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PHRM 864: Therapeutics IV > Intro to Neoplasia, Pathology and Chemo > Flashcards

Intro to Neoplasia, Pathology and Chemo Flashcards

1
Q

What are some of the basic terminology for Cancer? [Neoplasm, Tumor, Cancer]

A
  • Neoplasm: New Growth that could benign or malignant
  • Tumor: Lump or swelling
  • Cancer: malignant neoplasm
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2
Q

What are the “plasias” within cancer?

A
  • Hyperplasia: SIZE increase due to increase number of cells
  • Metaplasia: SUBSTITUTION of one tissue with another
  • Dysplasia: Loss of NORMAL architecture
  • Anaplasia: Loss of STRUCTURAL differentiation
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3
Q

What is important to understand with the intestinal epithelium as it relates to cancer development?

A
  • it is very organized and TURNS OVER alot; increasing the risk of cancer
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4
Q

What are the “omas” within cancer?

A
  • Carcinoma: Squamous Epithelium
  • Adenomacarincoma: Glandular Tissue
  • Sarcoma: Mesencyhmal Tissue
  • Lymphoma & Leukemia: Hetopoietic Tissue [Lymph & WBC]
  • Melanoma: Pigment Cells
  • Blastoma: Precursor Cells [KIDS]
  • Teratoma: Different cell/tissue types
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5
Q

What are the stages of the Numerical Staging System?

A
  • 0: In situ -> Precancerous
  • I: Initial Invasion
  • II: Lymph involvement [4-9 Nodes]
  • III: Lymph involvement [<10 Nodes]
  • IV: Metastasis
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6
Q

What does TNM stand for within Cancer?

A
  • T: Primary Tumor
  • N: Lymph Nodes
  • M: Metastasis
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7
Q

What are the stages within Primary Tumor [T]?

A
  • TX: Cannot be evaluated
  • TO: NO TUMOR
  • Tis: Precancerous [In Situ]
  • T1, T2, T3, T4: Size/ Extent of invasion
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8
Q

What are the stages with Lymph Nodes [N]?

A
  • NX: Cannot be evaluated
  • NO: NOT in LYMPH NODES
  • N1, N2, N3: Number/Location of Nodes
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9
Q

What are the stages with Metastasis [M]?

A
  • MX: Cannot be evaluated
  • MO: NO METASTATSIS
  • M1: Metastasis
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10
Q

What does the example T4 N1 M1 mean when determining cancer?

A
  • T4: Sizable Tumor
  • N1: Within Lymph
  • M1: Metastasis [Moved]
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11
Q

What does tumor grade mean within cancer?

A
  • The description of the tumor
  • Well Differentiated: close to normal cells
  • Undifferentiated: grow/separate slower
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12
Q

What is the Tumor Grading scale?

A
  • GX: undetermined grade
  • G1: Well differentiated [low grade]
  • G2: Mod differentiated [intermediate grade]
  • G3: Poorly differentiated [high grade]
  • G4: Undifferentiated [high grade]
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13
Q

How is cancer characterized?

A
  • Uncontrolled cell growth
  • Invasion
  • Metastasis
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14
Q

What are the hallmarks of cancer?

A
  • Evading growth suppressors
  • Avoding immune destruction
  • Enabling replicative immortality
  • Tumor promoting inflammation
  • Activating invasion & metastasis
  • Inducing Angiogenesis
  • Genome instability & mutation
  • Resisting cell death
  • Deregulation cellular energetics
  • Sustaining proliferative signaling
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15
Q

What are some of the ways that cancer can be prevented?

Risk Factors for Cancer?

A
  • Smoking, Obesity, Alcohol, UV, Physical Radiation, Physical Inactivity, Poor Diet
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16
Q

In what way was cancer found out to be “contagious”?

A
  • Infectious agents that were able to pass through a filter = VIRUS
  • Rous Sarcoma Virus [RSV] was filtered then in injected
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17
Q

What is an example of an oncogene?

A
  • Src: capable of providing proliferation and tumor progression
  • RSV = v-SRC
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18
Q

What is an oncogene?

A
  • Over-expression of a gene that results in cancer development
19
Q

What is the genetic basis of cancer?

A
  • MUTATION and DELETION of a tumor suppressor that is homgenous and run in families
  • a phenotype
19
Q

What is the mechanism that allows a phenotype to be achieve through different mechanisms?

A
  • Convergent Evolution
20
Q

How are tumor suppressor mutations good at predicting chemotherapies?

A
  • They are Loss of Function mutations
20
Q

What is Synthetic Lethality?

A
  • Causing the blockage of one gene when the tumor blocks the other one = Cell Death
  • EX: BRAC with PARP
20
Q

What drug is know to be the PARP inhibitor?

And MOA?

A
  • Olapalib [Rucaparib, Niraparib, Talazoparib]
  • Used in cancers with BRAC 1/2 mutations
20
Q

Which type of cancers are resistant toward chemotherapies?

A
  • Lung, Pancreatic, and Brain
20
Q

What types of cancer are curable by chemotherapies?

A
  • Hodgkins, Childhood Leukemias & Lymphomas, Testicular
  • Breat, Colorectal, Bladder respond well to chemos
20
Q

What are the imporant parts of the cell cycle?

A
  • G1: gathers the blocking blocks
  • S: Replication of DNA
  • G2: Checks replicated DNA
  • M: Mitosis - Division
20
Q

What is it called when a cell decides to enter or not enter into the cell cycle?

A
  • R point: critical time point when cells decide to enter

“R” we entering?

20
Q

In what way is the cell cycle driven?

A
  • Cyclines with kinases [CDK4/6]
21
Q

What are cell cycle checkpoints?

A
  • Desision points where the cell decides to proceed through the cell cycle
22
Q

What happens in the G1 to S checkpoint?

A
  • Signals division, is there enough building blocks, any damages
23
Q

What happens in the S to G2 checkpoint?

A
  • Did replication occur, any damages
24
Q

What happens in the G2 to M checkpoint?

A
  • Did they separate properly
25
Q

What is the major target for chemotherapy drugs?

A
  • DNA replication = S phase
26
Q

What is the mechanism of action for the CDK4/6 inhibitors?

A
  • Basically tells the cell cycle to STOP cycling
27
Q

What is Palbocicilb [Abemaciclib, Ribociclib]?

A
  • CDK4/6 kinase inhibitor
  • Targets ALL replicating cells
28
Q

What are some of the side effects for Palbociclib?

A
  • Nausea, Fatigue, Diarrhea, Vomiting
29
Q

What is true based around tumor suppressor genes?

A
  • They produce proteins that block the activity of cyclins.
30
Q

What type of Chemotherapy interferes with DNA synthesis?

A
  • S-phase specific
31
Q

What phase of the cell cycle is the target for Palbociclib?

A
  • G1 as it is the master regulator
32
Q

What happens when NORMAL cells are exposed to certain chemotherapies that cause DNA damage?

A
  • Cells stop in G1 until repaired
  • Then go to S [If S without repair then apoptose]
  • Divide
33
Q

What happens when CANCER cells are exposed to certain chemotherapies that cause DNA damages?

A
  • Cells DONT stop in G1 [replicating damages]
  • Causes apoptosis or necrosis [inflammation]
34
Q

What are some ways that chemotherapy becomes resistant?

A
  • Increased transport out of the cell
  • Reduced transport into the cell
  • Decreased activation of prodrug
  • Increased detoxification of drugs
35
Q
A

PHRM 864: Therapeutics IV (28 decks)

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