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PDA 3 > Masamha Exam 4 Materials > Flashcards

Masamha Exam 4 Materials Flashcards

1
Q

What are the other terms for cancer?

A

neoplasm/tumor-abnormal mass

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2
Q

Define: Tumorigenesis

A

initial formation of tumors

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3
Q

Define: Carcinogenesis

A

biological features of cancer development

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4
Q

Define: Benign tumor

A

limited to tissue of origin

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5
Q

Define: Malignant tumor

A

neoplasm invade nearby tissue and metasize (spead to distant sites in the body)

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6
Q

How is cancer classified?

A
  1. organ/location where cancer starts in the body (primary site)
  2. cell/tissue of origin
    - carcinomas= epithelial tissues
    - gilomas= glial cells of the CNS
    - lymphomas= lymphocytes
    - leukemias= hematopoietic cells
    - sarcomas= bone, connective and soft tissue
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7
Q

How can breast cancer be further subtyped by hormone receptor (HR)?

A
  • estrogen receptor (ER)
  • progesterone receptor (PR)
  • human epidermal growth factor 2 (HER2)
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8
Q

What are the mechanisms that control gene expression?

A
  • covalent changes to DNA (ex. methylation)
  • changes to histone (acetylation of histones)
  • long non-coding RNAs
  • small noncoding microRNAs (miRNA)
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9
Q

How do microRNAs regulate gene expression?

A

negative regulate gene expression

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10
Q

How do miRNA bind to RNA to regulate gene expression?

A

binds target sites within the 3’ UTR of gene, binds “seed region” 6-8nt long

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11
Q

What is the use of different miRNA expression?

A
  • distinguish between healthy and tumor tissue
  • sub-type cancers
  • determine the level of tumor/cancer progression
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12
Q

How may miRNA sub-typing be used for cancer therapy?

A
  • chemotherapeutic drug resistance
  • predict patients response to drug
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13
Q

What causes miRNA deregulation in cancer?

A
  • genomic deletion/amplications of the miRNA
  • mutations (alter proper miRNA processing, altered target site, altered seed region sequence)
  • changes in the 3’UTR length can eliminate target sites
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14
Q

What are the genetic changes seen in cancer?

A

DNA of specific “cancer genes”, miRNA, IncRNA
- mutations (single nucleotide changes)
- INDELS of DNA fragments
- copy number variations (increases/decreases)
- chromosomal translocations -> fusion genes

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15
Q

What is BCR-ABL (Philadelphia Chromosome)?

A

chromosomal translocation, accounts for ~90% of chronic myelogenous leukemia patients

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16
Q

What is the mechanism of action of Imatinib?

A

targets and blocks activity of Alb tyrosine kinase

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17
Q

What is the cause retinoblastoma?

A

retinoblastoma (RB1) gene (1/3 hereditary)

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18
Q

What are the herititary mutations that can cause breast and ovarian cancer?

A

BRCA1 and BRCA2

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19
Q

What are the “random errors” called that can cause cancer?

A

somatic

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20
Q

What is the potential enviromental damage that can be done to DNA that causes cancer?

A
  • radiation
  • chemical carcinogens
21
Q

What test tests for the carcinogenicity/mutagenicity potential of chemicals?

A

Ames test

22
Q

Describe the Ames test:

A
  1. a specific strain of salmonella that cannot produce histidine is added to 2 test plates
  2. one plate is given a small amount of histidine and no carcinogen
  3. one plate is given a small amount of histidine and carinogen being tested
  4. if many colonies produce histidine with the carcinogen then it can be confirmed that it is a mutagen due to the restored histadine gene
  5. the plate without the carcinogen may also have few colonies producig colonies due to natural mutations of gained back histidine function
23
Q

What viruses may cause cancer?

A

HPV

24
Q

How do viruses cause cancer?

A

direct transformation, affect expression of oncogenes/cytokines

25
Q

Describe the mechanism of how HPV can cause cancer?

A
  1. HPV infects the epithelial cells of the cervical mucosa and intergrates into the cellular genome
  2. over weeks HPV replicates
  3. 90% of patients will heal within 2 years
  4. in 0.8% of cases, years later HPV DNA becomes intergrated into tumor cell DNA and invasive cancer can develop
26
Q

What is the FDA approved HPV vaccine for prevention of cancer?

A

Gradasil 9 (HPV 6, 11, 18, 31, 33, 45, 52, 58)

preferred due to the strain coverage

27
Q

What is the mechanism of action of Gradasil 9?

A

contains virus-like particles (VLPs)= acts as antigen which is strongly immunogenic= antibodies produced, so in future encounters with HPV the antibodies can bind to prevent human cell infection

28
Q

What are the observable properties of cancer cells in cell cultures?

A
  • cells DO NOT exhibit contact inhibit
  • cells DO NOT exhibit density-dependent growth inhibition
  • cancer cells have altered cell morphology (de-differentiation, less specialized)
  • anchorage independent growth, able to proliferate in soft agar
  • reduced or no requirements for growth factors
  • immortality in late stages (normal cells may divide a finite times, Hayflick limit)
  • can be injected into susceptible
29
Q

Define Oncogenes:

A

normal genes that contribute to cancer once mutated/altered due to increased/decreased expression

30
Q

What are examples of oncogenes?

A
  • RAS
  • CCND1
  • HER2
31
Q

How may a proto-oncogene may become an oncogene?

A
  • deletion or point mutation in coding sequence may create a hyperactive protein
  • gene amplification allowing normal proteins to be overproduced
  • chromosomal rearrangement may cause nearby regulatory DNA sequence causes normal protein to be overproduced
  • chromosomal rearrangement may cause fusion gene to be over produced or hyperactive
32
Q

Define tumor suppressor genes:

A

genes that normally function as barriers of unregulated cell growth

33
Q

How can tumor suppressor genes be mutated in cancer?

A
  • point mutations (inactive)
  • large deletions (not expressed)

results to decreased/no expression

34
Q

What are the examples of tumor suppressor genes?

A
  • TP53 gene (p53 protein)
  • RB1
  • APC
  • PTEN
  • BRCA1 and BRCA2
35
Q

What is Knudson’s “two hit” hypothesis?

A

both alleles (copies) of a tumor supressor must be inactivated in cancer

36
Q

How can the molecular (genetic) signature of cancer be determined?

A
  • microarrays
  • next-generation sequencing (NGS)/massive parallel sequencing (MPS) technologies
37
Q

What are the “hallmarks” of cancer?

A
  1. sustained cellular proliferation
  2. evading growth suppressors
  3. resisting cell death
  4. enabling replicative immortality
  5. inducing angiogenesis
  6. activating invasion and metastasis
  7. genome instability and mutations
  8. deregulated metabolism
38
Q

How can sustained cell proliferation be targeted by drug therapy?

A
  • EGFR inhibitors
  • CKDis

several inhibitors

39
Q

How can evading growth suppressors be targeted by drug therapy?

A
  • cyclin dependent kinase inhibitors
  • checkpoint inhibitors
40
Q

How can resisting cell death be targeted by drug therapy?

A

BH3 proteins

41
Q

How can enabling replicative immortality be targeted by drug therapy?

A

telomerase inhibitors

42
Q

How can inducing angiogenesis be targeted by drug therapy?

A

inhibitors of VEGF signaling

43
Q

How can metastasis be targeted by drug therapy?

A

potentially inhibitors of HGF/cMET

44
Q

How can genome instability and mutations be targeted by drug therapy?

A

PARP inhibitors

45
Q

How is metabolism deregulated in cancer?

A

tumor cells up-regulate the uptake of glucose and glutamine

46
Q

Describe PET scanning with glucose (F-FDG-PET)?

A

scan with glucose tagging due to increased glucose usage in tumor cells used for staging, recurrance, and treatment response

47
Q

How to miRNA contribute to cancer?

A

may be oncogenes or tumor suppressors (or both)

48
Q
A

PDA 3 (5 decks)

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