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Therapeutics > Exam 1 Lecture 1 > Flashcards

Exam 1 Lecture 1 Flashcards

1
Q

Median age of being diagnosed with cancer

A

67

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2
Q

Define Neoplasm, tumor and cancer

A

Neoplasm- New growth that is benign or malignant
Tumor- Lump or swelling
Cancer- any MALIGNANT neoplasm

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3
Q

What are the non-cancerous plasias

A

Hyperplasia
Metaplasia
Dysplasia
Anaplasia

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4
Q

Define hyperplasia, Metaplasia, dysplasia and anaplasia

A

Hyperplasia- An increase in organ tissue size due to an increase in the number of cells

Metaplasia- Change of one type of adult tissue to another type of adult tissue

Dysplasia- An abnormal cellular proliferation in which there is loss of normal architecture

Anaplasia- cell dedifferentiation

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5
Q

What are the different types of -Omas in cancer

A
  1. Epithelial origin (carcinoma/ adenocarcinoma)
  2. Sarcoma
  3. Lymphoma
  4. Melanoma
  5. Blastoma
  6. Teratoma
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6
Q

What are the two different types of Omas from epithelial origin and what is their difference

A

Carcinoma- Malignant neoplasm of squamous epithelial cell origin

Adenocarcinoma- Malignant neoplasm derived from glandular tissue

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7
Q

Define Sarcoma, Lymphoma, Melanoma, Blastoma, Teratoma

A

Sarcoma- malignant neoplasm with origin in mesenchymal tissue (bone, muscle, fat)

Lymphoma (leukemia)- Malignant neoplasm of hematopoietic tissue (blood)

Melanoma- type of cancer of skin or eye

Blastoma- Malignancies common in children

Teratoma- Germ cell neoplasm made of several differentiated tissue types

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8
Q

In hematopoiesis, hematopoietic stem cells turn into either________ or _______

A

Myeloid or lymphoid progenitor.

Lymphomas arise from lymphoid progenitors.

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9
Q

Describe the numerical staging system in cancer

A

0- In situ carcinoma, no sign of local invasion.

I- Microscopic invasion of surrounding tissue

II- 4-9 surrounding lymph nodes are involved

III- 10 or more surrounding lymph nodes involved

IV- distant metastasis are detected

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10
Q

What is the TMN staging

A

T- Tumor
M- Distant Metastasis
N- Regional lymph nodes

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11
Q

Describe the Ts in TMN

A

Tx- Primary tumor cannot be evaluated
T0- No evidence of primary tumor
Tis- Carcinoma in situ (CIS)
T1, T2, T3, T4- size/extent of invasion

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12
Q

What is CIS (carcinoma in situ)

A

Abnormal cells are present but have not spread to neighboring tissue, although not cancer, it may become cancer.

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13
Q

Describe the N in TMN

A

NX- regional lymph nodes can not be evaluated
N0- No regional lymph nodes involved
N1, N2, N3- Degree of node involvement

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14
Q

Describe the M in TMN

A

Mx- Distant metastasis can not be evaluated
M0- No distant metastasis
M1- Distant metastasis present

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15
Q

describe in situ, localized, regional and distant

A

In situ- abnormal cells are present only in layer of cells in which they developed

Localized- Cancer is limited to organ in which it began

Regional- Cancer has spread beyond the primary site to nearby lymph nodes or tissues/organs

Distant- Cancer has spread from primaru site to distant tissues/organs

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16
Q

Describe the difference between differentiated and poorly differentiated tumors

A

If the cells of the tumor resemble normal tissue, it is called well- differentiated, these tumors tend to grow and spread at a slower rate than undifferentiated or poorly differentiated

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17
Q

Describe tumor grading

A

Gx- Grade cannot be assessed
G1- Well differentiated (low grade)
G2- Moderately differentiated
G3- Poorly differentiated
G4- undifferentiated

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18
Q

What is cancer characterized by? What is its difference with benign

A

Abnormal cell growth and tissue invasion, metastasis ( benign only has uncontrolled cell growth)

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19
Q

What is the progression of cancer

A

Hyperplasia to dysplasia to insitu to invasive cancer

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20
Q

V-Src is a (oncogene or tumor suppressor)

A

oncogene

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21
Q

What is an oncogene? What is a proto onco gene

A

Oncogenes cause cancer

Any gene in a healthy cell capable of promoting tumor growth is a proto onco gene

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22
Q

RB1 is a (oncogene or tumor suppressor)

A

Tumor suppressor

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23
Q

Describe the idea of loss of heterozygosity

A

If you have two normal copies of the gene, you need to have it mutated twice to turn cancerous. It is called loss of heterozygosity if a pateint is predisposed to having cancer due to having one normal and one abnormal gene.

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24
Q

WHat is NSCLC? What percent of NSCLC pts have EGFR mutation. What is EGFR

A

Non small cell lung cancer. 15-30% of NSCLC pts have eGFR mutration. EGFR is a tyrosing kinase. Tyrosine kinases act as oncogenes

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25
Q

LOF or GOF of tumor suppressors lead to chemotherapy?

A

LOF

26
Q

What are BRCA1 and BRCA2? WHat is PARP?

A

BRCA 1 and BRCA2 are tumor suppressors that encode for proteins involved in DNA repair.
PARP also repairs DNA.

27
Q

BRCA mutations in breast cancer increase susceptibility to ________

A

PARP inhibitors.

28
Q

Name a PARP inhibitor? How do they work?

A

Olaparib.
They work by trapping PARP to DNA such that PARP can no longer come off

29
Q

Describe each cycle in the cell cycle

A

G0/G1- Cell is in cycle arrest or accumulating building blocks required for division

S- Cell duplicates each of the 46 chromosomes

G2- Cell double checks duplicated chromosomes for error for chromosomal segregation

M- Mitosis

30
Q

control of cell cycle is done by

A

Cyclins

31
Q

Describe R- point. What cycle does it exist in?

A

R- point (restriction point) is the critical time point when cells decide whether or not to enter cell cycle. It is in G1 phase.

32
Q

Which cyclin controls the entire process in G1 phase? What does it bind?

A

Cyclin D controls entire process in G1 phase by binding CDK 4/6

33
Q

How do the cells move past R point

A

Cell accumulates cyclin D and binds to CDK 4/6. It activates cell to move past R point.

34
Q

What happens to cycline when we begin to approach G2

A

Cyclin E and cyclin A begin to cooperate and cyclin A slowly begins to take over when it progresses to G2. Cyclin A binds CDK 1.

35
Q

How do cells go from G1 to S phase

A

Cyclin E takes over and binds CDK 2.

36
Q

Which cyclin is present in mitosis

A

Cyclin B

37
Q

What are questions the cell asks between each cell cycle checkpoint?

A

G1 to S- Is there mitogenic signal telling cell to proceed? Are there sufficient quantities of building blocks? Is there unrepaired DNA damage?

S to G2- Has the genome been replicated? Any errors present?

G2 to M- Have sister chromatids separated?

38
Q

What are some DNA damaging agents (non cell specific)

G1 (mitogenic signalling) damaging agents

S (DNA replication)damaging agents

G2 (sister chromatid separation) damaging agents

M (chromosome segregation) damaging agents

A
  1. DNA damaging- alkylators, intercalators
  2. G1 (mitogenic signalling)- Kinase inhibitors, hormone inhibitors
  3. S (DNA replication)- Antimetabolites, Anti folates, topol inhibitors
  4. G2 (sister chromatid separation)- Topo2 inhibitors
  5. M (chromosome segregation)- targetted by microtubule inhibitors
39
Q

What are tumor suppressors? What are oncogenes?
a) P53
b) Ras
C) Rb1
D) P16

A

only Ras is an oncogene (most common oncogenic mutation)
P53, Rb1, P16 are all tumor suppressors,

40
Q

What kind of drug is pablociclib? What does it target? what is its MOA?

A

Palbociclib is a CDK 4/6 kinase inhibitor

Targets all replicating cells (are not target therapy)

Prevent i/a of cyclin D with CDK 4/6, no phosphorylation of Rb1.

41
Q

WHat is a normal cell reponse to DNA damage?

A

When normal cells are exposed to certain chemotherapy

Cells halt in G1 until DNA repaired. Cells proceed to S. If cell proceeds to S without repairing DNA they apoptose

42
Q

Cancer cell reponse to DNA damage

A

When tumor cells have lost G1/S checkpoint control, they are treated with chemotherapy

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 (cell death that results in lysis and inflammation)

43
Q

What are drugs that do not require cycling cells and what are they effective against

A

These drugs are effective against cancer cells resting in G0 and cells throughout the cell cycle

DNA alkylating agents

44
Q

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

A

Cell cycle non-specific

45
Q

When are cell cycle non-specific drugs useful?

A

These drugs are most effective when tumor cells are progressing through cell cycle. However they are NOT dependent on being in a specific phase.

46
Q

Do Cell cycle non specific drugs have efficacy against cells in G0?

A

Many of these agents have some efficacy against cells resting in G0, but are more effective against cells progressing through cell cycle.

47
Q

What are phase specific drugs?

A

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

48
Q

Limitation of phase specificity?

A

Higher drug dose may not result in greater tumor cell killing. Increased cell kill requires prolonged exposure.

49
Q

Why does chemotherapy have side effects?

A

Chemotherapies also kill rapidly dividing cells in the body (epithelial, blood cells) Cause GI, nausea, vomiting.

50
Q

consideration for chemotherapy

A

Chemotherapy kills a constant fraction not a constant number of tumor cells. It is impossible to kill all tumor cells with a single dose of drug. It selects for cells resistant to drug

51
Q

Norton simon hypothesis of chemotherapy

A

Give dose intensive and early chemo at short intervals and use a combination of drugs with a distinct MOA.

52
Q

Why is the norton simon hypothesis useful?

A

As tumors grow, their doubling time slows. When tumor burden is decreased by chemotherapy, the remaining cells will enter exponential growth.

53
Q

factors increasing success rates of chemotherapy

A

Small tumors
Early diagnosis
Increased drug intensity.

54
Q

Theories to design combination therapy chemotherapy

A

Use a combination of drugs, each of which is atleast partially effective against a particular tumor. Individual drugs in combination should be used at maximal dose.

Use drugs with different MOA or different cell cycle specificities.

55
Q

Advantages of combination chemotherapy

A

no additive toxicity for drugs with non-overlapping toxicities, increased cell killing.

56
Q

What are the different ways drug resistance occurs?

A
  1. Increased transport of drugs out of cell through efflux pumps. (PGP, MRP (multi drug resistance protein))
  2. reduced transport into cell (loss of importer)
  3. Decreased activation of prodrug
  4. Detoxify drug
57
Q

What are some changes in drug target or function that could occur in chemo?

A
  1. increased expression of drug target through gene amplification or expression. Upregulation of drug target makes it harder to inhibit
  2. Emergence of mutant, structurally altered target.
  3. emergence of cells bearing alterations in genes whose products are functionally dependent drug targets.
58
Q

What are some physiological changes that promote resistance

A

1.Refuge of cancer cells in drug protected anatomical sites (BBB)

  1. Massive stromalization (Carcinomas develop desmoplastic (stringy) stroma. Impedes drug transport)
  2. Changes in cell state such as EMT (epithelial mesenchymal transition) Slows cell cycle and increases drug efflux.
59
Q

What are some cell survival mechanism of cancerous cells

A
  1. Activation of anti-apoptotic regulators (increase in proteins that help cancer cells bypass cell death.)
  2. increased repair of damage caused by chemo
60
Q

What are some limitations of chemo

A

Resistance- selective proliferation of surviving cells
Narrow therapeutic index of chemo drugs.

Therapeutics (36 decks)

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