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Pathology Jim > Pathology Week 7 E > Flashcards

Pathology Week 7 E Flashcards

1
Q

Define Oncogenesis

A

The process initiating and promoting the development of neoplasm through the action of biological, chemical or physical agents

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2
Q

Define pathogenesis

A

The production and development of disease

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3
Q

Define carcinogenesis

A

The development of cancer

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4
Q

Define a carcinogen

A

A substance capable of causing cancer in living tissue

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5
Q

What are the factors that play a role in the pathogenesis of cancer?

A

Accumulated genetic abnormalities

Environmental carcinogenic insults

Growth factor activation

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6
Q

What is the pathogenesis sequence of cancer?

A

1 - Induction: fixation into the genome, avoidance of apoptosis and immune rejection.

2 - Promotion: stimulation of cell expansion of mutated clone, continued avoidance of apoptosis and immune surveillance.

3 - Conversion/ Transformation: epigenetic &/or secondary mutation, immortalisation and activation of telomerase allowing limitless cell division, loss of cell contact inhibition, angiogenesis of primary tumour.

4 - Progression: tertiary mutations, outgrowth of tumour

5 - Metastasis: breach of vascular endothelium, lodging and binding of capillary beds, invasion of secondary sites.

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7
Q

What are the 7 classes of proteins controlling cell growth?

A

I - Growth factors

II - Growth factor receptors

III - Signal transduction proteins

IV - Transcription factors

V - Pro- or anti-apoptotic proteins

VI - Cell cycle control proteins

VII - DNA repair proteins

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8
Q

What is significant about proteins class I-IV?

A

Mutations changing the structure of expression of proteins in classes I-IV generally give rise to dominantly active oncogenes. Viral proteins that activate growth factor receptors may also induce cancer.

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9
Q

What is the role of class V proteins?

A

Mutations changing the structure or function of class V proteins reduces the rate of cellular attrition, allowing the cell to live longer. (Makes it less susceptible to apoptosis)

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10
Q

What is the function of class VI proteins?

A

They act as tumour suppressors. Mutations in the gene creating these proteins is likely to produce proteins that have an altered or impair ability to perform the function of suppressing tumours, therefore the mutant cells have a higher probability of becoming tumour.

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11
Q

What will mutations in a class VII cause?

A

Mutations greatly increase the probability that the mutant cells will become tumour cells

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12
Q

What are the 2 main types of genes that play a role in cancer development?

A

Tumour suppressor genes

Oncogenes

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13
Q

What are proto-oncogenes?

A

Normal genes, some of which provide signals that lead to cell division while other relate to apoptosis. Mutations in proto-oncogenes increases the risk of neoplasia and mutated proto-oncogenes are called oncogenes.

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14
Q

What are oncogenes?

A

Any gene that causes the transformation of normal cells into cancerous cells. They result from the mutation and activation of proto-oncogenes. The key feature of oncogene activity is that a single altered copy leads to unregulated growth. Cell growth caused by oncogenes can occur in the absence of normal growth signals such as those provided by growth factors.

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15
Q

What are the risk % associated with the BRCA gene in regards to breast cancer and ovarian cancer?

A

80-90% lifetime risk of beat cancer

40-50% lifetime risk of ovarian cancer

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16
Q

What is the full name for BRCA1?

A

Breast cancer 1, early onset gene

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17
Q

What is the normal function BRCA1?

A

Plays a role in maintaining the stability of a cells genetic information and provides instructions for making the BRCA1 protein. It plays a role in DNA repair and a critical role in embryonic development and interacts with other tumour suppressor proteins to regulate cell division.

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18
Q

What is the full name for BRCA2?

A

Breast cancer 2, early onset gene

19
Q

What are the normal functions of the BRCA2 gene?

A

Plats a role in maintaining the stability of a cells genetic information. The gene codes for the BRCA2 protein which has a role in DNA repair. This protein may also have a role in the regulation if

20
Q

What are tumour suppressor genes?

A

Normal genes that:

Slow down cell division

Repair DNA mistakes

Tell cells when to undergo apoptosis

Their normal function is to inhibit cell proliferation

21
Q

What happens when tumour suppressor genes are not activated?

A

This results in unregulated cell growth and may result in neoplasia

22
Q

What is TP53?

A

It is a tumour suppressor gene that codes for the synthesis of tumour protein p53. TP53 stops cells from growing and dividing too fast or in an uncontrolled way. TP53 is located in the nucleus of cells throughout the body where it binds directly to the DNA. If the DNA is able to be repaired TP53 activates repair genes. If the DNA is beyond repair it is prevented from dividing and it undergoes apoptosis. Therefore TP53 prevents the development of tumours by blocking the division of cells with mutated or damaged DNA

23
Q

What is TP53 also known as?

A

The guardian of the genome

24
Q

What will a mutate in TP53 result in?

A

These TP53 genes will produce faulty P53 proteins, which will be unable to do their job of recognising, repairing or initiating apoptosis in defective DNA.

25
Q

What is RB1 stand for? What does it do?

A

Retinoblastoma 1 geneIt codes for the synthesis of a tumour suppressor protein called pRB.Under certain conditions pRB stops other proteins from triggering DNA replication.

pRB is the first major checkpoint in the process of monitoring the DNA replication in the process of cell divisonIt also plays a role in apoptosis and cell differentiation.

26
Q

What is it known as when the mutation of a single allele of a proto-oncogene leads to cellular transformation?

A

These mutations are considered dominant

27
Q

What must be altered in order for cellular transformation of tumour suppressor genes?

A

Both alleles of the gene must be mutated

28
Q

What is a mutagen?

A

A substance, preparation or other factor that is capable of inducing mutation

29
Q

What are 4 examples of mutagens?

A

Radiation and chemicals

Chromosome rearrangements

Oxidative stress

Viral Infections

30
Q

What impact does radiation and chemicals normally have on genes?

A

Small genetic changes

31
Q

When do chromosome rearrangements occur?

A

Occur during meiosis, may result in large changes.

32
Q

How may oxidative stress be generated? What does oxidative stress do?

A

Oxidants may be generated during normal metabolism, inflammation etc. Oxidants released during chronic inflammation damage genes (e.g. TP53) and regulatory proteins (e.g. caspases) which can result in neoplasia

33
Q

How can viral infections result in neoplasia?

A

Viruses can excise of insert genetic material into their host cell’s genome. The genetic changes that occur are not regulated appropriately. When the affected genes are associated with cell regulation and apoptosis, oncogenesis may occur. Viruses can also inhibit caspases, blocking apoptosis (Epstein Barr Virus)

34
Q

What is Carcinogenesis?

A

A multistage process where normal cells progress to cancer through a gradual accumulation of genetic errors.

35
Q

Which cell cycle check point does pRB regulate?

A

G1/ S

36
Q

Which cell cycle check point does p53 regulate?

A

G2/M

37
Q

What is the role of NK (natural killer) cells in the destruction of cancer cells? How are NK cells activated?

A

They are a type of lymphocyte that find and destroy virus affected or tumour cells. Prior activation by the immune system is not needed for NK to do their job (they are activated by double stranded RNA)

38
Q

How do cytotoxic t cells help protect against cancer? What activates cytotoxic t cells?

A

Cytotoxic T cells attack damaged or dysfunctional cells, e.g. virus infected and cancer cells. Antigen presentation induces t cells to become cytotoxic

T cells are antigen specific and are able to search out and kill specific types of cells (e.g. infected or tumours)

When T cells find cells carrying the antigen they are looking for they secrete monokines to attract macrophages to the area, they also release granzymes (proteases)

39
Q

What are CD8 receptors? How do they assist in tumour or infected cell recognition?

A

A membrane glycoprotein found on the surface of cytotoxic T cells. It recognises and binds to abnormal antigens on the surface of disease cells. Once binding occur the cytotoxic t cell induces the destruction of the abnormal cell by macrophages

40
Q

How do antibodies help to protect against cancer?

A

They bind to abnormal antigens on the surface of pathological cells and induce death of the cell by activating complement.

41
Q

How do macrophages help to protect against cancer?

A

They kill tumour cells that have been damaged or marked by complement.

42
Q

What are the characteristics of neoplastic cells?

A

Angiogenesis

Defective DNA repair

Unrestricted proliferation

Insensitive to growth inhibition

Evade apoptosis

Invade local tissues

Metastasis

Self sufficient in growth signals

avoid driving under influence especially if mega shitfaced

43
Q
A

Pathology Jim (6 decks)

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