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Human Genetics > Cancer > Flashcards

Cancer Flashcards

0
Q

What are the 4 stages of a cells life cycle?

A

Stasis
Mitosis
Differentiation
Apoptosis

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1
Q

What is the abcd of melanoma growth

A

Asymmetry
Borders (uneven)
Colour
Diameter

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2
Q

A) What are the two main ways that mutations occur?
B) What usually happens to a damaged cell? (2)
C) Why do cancer cells not die?

A

A) replication errors (accumulate with age) and exposure to DNA damaging agents
B) cell will repair the damage, or die
C) cells have faulty repair or apoptosis genes

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3
Q

Give some examples of genes
A) in controlling cell growth
B) in DNA repair and genome stability
C) in controlling cell death

A

A) RAS, ABL, SRC, RB, MDM2
B) p53, telomerase, ATM, BRCA
C) Bcl-2 family genes, myc

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4
Q

What are oncogenes?

A

Mutant or normal copies of cellular genes
Control cell growth
Have the potential to cause cancer

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5
Q

What are anti-oncogenes?

A

Also called tumour suppressors

Genes whose function is lost in tumours either by deletion or null mutation or down regulation by miRNAs

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6
Q

What phenotype do oncogenes usually have?

A

Dominant

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7
Q

How are oncogenes activated? (3)

A
  • Point mutation - May alter function of normal
  • Over expression of normal gene product - gene amplification, translocation to transcription ally active site, reduced expression if controlling miRNA
  • creation of a novel gene by translocation
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8
Q

What is a homogeneously staining region?

A

A type of change in a chromosomes structure which is frequently observed in the nucleus of human cancer cells, where a segment of the chromosome has been tandemly duplicated many times

They have various lengths and staining intensity after G banding

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9
Q

MiRNAs are a class of ______ RNA molecules. miRNA molecules bind to target ____ molecules and prevent ______ of the protein? miRNAs are known to regulate _______ expression. If a _____ that normally down regulates oncogene expression is itself down regulated then ______ of the oncogene will be translated.

A

MiRNAs are a class of regulatory RNA molecules. miRNA molecules bind to target mRNA molecules and prevent translation of the protein. miRNAs are known to regulate oncogene expression. If a miRNA that normally down regulates oncogene expression is itself down regulated then more of the oncogene will be translated.

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10
Q

miR-16-1 usually regulates ____ expression
miR-16-1 expression is reduced in ______, thus ____ expression of ___

miRNA of the let-7 family regulate _____ expression
Reduced expression is let-7 in lung tumours is associated with _____ expression of ______

A

miR-16-1 usually regulates Bcl-2 expression
miR-16-1 expression is reduced in chronic lymphocytic leukaemia and increases expression of Bcl-2

miRNA of the let-7 family regulate Ras expression
Reduced expression is let-7 in lung tumours is associated with increased_ expression of Ras

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11
Q

How is tumour suppressor activity lost? (6)

A 
(Both alleles of gene need to be inactive)
Point mutations
Deletion (loss of heterozygosity)
Methylation (= gene silencing)
Down regulation by miRNAs
Mitotic non disjunction
Mitotic recombination (rare)
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12
Q

How can ts genes be silenced?

A

By epigenetic modifications of the DNA (eg. Methylation)

Over expression of miRNAs

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13
Q

Where and how are oncogenes found..

A

Often Located at translocation break points
Present in HSR or double minutes
Found by transducing retroviruses and identified as miRNA target

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14
Q

What are DNA double minutes?

A

Small fragments of extra chromosomal DNA which are a manifestation of gene amplification during the development of tumours which give the cells selective advantages for growth and survival

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15
Q 
Ts genes:
Region is \_\_\_\_\_\_ in tumour cells
Loss of \_\_\_\_\_zygosity
Mutated in \_\_\_\_\_\_\_\_\_
Identified as a \_\_\_\_\_\_\_\_\_
A 
Ts genes:
Region is deleted in tumour cells
Loss of heterozygosity
Mutated in familial cancer syndromes
Identified as a miRNA
16
Q

Write down the multistep process of normal cell -> metastasis

A
  • Normal cell needs growth factor for growth and survival – no factor, cell differentiates or dies
  • Cell becomes factor independent – can grow or differentiate when factor absent, but if cell cycle disrupted will die
  • Cell becomes unresponsive to cell cycle control – cannot differentiate, can grow or die
  • Cell becomes resistant to apoptosis – cell grows, cannot die
  • Cell cannot repair damaged DNA – as it cannot die by apoptosis, damaged cells survive – tumour genetically unstable and mutations accumulate
  • Cell loses contacts with surrounding cells – spreads to other sites
17
Q

Give 2 familiar cancer syndromes that are specific to certain tissues
Give 2 familiar cancer syndromes that affect multiple tissues

A 
Early onset Breast cancer (BRA2)
Neurofibromatosis (NF1/2)
---
Li-Fraumeni syndrome (p53)
Ataxia telangiectasia (ATM)
18
Q

Give 4 reasons that cancer mortality is still high

A
  • Tumour is too advanced before diagnosis
  • Tumour becomes resistant to treatment
  • No effective treatment available for that tumour
  • Opportunistic infections occur due to poor immune system.
19
Q

What is the first line of defence against a tumour, give some disadvantages to this..

A

Surgical removal

Can be disabling or disfiguring, or may promote the spread of the tumour.

20
Q

Chemotherapy -
give the effect of the following agent on DNA
and an example..
Alkylating agents -

A

Alkylating agents - Damages DNA. Used in treating blood cancers, lung, breast ovarian. e.g. cisplatin, chlorambucil.

21
Q

Chemotherapy -
give the effect of the following agent on DNA
and an example..
Nitrosoureas

A

Nitrosoureas - Damages DNA, crosses blood-brain barrier. Used for brain tumours. e.g. Streptozocin

22
Q

Chemotherapy -
give the effect of the following agent on DNA
and an example..
Antimetabolites

A

Antimetabolites - Targets cells in S phase and interferes with DNA and RNA synthesis.e.g. 5-fluorouracil, methotrexate.

23
Q

Chemotherapy -
give the effect of the following agent on DNA
and an example..
Anthracyclines -

A

Anthracyclines - interferes with enzymes involved in replication e.g. doxorubicin.

24
Q

Chemotherapy -
give the effect of the following agent on DNA
and an example..
Topoisomerase inhibitors -

A

Topoisomerase inhibitors - Interferes with accurate DNA replication e.g. etoposide

25
Q

Chemotherapy -
give the effect of the following agent on DNA
and an example..
Mitotic inhibitors -

A

Mitotic inhibitors - Block mitosis M phase e.g. paclitaxel, vinblastine

26
Q

What role do corticosteroids play in chemotherapy?

A

Corticosteroids - commonly used as anti-emetics to help prevent nausea and vomiting caused by chemotherapy

27
Q

Give 3 problems with chemotherapy

A

1) The side effects - damages any fast growing cells
2) Tumours develop resistance to drugs
3) Some tissues are hard to target (may have reduced efficacy by time it reaches tumour OR blood-brain barrier)

28
Q

What are immunomodulatory drugs?

A

Boost the body’s own immune system to help attack the tumour

29
Q

(Novel cancer therapies) What is:
used to treat CML and GIST (GI stromal tumour). Inhibits tyrosine kinase ( a novel TK is produced by the Brc-Abl translocation in CML)

A

Glivec

30
Q

(Novel cancer therapies) What is:

a new therapy to treat non small cell lung cancer – blocks the epidermal growth factor receptor (EGFr)

A

In trial – Iressa

31
Q

(Novel cancer therapies) What is:

used in advanced pancreatic cancer, blocks EGFr

A

Tarceva

32
Q

(Novel cancer therapies) What is:

used in advanced pancreatic cancer, blocks EGFr

A

Tarceva

33
Q

What is the antibody that binds to the Her2 antigen that is expressed on a subset of breast cancers that is used in cancer treatment.

A

Herceptin

34
Q

What is the antibody that binds to the Her2 antigen that is expressed on a subset of breast cancers

A

Herceptin

35
Q

What exploits the DNA repair deficit in BRCA positive breast cancer cells leading to irreparable double strand breaks, used in cancer treatment.

A

Olaparib

Human Genetics (7 decks)

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