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SG Molecular > Lecture 29: Cancer 2 > Flashcards

Lecture 29: Cancer 2 Flashcards

1
Q

What type of proteins are usually encoded by tumor suppressor genes?

A

Proteins that inhibit cell proliferation

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2
Q

What are the 2 major categories of proteins that tumor suppressor genes encode?

A

Proteins that normally restrict cell growth and proliferation

Proteins that maintain integrity of the genome

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3
Q

What are examples of proteins that normally restrict cell growth and proliferation?

A

Rb, CKI, proteins that promote apoptosis (caspases)

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4
Q

What are examples of proteins that maintain the integrity of the genome?

A

ATM, ATR (checkpoint control - detect DNA damage), DNA repair enzymes or pathways

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5
Q

What type of gene is Rb?

A

A tumor suppressor - it prevents over-proliferation of cells and inhibits cell division

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6
Q

What are the 2 forms of retinoblastoma?

A

Hereditary

Sporadic

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7
Q

Are the majority of Retinoblastoma cases hereditary or sporadic?

A

Sporadic = 60%

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8
Q

What is the difference between hereditary and sporadic retinoblastoma?

A

Hereditary = familial, BOTH eyes are affected

Sporadic = NO family history, single tumor in one eye

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9
Q

Which type of retinoblastoma is associated with a loss of heterozygosity?

A

Hereditary

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10
Q

What leads to the loss of heterozygosity?

A

Person initially starts one Rb deletion in every cell (inherited), then somatic event occurs and eliminates the one good copy –> tumor forms

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11
Q

In the sporadic form of Rb, you start off with all normal cells - no mutations of Rb. What hypothesis describes the development of Retinoblastoma in this case?

A

Two-hit hypothesis - first Rb gene obtains mutation, then another mutation must occur to develop Retinoblastoma

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12
Q

What binds to the promoters of G1/S cyclin and S cyclin genes to drive the cell cycle and what is the effect of the Rb protein on this interaction?

A

E2F - this is inhibited by interaction with the Rb protein, so Rb inhibits cell division

When Rb is mutated, cell division proceeds uncontrolled –> cancer

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13
Q

True or false: The Rb pathway includes tumor suppressor genes only, not oncogenes

A

False – the Rb pathway can include both tumor suppressor genes and oncogenes

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14
Q

What is the action of an active CKI (p16)?

A

Inhibits Cdk, so Cdk-cyclin complex will not phosphorylate Rb

Rb then binds E2F and blocks it, inhibiting cell proliferation

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15
Q

What is the action of Cdk-cyclin in the absence of a CKI?

A

Cdk will remain permanently active, Cdk-cyclin complex can now phosphorylate Rb

Rb will be inactive and E2F will drive S-Cdk activation by making more cyclins

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16
Q

What type of gene are Cdks or cyclins considered when they are overproduced, why?

A

Oncogenes - bc overproduction can overcome the amount of CKIs and lead to uncontrolled growth –> cancer

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17
Q

What type of genes are CKI and Rb considered, why?

A

Tumor suppressor genes, because if these are lost, there is no control of Cdk-cycling or suppression of entry into the cell cycle –> cancer

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18
Q

What tumor suppressor gene is considered the guardian of the genomic galaxy because it is mutated in the majority of cancers

A

p53

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19
Q

What are the 4 processes that p53 is primarily involved in?

A
  1. Cell cycle arrest
  2. DNA repair
  3. Apoptosis
  4. Block of angiogenesis
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20
Q

If you lose p53, what functions are you losing?

A
  1. Loss of checkpoint control in cell cycle
  2. Loss of cell cycle arrest d/t DNA damage
  3. Loss of DNA repair
  4. Loss of apoptosis d/t DNA damage
21
Q

What are the 2 functions of p53 as a gene regulatory protein?

A

Stimulates transcription of gene encoding CKI called p21

Activates expression of pro-apoptotic proteins BH123 and BH-3

22
Q

What 2 conditions are caused by papilloma viruses?

A

Warts and cervical cancer

23
Q

How does viral DNA exist in human cells after infection with the virus?

A

Extrachromosomal material - like a plasmid

24
Q

What occurs if viral DNA integrates into host DNA in terms of tumor development?

A

Viral DNA will interfere with control of cell division in basal cells –> malignant tumor development

25
Q

True or false - papilloma viruses lead to malignant tumor development after infection of host cell prior to integration into host genome

A

False - prior to integration into host genome, HPV causes benign warts. If accidental integration of viral DNA occurs, unregulated production of viral proteins drives cell proliferation leading to a malignant tumor

26
Q

What are the 2 viral proteins of papilloma virus?

A

E6 and E7

27
Q

The viral proteins of papilloma virus E6 and E7 bind to which 2 tumor suppressor genes? What does this cause?

A

Rb and p53

Uncontrolled cell proliferation

28
Q

In a tumor cell resulting from HPV, viral protein _____ binds to Rb so _____ can cause overexpression of G1/S-Cdk and S-Cdk and cells grow and divide

Viral protein ____ binds to p53 and inactivates it so ______ is not produced –> Cdk’s can act uncontrollably

A

E7; E2F

E6; CKI

29
Q

A ______________ is a normal gene, usually involved in regulation of cell proliferation that can be converted into a cancer-causing oncogene by a mutation

A

Proto-oncogene

30
Q

Transgenic (Tg) mice are a tool for studying oncogenes. What is the difference in the results in:

Myc Tg mice

Ras Tg mice

Myc Tg x Ras Tg mice

A

Myc Tg mice - cell proliferation occurs but most cells to not give rise to cancer

Ras Tg mice - more severe - tumors occur earlier

Myc Tg x Ras Tg - Develops tumors earlier and faster

31
Q

Is Bcl-2 an oncogene or tumor suppressor gene?

A

Oncogene

32
Q

How does Bcl2 function as an oncogene?

A

A Bcl2 mutation stops apoptosis

33
Q

For most cancers, the first step of metastasis is local invasion - is this an easy or difficult step?

A

Difficult! Only a few cancer cells will pass this barrier

34
Q

The initial entry into blood or lymphatic vessels is facilitated by ___________ of new blood or lymphatic vessels. Is this an easy or difficult step?

A

Easy - most cancer cells have acquired this ability before becoming invasive through mutations in genes that control apoptosis

35
Q

Many cancer cells survive in circulation and exit at remote sites to colonize new tissues - is this an easy or difficult step?

A

Difficult - some cells die after entering foreign tissues, others fail to proliferate. Only a few metastasis-competent cells continue to proliferate in foreign tissue and form tumors

36
Q

Colorectal cancer is one of the most preventable cancers. Where does it arise?

A

In the epithelial lining of the large intestine (highly organized, renewed by stem cells every week)

37
Q

There are 600,000 deaths annually from colon cancer, what percentage of total cancer deaths are due to colorectal cancer?

A

10%

38
Q

Colonoscopies are important for early detection of colorectal cancer - they detect small, protruding tumors called polyps, which are considered ___________

A

Adenomas

39
Q

What happens when a colorectal polyp (adenoma) is left alone

A

A malignant tumor develops

40
Q

40% of colorectal cancers have point mutations in ______

60% have an inactivating mutation of _______

An important loss is a ______ mutation

A

K-Ras
p53
APC

41
Q

Familial adenomatous polyposis coli is characterized by hundreds of polyps - of which at least one will certainly become malignant. What will ultimately cause this malignancy?

A

Inactivation of tumor suppressor gene APC - leading to loss of heterozygosity so NO APC is transcribed

[because in familial cases they already only have one functioning copy of APC]

42
Q

T/F: most colorectal cancers are hereditary

A

False, more than 80% show inactivation of both copies of APC acquired throughout lifetime

43
Q

What is Hereditary non-polyposis colorectal cancer (HPNCC)?

A

In most cases of colon cancer, there is high degree of genetic instability (multiple copies of chromosomes); with HPNCC, there is a normal number, or near-normal number of chromosomes

44
Q

What is the purpose of chemotherapy and how does this lead to the common side effects of hair loss, nausea, anemia & immune dysfunction?

A

Chemotherapy stops cell division, and this includes hair follicle cells, stomach-lining cells, and blood-producing cells

45
Q

The Philadelphia Chromosome has a reciprocal translocation between chromosomes 9 and 22, which is responsible for chronic myelogenous leukemia. What does this translocation do to bring about CML?

A

There is a break point in two genes - Bcr (22) and Abl (9), these come together and fuse

When the N-terminus of Bcr joins Abl, it makes it hyperactive as a tyrosine kinase leading to a high degree of cell proliferation

46
Q

CML involves a Bcr-Abl protein, what is the treatment for CML?

A

Gleevec - inhibits tyrosine kinase activity by taking the place of ATP on Bcr-Abl so the substrate does not change, and causes disappearance of Philadelphia chromosome in 80% of patients

47
Q

What is the reason for combination therapy to treat cancer?

A

Treating patients with drugs simultaneously is an advantage for cancer therapy because it can kill different types of cells that might have the ability to survive one treatment alone

48
Q

Cancers can be very heterogenous - meaning that they are different in everyone. What is the future of cancer treatment?

A

Custom-driven treatments selected to target specific disregulated cancer-critical proteins

Personalized-medicine!!!

49
Q

What is the basis of Anti-angiogenesis therapy?

A

Prevents new blood vessel formation by tumors. In mice, repeated treatments with this therapy resulted in the tumor growing back 6 times, but on the 7th time there was no tumor growth. However this does not translate to human use - only works in some

SG Molecular (7 decks)

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