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Biochemical Pharmacology > Cancer and Cell Cycle > Flashcards

Cancer and Cell Cycle Flashcards

1
Q

What is cancer?

A

A genetic disease where mutations in DNA cause cells to grow and divide uncontrollably, forming tumours.

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2
Q

What is metastasis in cancer?

A

The process where cancerous cells spread and invade other parts of the body.

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3
Q

What is the cancer prevalence in the UK?

A

1 in 2 people born after 1960 in the UK will be diagnosed with some form of cancer during their lifetime, due to longer life expectancy.

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4
Q

What were the most common causes of cancer death in 2020?

A
  1. Lung
  2. Colon and rectum
  3. Liver
  4. Stomach
  5. Breast cancer.
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5
Q

What are the factors that contribute to an individual’s risk of developing cancer?

A
  • Genetic make-up
  • Age
  • Exposure to ultraviolet radiation
  • Tobacco smoke
  • Diet
  • Biological factors (HPV virus)
  • Oxidative stress.
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6
Q

How does genetic variation increase the risk of cancer?

A

BRCA1 gene can cause:

  • 10-15% chance of breast cancer
  • 15-20% chance of cervical cancer.
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7
Q

What is oxidative stress and how does it contribute to cancer risk?

A
  • An imbalance between free radicals and antioxidants in the body.
  • Can damage DNA and contribute to an increased risk of cancer.
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8
Q

What is the cell cycle?

A

The series of events that occur in a cell as it grows and divides into two daughter cells.

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9
Q

What is the importance of the cell cycle?

A

The timing and rate of cell division is crucial to normal growth, development, and maintenance of an organism.
The number of times a cell divides is dependent

  • Skin cells and GIT cells divide frequently
  • Liver cells only divide if they need to repair
  • Nerve cells don’t divide regularly.
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10
Q

What are cell cycle checkpoints and what is their role in regulating the cell cycle?

A

Surveillance mechanisms that ensure the next cell cycle event does not occur prior to the completion of the preceding one.

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11
Q

What are checkpoint pathways comprised of?

A

G1- checks cell is ready for replications, are conditions favourable - before S phase
G2 - check DNA is not damaged - before mitosis
M - ensures proper allignment of chromosome on mitotic spindle

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12
Q

How does DNA damage lead to cancer?

A
  • Changes to a cell’s DNA can cause mutations.
  • If these mutations occur in genes that control growth, uncontrolled cell division can occur, leading to tumour formation and cancer.
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13
Q

What are some changes in cells that can cause cancer?

A
  • Genome changes ranging from point mutations to whole chromosome gain or loss
  • The ability to produce their own vascular supply and metastasize
  • Acquiring migratory properties that enable them to invade surrounding tissues and establish secondary sites of growth.
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14
Q

How do healthy cells differ from cancer cells?

A

Healthy cells

  • have contact inhibition
  • elongated morphology
  • align in an orderly fashion

Cancer cells

  • have no contact inhibition
  • rounded cells
  • overgrown 3D clusters of cells
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15
Q

What is the role of fibroblasts in tumor growth?

A

A type of connective tissue that secretes collagen

Within the tumour:

  • Used for growth advantage
  • use of structural proteins for tumor formation
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16
Q

What is the relationship between age and the incidence of human cancers according to the multi-hit model?

A

increases as a function of age.

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17
Q

How do cancers arise according to the multi-hit model?

A
  • Through an evolutionary process of clonal selection
  • Cells with advantageous genetic alterations are selected for survival and growth.
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18
Q

What is a prediction of the multi-hit model regarding the genetic alterations in tumor cells?

A

Tumor cells in a given tumor should have at least some genetic alterations in common.

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19
Q

Why does cancer incidence increase with age according to the multi-hit model?

A

Because it can take decades for the required multiple mutations to occur.

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20
Q

What is the approximate annual incidence rate of cancer according to the multi-hit model?

A

Roughly 1 in 100,000.

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21
Q

How does the incidence of cancer change as we age?

A

Increases with age.
The older we are, the higher the incidence rate.

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22
Q

What is the initial event in the multi-hit model of colon cancer?

A

APC tumour-suppressor gene mutation in a single epithelial cell
Leading to:

  • Cell division
  • The formation of a localized polyp of benign tumor cells.
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23
Q

What are the consequences of the expression of a constitutively active Ras oncoprotein and loss of the tumor-suppressor gene p53 in the multi-hit model of colon cancer?

A

It generates a malignant cell

  • Sustains its proliferation by preventing P53 from shutting it down
  • Allowing it to transition from a benign to a malignant state.
24
Q

How do some tumor cells in colon cancer spread to other sites in the body?

A

Invade blood vessels, which distribute them to other sites in the body.

25
Q

What is the role of additional mutations in the multi-hit model of colon cancer?

A

Permit the tumor cells to:

  • Exit from the blood vessels
  • Proliferate at distant sites

leading to the formation of secondary tumors.

26
Q

What is the significance of APC mutation in the multi-hit model of colon cancer?

A

Loss of APC leads to the initial growth of small polyps

27
Q

What is COSMIC?

A

A catalogue of mutations found in cancer genes in human tumors.

28
Q

What are proto-oncogenes?

A

Genes that function to promote cell growth in a controlled manner.

  • When these genes acquire mutations that result in continually active proteins they become oncogenes.
  • Cause uncontrolled cell growth and division -> leads to cancer
29
Q

What are some examples of mutations in proto-oncogenes?

A

Oncogenic mutations in proto-oncogenes that encode cell surface receptors
HER2 receptor
* mutated in the transmembrane region
* valine replaced by glutamine
* results in over-production or unregulated activity

EGF receptor
* mutated through partial gene deletion,
* results in the loss of the extracellular ligand binding domain.

30
Q

What are tumor suppressor genes?

A

Genes that function to inhibit cell proliferation and tumor development.
They halt the cell cycle to:

  • Prevent unnecessary division
  • Promote DNA repair
  • Promote apoptosis.
31
Q

What is p53?

A
  • Best-known tumor suppressor gene.
  • “guardian of the genome”
  • Functions to prevent the formation of cancerous cells.

p53 gene is mutated in more than 50% of all cancers

32
Q

What are the seven types of proteins that can lead to cancer?

A

Types 1 - 4
Mutant forms of proteins that normally promote cell growth can give rise to dominantly acting oncogenes

Types 5 - 6
Tumour-suppressor gene mutations

Type 7
Both tumour suppressors and oncoproteins
apoptotic proteins.

33
Q

What are the drawbacks of conventional chemotherapy?

A
  • Non-specific
  • Targets rapidly dividing cells (includes healthy cells)

This can lead to side effects such as

  • hair loss
  • low blood counts
  • nausea/vomiting
34
Q

What is targeted cancer therapy?

A

Drugs designed to target components responsible for, and unique to, the cancer.
Results in:

  • fewer side effects
  • increased efficacy

compared to conventional chemotherapy.

35
Q

What is Trastuzumab?

A

Trastuzumab is a targeted therapy drug used to treat HER2-positive breast cancer.

36
Q

What is the primary target of Trastuzumab in the treatment of breast tumors?

A

HER2 receptors on breast tumor cells.

37
Q

How does Trastuzumab block the activation of HER2 receptors?

A

Trastuzumab binds to the HER2 receptors
preventing their activation
interrupting the signaling cascade that drives tumor growth and progression.

38
Q

What is the effect of Trastuzumab on HER2 protein?

A

Induces internalization and degradation of the cell

39
Q

Besides blocking HER2 activation, what additional mechanism does Trastuzumab utilize?

A

Can stimulate the immune system to recognize and target HER2-overexpressing cells, contributing to the elimination of tumor cells.

40
Q

What downstream signaling pathways are associated with the HER2 receptor?

A

PI3K
mTOR
MAPK
which regulate cell proliferation and survival.

41
Q

How does Trastuzumab disrupt the signaling pathways in HER2-positive breast tumors?

A
  • Blocks the phosphorylation of proteins involved in the downstream signaling pathways.
  • This prevents the activation of proteins that contribute to cell growth and division.
42
Q

What is the result of Trastuzumab’s blockage of phosphorylation and signaling?

A
  • By disrupting the inner phosphorylation cascade,
  • Trastuzumab prevents tumor cells from dividing and making copies of themselves,
  • leading to the regression and elimination of the tumor cells over time.
43
Q

What is Pembrolizumab?

A
  • Highly selective
  • Humanized monoclonal IgG4-kappa isotype antibody
  • Against PD-1

Second most popular drug in the world

44
Q

What mechanism does Pembrolizumab target?

A

PD-1 receptor
A negative regulator of T cell effector mechanisms that limits immune responses against cancer.

  • When PD-1 is active, it turns off T cells
  • If T cells are not active, the immune system cannot function.
45
Q

What is the mechanism of action of anti-PD-1 antibodies?

A
  • It works by stopping the deactivation of T cells
  • Allowing them to remain active and carry out their anti-tumor functions.
46
Q

How does PD-1 inhibit T cell activity?

A
  • PD-1, when expressed on antigen-stimulated T cells, induces downstream signaling that inhibits T cell proliferation, cytokine release, and cytotoxicity.
  • This inhibition suppresses the immune response against tumors.
47
Q

How do many tumours suppress cytotoxic T-cell activity, and what effect does this have on T cells?

A
  1. Many tumours suppress cytotoxic T-cell activity by expressing PD-1 ligand (PD-L1) on the cell surface.
  2. PD-L1 activates PD-1 on the surface of a T cell
  3. The T cell goes dead automatically
  4. Cannot function once PD-L1 has blocked it.
48
Q

What are the effects of anti-PD-1 antibodies like Pembrolizumab?

A

Anti-PD-1 antibodies can reverse T-cell suppression
induce long-lasting antitumor responses
in patients with advanced solid tumours

49
Q

Why is it important to keep T cells blocked rather than blocking the tumor directly?

A
  • Blocking T cells prevents them from entering an anergic state and allows them to maintain their anti-tumor activity.
  • Blocking the tumor directly may lead to tumor adaptation and the development of resistance mechanisms.
50
Q

What is Chronic Myelogenous Leukaemia (CML)?

A

CML is a cancer of the white blood cells and accounts for 10-15% of all leukemia cases.

51
Q

How does CML result from a chromosomal translocation?

A

Results from:

  • ABL gene from the end of chromosome 9
    fused to
  • BCR gene on the end of chromosome 22

Creating a BCR-ABL fusion gene - Philadelphia chromosome.

52
Q

What is the result of the BCR-ABL fusion gene?

A

A constitutively active BCR-ABL fusion protein

Which:

  • phosphorylates multiple signal transduction proteins
  • Is heavily involved with proliferation.
53
Q

What is Imatinib (Glivec)?

A

A selective small-molecule tyrosine kinase inhibitor

54
Q

What is the mechanism of action of Imatinib (Glivec) in the treatment of CML?

A
  • Binds to the active site of the BCR-ABL kinase
  • inhibiting its enzyme activity
  • stabilizing the inactive non-ATP binding form.

This prevents phosphorylation of substrates, resulting in the downregulation of signaling pathways required for leukemogenesis.

55
Q

How can personalized medicine potentially improve the treatment of cancer?

A

Cancer results from a series of genetic changes, and personalized medicine can select the best drugs that target certain mutations.
Understanding the genome of a certain cancer can help understand it better and make better drugs, leading to further genetic research and development of more targeted therapeutics.

Biochemical Pharmacology (9 decks)

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