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Biology Hwa Chong > Molecular Basis of Cancer > Flashcards

Molecular Basis of Cancer Flashcards

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1
Q

What is cancer

A

A disease that results from uncontrolled cell division. Mutations in the genes that control cell division may result in a dysregulation of cellular checkpoints, such that a cell divides uncontrollably

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2
Q

List the important characteristics of cancer cells

hint 8 points

A
  1. High rate of cell division
  2. Genome instability and mutation
  3. Replicative immortality
  4. Loss of anchorage dependence
  5. Lack of contact inhibition and density-dependent inhibition
  6. Inducing Angiogenesis
  7. Metastasis
  8. Avoiding immune destruction
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3
Q

G2 checkpoint__assessment of DNA replication

A
  • Occurs at G2
  • Checks if DNA has replicated successfully without damage
  • If there is irreparable damage, apoptosis occurs

If passed, proteins will signal the cell to begin the molecular processes that will alow the cell to divide via mitosis

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4
Q

M checkpoint__assessment of mitosis

A
  • Occurs at metaphase
  • Checks if there is successful formation of spindle fibres and attachment of spindle fibres to the kinetochore of chromosomes
  • Ensures that there is successful separation of DNA to the 2 daughter cells
  • If spindle fibres are not formed or attachment to centromere is inadequate, mitosis is arrested
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5
Q

G1 checkpoint_assessment of cell growth

A

Occurs at G1

Checks for:

  • presence of proteins called growth factors that are required to stimulate cell division
  • DNA damage and cell size
  • Nutrients are sufficient

If there is irreparable damage, apoptosis occurs, if not cell is committed to divide

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6
Q

What happens to mature cells

A

They pass into the G0 phase and may never divide again

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7
Q

What is something important on page 12

A

Uncontrollable cell division may not always mean that tumour cells divide more rapidly than normal cells. The crucial issue is the relationship between accumulation of new cells occurs

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8
Q

So what is this relationship expressed in cancer cells vs normal cells

A

In normal tissues, the rate of cell division and rate of cell loss are kept in balance so no net accumulation of new cells occur

In cancer cells, since they have escaped precise cell control, the rate of cell division far exceeds the rate of cell loss. This results in net uncontrolled proliferation of new cells

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9
Q

What are the 2 classes of cancer-critical genes

A

These genes exert their effects by acting on the cell cycle control machinery

  1. Tumour Suppressor gene
    Normal genes encodes a protein which inhibits uncontrolled cell division
  2. Proto-oncogene
    Normal gene encodes a protein which stimulates normal cell division
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10
Q

Functions of tumour-suppressor proteins

Five points

A
  1. Take part in cell signaling pathways to inhibit the cell cycle
  2. Halt cell division if DNA is damaged
  3. Trigger DNA repair mechanisms, preventing cells from accumulating DNA damage
  4. Initiate apoptosis
  5. Maintain cell adhesion
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11
Q

Why to abolish the function of tumour suppressor genes totally must 2 copies of the gene be mutated

A

In a diploid organism, there are two copies of every gene.

If the function of only one copy of a TSG is lost, cell cycle activity remains normal, as the other copy of the gene is still able to produce sufficient quantity of functional normal gene product to regulate normal cell cycle

Mutated TSG is thus recessive

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12
Q

Why is the p53 gene known as the “Guardian of the Genome”

A

It has triple involvement in cell cycle control, in apoptosis, and in maintenance of genetic stability - all aspects in protecting the organsim against cellular damage and disorder

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13
Q

What is p53

A

A transcription factor that binds to DNA to trigger transcription of genes involved in cell cycle inhibition

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14
Q

What are the mechanisms of p53

A
  • It can activate DNA repair proteins when DNA has sustained damage (making it an impt factor in ageing)
  • It can arrest growth by holding the cell cycle at the G/S regulation point on DNA damage recognition. This ensures damaged DNA is not replicated and gives time for the cell to repair DNA damage.
  • It can initiate apoptosis by activating suicide genes, to ensure that cell with damaged DNA does not continue to proliferate.
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15
Q

One example of how p53 arrests growth

A
  • Activated p53 protein binds to specifc DNA control elements and promotes transcription for the relevant genes like p21
  • p21 protein stops the cell cycle by binding to proteins that are involved in cell cycle progression such as Cyclin-dependent kinases (Cdks)
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16
Q

Function of proto-oncogene (POG) products

A
  1. Growth factors
  2. Growth factor receptors
  3. Protein kinase
  4. Inhibitors of apoptosis
  5. Transcription factors
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17
Q

Oncogenes?

A

Proto-oncogenes can undergo gain of function mutations and be converted to oncogenes.

Hence, oncogene is a gene that encodes a protein that promotes excessive cell division. This will cause cell division to be uncontrolled.

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18
Q

Why a mutation of 1 of the 2 copies of the proto-oncogene is sufficient to cuase abnormal cell proliferation

and what kind of mutation is it?

A

The oncogene acts in a dominant manner.

The mutation is a gain in function mutation. This type of mutation causes the genes to gain function, such as being over-expressed or to encode for a hyperactive protein.

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19
Q

ras, a Proto-oncogene what does it encode for?

A

A small protein known as the ras protein which belongs to a super familyof proteins known as “low-molecular weight G-proteins”

RECAP
G-proteins are a class of proteins that bind to guanine nucleotides (GTP and GDP), and are involved in signal transduction
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20
Q

How are ras Proteins involved in the cell cycle-stimulating pathway

A
  • when activated, relays signals from a growth factor receptor to a series of protein kinases known as the phophorylation cascade
  • The last protein kinase of the signal transduction pathway activates transcription of genes encoding proteins that stimulate cell division.
  • The pathway is normally activated only when a growth factor binds to its receptor in the plasma membrane.
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21
Q

How does the gain in function mutation affect the cell cycle-stimulating pathway

A
  • The mutation leades to changes in the three-dimensional confromation of the ras protein.
  • This causes GTP to remain bonded to the ras protein as a ras-GTP complex and thus it is in a constant “active” state, even in the absence of growth factor.
  • This results in an increase in cell signaling, transcription and consequently stimulates the cell cycle.

This shows how a hyperactive ras protein leads to excessive cell division.

22
Q

What are the consequences of conversion of a proto-oncogene to a oncogene

A
  1. Quantitative change
    Tumour formation is induced by an increase in the absolute number of oncogene product
  2. Qualitative change
    Tumour formation is induced by a hyperactive oncogene product
23
Q

What steps are in the multi-step model of cancer progression

A
  1. Accumulation of mutations
  2. Activation of telomerase
  3. Angiogenesis
  4. Metastasis
24
Q

What evidence support the multi-step model of cancer progression

A
  • incidences of most cancer rise exponentially with age
  • delay between exposure to carcinogens and appearance of cancer
  • cancers develop progressively, from benign tumours to increasingly malignant cells
25
Q

Why must many mutations be accumulated

A

A single mutation is not enough to convert a healthy cell into a cancer cell.

The genesis of a cancer typically requires gradual accumulation of several independent mutations in cancer-critical genes in a single cell lineage.

A tumour develops through repeated rounds of mutation and proliferation, giving rise eventually to a clone of fully malignant cancer cells.

26
Q

What are some cancer-critical genes

A
  • proto-oncogene
  • tumour suppressor gene
  • telomerase gene
  • angiogenesis-activating protein genes
27
Q

Describe an accumulation of mutations leading to cancer

A

Every stage/step of cancer progression corresponds to one or a few mutations

  • At each step, a single cell undergoes a mutation that either enhances cell proliferation or decreases cell death, so that its progeny become the dominant clone in the tumour
  • Proliferation of each clone hastens the occurence of the next step of tumor progression by increasing the size of the cell population that is at risk of undergoing an additional mutation.
  • The final step is an invasion through basement membrane, an initial step in metastasis
28
Q

What are telomeres

A

Regions of long stretches of repetitive, non-coding DNA sequences located at the ends of all eukaryotic chromosomes.

29
Q

What is the hayflick limit?

A

During DNA replication, the ends of linear chromosomes shorten after each round of replication.

Once telomeres are shortened to a critical length after a number of rounds of replication, the cell stops dividing and goes into replicative cell senescence.

Telomere length functions as a natural check on the number of times a cell can divide which is the hayflick limit

30
Q

What is telomerase

A

A ribonucleoprotein complex that adds telomere repeat sequence to the 3’ ends of DNA.

The complex contains a reverse transcriptase enzyme and a single RNA molecule which acts as a template for synthesis of telomere repeat.

31
Q

How does telomerase aid cancer cells

A

Telomerase are usually not expressed in most human somatic cells.

Telomerase genes are activated in most human cancer cells, where telomerase is produced and maintains tolemere lengths so that cancer cells divide indefinitely.

Telomerase appears to allow cancer cells to evade apoptosis as well

32
Q

What is angiogenesis

A

To ensure its relentless growth, a tumour will stimulate the formation of new blood vessels, this is known as angiogenesis.

These blood vessels allow for an increased blood flow to the tumour, hence supplying nutrients and oxygen and removing toxic waste products.

They also provide pathways for cancer to spread to other sites in the body

33
Q

What are some angiogenesis-activating proteins

A
  • vascular endothelial growth (VEGF)

- fibroblast growth factor (FGF)

34
Q

Summarize the angiogenic process

A
  1. A tumour cell releases angiogenesis-activating proteins that attract endothelial cells and promote their proliferation
  2. Endothelial cells secrete protein-degrading enzymes called matrix metalloproteinases (MMPs)
  3. These proteases break down the blood vessel wall and the components of the extracellular matrix (ECM), allowing the endothelial cells to become organised into new networks of blood vessels
35
Q

What is after angiogenesis

A

After angiogenesis has been triggered at an initial tumour site, cancer cells begin to spread throughout the body.

This ability to spread is based in two distinct mechanisms: invasion and metastasis

36
Q

What is metastasis

A

The ability of cancer cells to enter the circulatory system and travel to distant sites, where they form secondary tumours called metastases that are no physically connected to the primary tumour

37
Q

Summarize the events of metastasis

A
  1. Cancer cells invade surrounding tissues and penetrate through the walls of lymphatic and blood vessels, thereby gaining access to the bloodstream
  2. The cancer cells are transported by the circulatory system throughout the body
  3. Cancer cells leave the bloodstream and enter particular organs, where they establish new secondary tumours at distant sites from the primary tumour
38
Q

All causative factors of cancer

A
  1. Lifestyle and diet
  2. Radiation exposure
  3. Age
  4. Genetic Predisposition
  5. Loss of immunity
  6. Viral infections
39
Q

how can cigarette and tobacco smking cause cancer?

A

When smoke is inhaled, chemicals like polycylic aromatic hydrocarbons (PAHs) enter the lungs and is spread around the rest of the body via the bloodstream.

40
Q

How does PAH harm the body

A

These organic compounds can bind to DNA of cells to form a physical complex known as adduct, which can cause mistakes in DNA synthesis during normal cell division. These mistakes introduce mutations into the DNA sequence, leading to gene mutation.

  • PAH tends to form adducts at several sites on the p53 gene in cells (esp lungs), which prevent the production of functional p53 protein.
  • Therefore, leading to a loss of normal growth control mechanisms and the cell divides uncontrollably leading to tumour formation (IMPT used as a conclusion for everything)
41
Q

How does exposure to chemical carcinogen affect the body

A

Nitrites seem to contribute significantly to cancer.

When meats are cooked over high temperatures, heterocyclic amines (HCAs) and PAHs are formed.

When the meat is consumed, HCAs and PAHs spread around the body

Chemical carcinogens are dangerous in high concentrations, acting directly on cellular DNA, introducing mutations into the DNA sequence

42
Q

How is HCA formed during cooking

A

When amino acids, sugars and creatine react at high temperatures

43
Q

How is PAHs formed during cooking

A

PAHs are formed when fat and juices from meat grilled directly over an open fire drip onto a fire, causing flames

These flames contain PAHs that then adhere to the surface of the meat.

PAHs can also be formed from smoking meat.

44
Q

How can food choices cause cancer

A

Animal (saturated) fats, especially from red meat, are associated with several different types of cancer, including colon, rectum and prostate.

A lack of dietary fiber is linked to increased risks of colorectal cancer.

Obesity also increases one’s risk of developing cancer

45
Q

How can ionising radiation cause cancer

A

Potential sources of ionising radiation (X-rays and Y-rays) include nuclear explosion.

  • Ionising radiation forms free radical of water which are chemically very reactive.
  • Free radicals can interact with cellular DNA to produce double stranded breaks leading to chromosomal rearrangements and deletions, hence affecting cancer critical genes like TSG and POG
  • Therefore, leading to a loss of normal growth control mechanisms and the cell divides uncontrollably leading to tumour formation (IMPT used as a conclusion for everything)
46
Q

How can UV radiation cause cancer

A

Exposure to the sun causes skin damage and maybe cancer

  • excessive exposure allow for the production of a covalent attachment between adjacent pyrimidines in one strand (thymine dimers) or base pair sub, deletion and insertion in cellular DNA
  • This causes mutation in cancer critical genes
  • Therefore, leading to a loss of normal growth control mechanisms and the cell divides uncontrollably leading to tumour formation (IMPT used as a conclusion for everything)
47
Q

What is the most harmful form of UV rays

A

Most harmful of this type of radiation is DNA-damaging UV-B rays.

These rays cause 90% if all skin cancers as they lead to distinctive mutation patterns during DNA replication.

48
Q

How does age cause cancer

A

If cancer results from an accumulation of mutations and if mutations occur throughout life then the longer we live, the more likely we are to get cancer

49
Q

How does genetic predisposition increase risk of cancer

A

An individual inheriting an oncogene or a mutant allele of a TSG is one step closer to accumulating necessary mutations for cancer to develop.

Predisposition to cancer is inherited not cancer itself

50
Q

Some examples of a cancer running in the family

A
  1. Familial colorectal cancer: individuals that inherit one mutant copy of the APC gene (TSG) have an increased disposition to develop colon cancer
  2. Hereditary breast cancer: Individuals that inherit one mutant copy of genes such as BRCA1, BRCA 2 and p53 (TSG) have an increased disposition to develop breast cancer
51
Q

How does loss of immunity cause cancer

A

When the immune system is suppressed by drugs, viruses like HIV, or even mental states of anxiety and depression, it is unable to detect and destroy cancerous cells due to absence or inadequate numbers of immune cells.

Hence tumours may develop.

Biology Hwa Chong (19 decks)

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