibrosis?

A

(1) A form of chronic myeloid leukemia with (2) fibrosis of the bone marrow (3) due to excessive platelet-derived growth factor (PDGF) (4) produced by increased megakaryocytes

60
Q

What leukemias is JAK2 kinase associated with?

A

(1) Polycythemia vera
(2) Essential thrombocytosis
(3) Myelofibrosis