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PHRM 864 > Intro to Neoplasia, Pathology and Chemotherapy > Flashcards

Intro to Neoplasia, Pathology and Chemotherapy Flashcards

1
Q

What is the median age of Cancer diagnosis?

A

67

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2
Q

Neoplasm

A

new growth, may be benign or malignant

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3
Q

Tumor

A

nonspecific term meaning lump or swelling

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4
Q

Cancer

A

any MALIGNANT neoplasm

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5
Q

Hyperplasia

A

an increase in organ or tissue size due to an increase in the number of cells

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6
Q

Metaplasia

A

an adaptive, substitution of one type of adult tissue to another type of adult tissue

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7
Q

Dysplasia

A

an abnormal cellular proliferation is which there is a loss of normal architecture

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8
Q

Anaplasia

A

a loss of structural differentiation. Cells differentiate

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9
Q

Carcinoma

A

malignant neoplasm of squamous epithelial cell origin

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10
Q

Adenocarcinoma

A

adeno=gland

malignant neoplasm derived from glandular tissue

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11
Q

Sarcoma

A

malignant neoplasm with origin in mesenchymal tissues or its derivatives

example: bone, muscle, fat

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12
Q

Lymphoma and Leukemia

A

malignant neoplasms of hematopoietic tissues

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13
Q

Melanoma

A

type of cancer of pigment producing cells in the skin or the eye

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14
Q

Blastoma

A

malignancies in precursor cells, often called blasts, which are more common in children

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15
Q

Teratoma

A

a germ cell neoplasm made of several different differentiated cell/tissue types

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16
Q

Myeloid leukemias

A

common myeloid progenitor

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17
Q

Lymphocytic leukemias

A

common lymphoid progenitor

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18
Q

Lymphomas

A

small lymphocyte–>T lymphocyte and B lymphocyte–> plasma cell

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19
Q

Stage 0

A

In situ carcinoma, no sign of local invasion

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20
Q

Stage 1

A

microscopic invasion of surrounding tissue

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21
Q

Stage 2

A

4-9 Surrounding Lymph nodes are involved

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22
Q

Stage 3

A

10 or more surrounding lymph nodes are involved

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23
Q

Stage 4

A

Distant metastases are detected

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24
Q

What is the numerical staging system based on?

A

largely based on tumor size, location, and number

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25
Q

Primary tumor

A

T

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26
Q

TX

A

Primary tumor cannot be evaluated

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27
Q

T0

A

No evidence of primary tumor

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28
Q

Tis

A

Carcinoma In Situ: Abnormal cells are present but have not spread to neighboring tissue; although not cancer, CIS may become cancer and is sometimes called preinvasive cancer

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29
Q

T1, T2, T3, T4

A

Size and/or extent of invasion of the primary tumor

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30
Q

Regional Lymph Nodes

A

N

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31
Q

NX

A

Regional lymph nodes cannot be evaluated

32
Q

N0

A

No regional lymph node involvement

33
Q

N1, N2, N3

A

Degree of regional lymph node involvement

34
Q

Distant Metastasis

A

M

35
Q

MX

A

Distant metastasis cannot be evaluated

36
Q

M0

A

No distant metastasis

37
Q

M1

A

Distant metastasis is present

38
Q

In situ

A

abnormal cells are present only in the layer of the cells in which they developed

39
Q

Localized

A

cancer is limited to the organ in which it began, without evidence of spread

40
Q

Regional

A

cancer has spread beyond the primary site to nearby lymph nodes or tissues and organs

41
Q

Distant

A

cancer has spread from the primary site to distant tissues or organs or to distant lymph nodes

42
Q

G1

A

Well differentiated (low grade)

43
Q

G4

A

Undifferentiated (high grade)

44
Q

Cancer is a disease of progression

A

Cell with mutation–>Hyperplasia–>Dysplasia–>In situ cancer–> Invasive cancer

45
Q

Hallmarks of cancer

A
  1. Sustaining proliferative signaling
  2. Avoiding immune destruction
  3. Enabling replicative immortality
  4. Activating invasion and metastasis
  5. Inducing or accessing vasculature
  6. Genome instability and mutation
  7. Resisting cell death
46
Q

For many tumors the growth of the primary tumor is not going to be life threatening

A

Cells from a primary tumor can sit in an organ for very long periods of time before metastasizing

Metastasized cells are considered a tumor from the PRIMARY SITE

47
Q

v-Src

A

ONCOGENE: gene that can cause cancer

RSV encodes a protein (v-Src) that is similar to the eukaryotic protein Src

any gene in a healthy cell capable of promoting tumor growth–> proto-oncogene

48
Q

Tumor Suppressor

A

RB1

Most tumor suppressors can be expressed from either chromosome, and will need to be homozygous deletion/mutation

Heterozygous mutations can be inherited and families show increased susceptibility to cancers

Also called “loss of heterozygosity”

49
Q

Genetic Basis of Cancer

A

Cancers often take 20 years or more to develop, although the time to cancer is decreased with increased mutation rate, such as through exposure to carcinogens

Carcinogen-induced cancers have very high mutation rates

50
Q

Targeting Oncogenic mutations

A

Activating mutations can predict susceptibility to targeted therapy

15-30% of NSCLC patients have an EGFR mutation

Mutations can be identified using sequencing technologies

Mutations in EGFR catalytic domain increase the intensity and duration of signaling in response to logand

51
Q

Tumor Suppressor Mutations

A

Loss of function mutations can predict susceptibility to chemotherapies

“Synthetic lethality”

Kill tumor cell while keeping healthy tumor in tact

52
Q

BRCA 1 and BRCA2

A

Tumor suppressors

The BRCA1 and 2 gene encode for proteins involved in DNA repair

The nonfunctional mutant alleles of BRCA1/2 are inherited as germline mutations

53
Q

BRCA mutations in breast cancer increase susceptibility to PARP inhibitors

A
54
Q

Olaparib

A

PARP inhibitor: binds to DNA when it is bound it recruits additional modifiers

For cancers with BRCA1/2 mutations it works by “trapping” PARP DNA–> unable to uncouple from DNA

55
Q

Chemotherapy

A

target the central dogma

56
Q

G0/G1

A

Cell is quiescent or accumulating building blocks required for division

CDK 4/6

G1: kinase inhibitors and hormone inhibitors

57
Q

S

A

cell replicating DNA

CDK1

Anti-metabolites, Antifolates, Topol inhibitors

58
Q

G2

A

Cell assembling machinery for chromosomal segregation and cytokinesis

Topo2 inhibitors

59
Q

M

A

mitosis

chromosome segregation

Microtubule inhibitors

60
Q

R-point

A

restriction point is the critical time point when cells decide whether or not to enter the cell cycle

61
Q

G1 to S

A

Is there a signal telling cell to proceed through cycle?

Are there sufficient quantities of the required nucleotide “building block?”

Is there unrepaired DNA damage?

62
Q

S to G2

A

Has the genome been replicated?

Are there any errors?

63
Q

G2 to M

A

Have sister chromatid arms been separated?

Has the machinery required for chromosomal segregation and cytokinesis been assembled?

64
Q

P16

A

Tumor suppressor

65
Q

TP53

A

Tumor suppressor

66
Q

RAS

A

Oncogene

67
Q

Palbociclib

A

Cdk4/6 kinase inhibitor

Aren’t exactly “targeted therapy” because they target all replicating cells

Adverse reactions: neutropenia, nausea, fatigue, diarrhea, vomiting

Approved for cancers arising due to BRCA1/2 mutations

68
Q

When normal cells are exposed to certain chemotherapy drugs that cause DNA damage

A

cells halt in G1 until DNA repaired

cells then proceed into S

If cells proceed into S without repairing DNA, they apoptose

preserves genomic integrity of daughter cells

69
Q

When tumor cells that have lost G1/S checkpoint control are treated with chemotherapy that causes DNA damage

A

Cells don’t halt in G1 and attempt to replicate damaged DNA

Attempting to replicate damaged DNA can trigger apoptosis

OR, if the apoptotic response has been lost cells replicate damaged DNA and acquire lethal genetic damage that results in necrosis

70
Q

Drugs that are more effective against cycling cells at many phases of the cell cycle are called cell cycle non-specific

A

These drugs are more effective when the tumor cells are progressing through the cell cycle, but they are not dependent upon the cell being in a specific phase of the cycle

Alkylating agents and DNA intercalation agents

71
Q

Phase-specific

A

drugs are most effective against tumor cells in a specific phase of the cell cycle

DNA synthesis (S phase) or Mitosis (M phase)

72
Q

Major dose-limiting toxicities of chemotherapy

A

Hematopoietic: WBC-infections, platelets-hemostasis, RBC-anemia

Gastrointestinal, N/V, loss of appetite

73
Q

Combination chemotherapy

A

use combinations of drugs each of which is at least partially effective against a particular tumor

a drug that is ineffective when used alone is often not approved for combination studies, although this is changing

individual drugs in combination should be used at max doses

use drugs with different mechanism of action or different cell cycle specificities

74
Q

CHOP

A

C: cyclophosphamide

H: Doxorubicin

O: Vincristine

P: Prednisone

75
Q

Drug resistance

A

Many tumors initially sensitive to chemotherapy become resistant

76
Q

Changes in drug targets/function

A

increased expression of drug target through gene amplification

emergence of a mutant, structurally altered target

emergence of cells with alterations in genes where the downstream effects are functionally redundant with the drug target

cells can rewire the pathway to bypass the need for drug target

PHRM 864 (9 decks)

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