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Pharmacy > 301 Cancer > Flashcards

301 Cancer Flashcards

1
Q

Epigenetics: what are stable or dynamic changes?

A

Stable: pass on to next generations
Dynamic: response to environmental stimuli

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1
Q

What are epigenetics?

A

Pattern of inheritance in which gene/chromosome is modified temporarily that changes gene expression & function/regulation of DNA, protein or RNA molecules without changing primary sequences

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2
Q

What happens in chromosome inactivation?

A

Allow only one X chromosome to remain active and inactivate the rest of them (forming Barr body from inactive ones)
This is why phenotypes associated with X are less severe than Y

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3
Q

What are Barr bodies?

A

Condensed inactive X chromosomes found in nuclei of female mammals: 1 of 2 C chromosomes randomly inactivated in dosage compensation so 1 Barr body visible in cell nucleus

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4
Q

What is dosage compensation?

A

Process by which organisms equalise expression of genes between members of different biological sexes

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5
Q

Number of Barr bodies:
Normal female
Normal male
Turner syndrome (female)
Triple X syndrome (female)
Klinefelter syndrome (male)

A

XX 1
XY 0
X0 0
XXX 2
XXY 1

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6
Q

What is genomic imprinting?

A

Expression of gene depends on parent sex
Marking of alleles can be changed between generations

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7
Q

What is DNA methylation?

A

Chemical marking process important in genomic imprinting
Methyl (CH3) group added to cytosine in DNA regions needed for gene regulation & expression

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8
Q

Where does DNA methylation take place and what does it result in?

A

Sperm (chromosome X0) or oocyte (not both)
Gene expression inhibition (silences genes)

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9
Q

What are classical genetic controlled by?

A

Promoters, enhancers or proteins binding sites that are present or absent in DNA sequences

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10
Q

What is the difference between genetic & epigenetic regulation?

A

E: do not involve change to DNA sequence or mutations to sequence
Implies modification of DNA & proteins, without changing DNA sequence
Regulation at level above genetic mechanism regulation

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11
Q

What is model organism in epigenetics?

A

Different advantage & all important for learning about processes & mechanisms involved in epigenetic regulation

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12
Q

Saccharomyces cerevisiae (budding yeast) has helped what?

A

Elucidate chromosome structure & telomere silencing (regulates gene transcription near telomeres - prevents premature aging & aging-related diseases)

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13
Q

Protozoan Tetrahymena thermophilia is used for what?

A

Study of RNAipathway that functions gene silencing

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14
Q

What is a classic genetic model used for epigenetic research?

A

Drosophila melanogaster

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15
Q

What is a plant model with considerable epigenetic mechanisms like mammals

A

Arabidopsis thaliana

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16
Q

When are mice used in epigenetic research?

A

Embryology

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17
Q

What are biological applications of epigenetics?

A

Control expression of embryonic development genes
Erasure & re-establishment of DNA methylation
Genetic imprinting
X-chromosome inactivation
Stem cell development
Somatic cell differentiation
Production of differentiated cells from adult stem cells & specific cell types

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18
Q

What is found to correlate with cancer?

A

DNA methylation biomarkers
Cancer tumour suppressor genes show hypermethylation but also hypomethylation are expressed in other cancers

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19
Q

What is not involved in epigenetic alterations to genome?

A

Change in nucleotide sequence
Managing and controlling alterations plays role in cancer prevention and treatment

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20
Q

Examples of epigenetic mechanisms applied in different cancer types

A

Silencing tumour suppressor
Activation of oncogenes
Histone modifications

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21
Q

Epigenetic therapy: tumour suppressor genes

A

Decrease of tumour growth
Induction of apoptosis
Suppression of invasion & metastasis

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22
Q

Epigenetic therapy:
Stem cell genes
miRNAs regulating stem cell genes in CICs

A

Decrease of self-renewal or survival of CICs
Differentiation of CICs

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23
Q

Epigenetic therapy:
Tumour suppressor genes
Drug response genes

A

Resensitisation to chemotherapy

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24
Q

FDA approved epigenetic chemotherapy

A

Azacitidine (Vidaza)
Decitabine (Dacogen)
Vorinostat (Zolinza)
Romidepsin (Istodax)

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25
Q

Epigenetic therapy: Azacitidine (Vidaza)

A

Make genes fight cancerous cells when given at low doses, shows effectiveness against certain lung cancers

26
Q

Epigenetic therapy: Azacitidine (Vidaza)

A

Make genes fight cancerous cells when given at low doses, shows effectiveness against certain lung cancers

27
Q

Epigenetic therapy: decitabine (Dacogen)

A

Treats myelodysplasia (affects blood cell production in bone marrow) and leukaemia

28
Q

Epigenetic therapy: Vorinostat (Zolinza)

A

Treats immune system cancer (cutaneous T-cell lymphoma)

29
Q

Epigenetic therapy: romidepsin (Istodax)

A

Epigenetic injection therapy (like Vorinostat and romidepsin)
Treats peripheral T-cell lymphoma in patients who have received 1+ prior treatment

30
Q

Epigenetic therapy: romidepsin (Istodax)

A

Epigenetic injection therapy (like Vorinostat and romidepsin)
Treats peripheral T-cell lymphoma in patients who have received 1+ prior treatment

31
Q

What is carcinogenesis?

A

Molecular process where cancer develops

32
Q

External, lifestyle and environmental factors in carcinogenesis

A

Ex: chemicals, viruses, diet & radiation
Env: chemicals (air pollutants, asbestos)
Life: diet, smoke, alcohol, direct sun exposure

33
Q

What is cancer development?

A

Multi-stage process involving damage to genetic material of cells (DNA)
Damage of genes that regulate normal cell growth and division

34
Q

What are carcinogens?

A

Agents causing cancer
Classified as genotoxic or nongenotoxic (epigenetic)

35
Q

What are genotoxins?

A

Cause irreversible genetic damage (mutations) by binding to DNA

36
Q

Examples of genotoxins

A

Chemical agents like N-methyl-N-nitrosourea or non-chemical agents UV light

37
Q

Why can viruses act as carcinogens?

A

Interact with DNA (HBV and liver and HPV and cervix)

38
Q

Stages of carcinogenesis

A
  1. Initiation
  2. Promotion
  3. Transformation
  4. Progression
39
Q

Stages of carcinogenesis: initiation

A

Involve random change in genetic makeup of cell
>1 agent acts together as carcinogens
Carcinogen interacts with DNA causing damage at gene location that regulates cell growth
If cell repair systems do not occur, cell may turn cancerous

40
Q

What is the 1st stage in neoplastic development?

A

Initiation stage of carcinogenesis

41
Q

Stages of carcinogenesis: progression

A

Malignant conversion stage
Irreversible
Changes in structure of genome, increased growth rate
Invasiveness
Metastatic capability
Biochemical changes & neoplastic cells born
Expansion of tumour cells
Genetic material of tumour is more fragile and go through additional mechanisms

42
Q

Stages of carcinogenesis: promotion

A

Initial cell damage rarely results in cancer due to cell mechanisms to repair damaged DNA
Reversible and revocable if stimulus stops
Promoted not always carcinogen but enhances carcinogenicity
Continually controlled through environmental alterations
Cigarette smoke, bile acids & chemical pollutants involved in promotion

43
Q

When does cancer occur?

A

When tumour suppressor genes inactivated and oncogenes are activated

44
Q

What are tumour suppressor genes associated with?

A

Healthy cell activities like cell growth, cell differentiation & apoptosis

45
Q

What do tumour suppressor genes produce?

A

Proteins that inhibit cell reproduction during inappropriate growth times (control cell division during repair times)

46
Q

What are proto-oncogenes?

A

Altered version of normal genes, regulate cell growth and survival

47
Q

What activate proto-oncogenes?

A

Mutations

48
Q

Mechanism of oncogene action

A

Cell surface receptors
Intercellular signal transduction pathways
DNA-binding nuclear protein (transcription factor)
Cell cycle proteins (cyclins & cyclin-dependent protein kinases)
Inhibitors of apoptosis

49
Q

What do oncogenes trigger?

A

Signal transduction (cascade of biochemical signals)
These signals control genes that regulate cell growth and division

50
Q

What is important for cancer to occur?

A

Activation of oncogenes and inactivation of tumour suppressor genes

51
Q

What tumour suppressor genes are associated with cell growth and differentiation?

A

P53 and DCC

52
Q

What are the most common mutations seen in humans?

A

Mutations that inactivate tumour suppressor gene p53

53
Q

Colon carcinogenesis

A
  1. Mutations of APC: sometimes inherited, leads to dysplasia or polyp formations on mucous membrane surface
  2. DCC: subsequent mutations lead to late adenoma and then carcinoma
  3. Changes in p53 genes: progressive changes seen in colonic epithelium as polyps remain dormant for years
  4. DNA microsatellite instability (MSI): hyper mutable phenotype caused by loss of DNA repair activity
54
Q

p53 mutations lead to what?

A

Over expression of oncogenes and deletion of anti-oncogenes and DNA repair gene

55
Q

What does APC stand for?

A

Adenomatous polyposis coli

56
Q

What does DCC mean?

A

Deletion in colon cancer gene

57
Q

What are the tumour markers for:
Lung cancer
Liver cancer
Prostate cancer
Testicular cancer
Breast cancer
Stomach cancer
Colon cancer
Pancreatic cancer
Ovarian cancer

A

CA125, CEA
AFP
PSA
AFP, HCG
CA125, CEA, HER2
CEA
CEA
CA125, CEA
CA125, CEA

58
Q

What are tumour markers and can be detected where?

A

Substances produced by cells (normal or cancer) of body in response to cancer or benign conditions
Blood, urine, stool, tumour tissue and other body fluid samples

59
Q

Benefits of tumour markers in cancer care

A

Used in highly sensitive and specific screening tests for early detection
Elevated levels suggest but do not diagnose
Combine with other tests for diagnosis
Used to manage some types of cancer
Helps doctors know stage & suitable therapy
Determines whether tumour responds to treatment

60
Q

Limitations of tumour markers in cancer care

A

Tumour markers may increase in non-cancerous conditions
Not all patients have elevated tumour markers
Tumour markers not identified for all types of cancer

61
Q

Alpha-fetoprotein (AFP):
Cancer types
Tissue analysed
How used?

A

Liver, germ cell tumours
Blood
Diagnose liver cancer and follow treatment response, assess stage, prognosis and response to treatment to germ cell tumours

62
Q

Beta-2-microglobulin (B2M):
Cancer types
Tissue analysed
How used?

A

Multiple myeloma, chronic lymphocytic leukaemia and some lymphomas
Urine or blood
Assess stage, prognosis and treatment response

Pharmacy (11 decks)

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