MDSA01H3 Lecture Notes - Lecture 10: Retina, Retinoblastoma Protein, Oncogene

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greentrout185

26 Dec 2016

School

UTSC

Department

Media Studies

Course

MDSA01H3

Professor

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Metacognition- thinking about your learning technique and you are learning. Cancer is a defect in the ability of cell division. Normal cells are somehow modified into a cancer cell, we see it as a genetic change. Mutations moving forward through rounds of cell division that abnormal cell is now proliferating and carrying on that genetic change. Leukemia- blood cells do not mature, individual will not have mature t cells and be able to fight infections. Cancer can also cause problems in the tumor(the accumulating mass of abnormal cells) and the functioning of the tumor around it. But for the skull there is no more space for it to grow so there is a lot of pressure on the brain. Solid tumors are not always the exact same cells. The right side pic- is the multi hit concept that is added onto the proliferated activity. These are what will change the phenotype and change the behaviour of those cells.

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1.In 1971, Dr. Judah Folkman published the âangiogenic hypothesisâ suggesting that a tumor cannot grow beyond 1â2 millimeters without the development of new blood vessels (angiogenesis) that provide access to oxygen and nutrients. During the 1990s, it was discovered that vascular endothelial growth factor (VEGF) stimulates migration and proliferation of the cells that form blood vessels, leading to the formation of new blood vessels. VEGF binds to receptor tyrosine kinases (RTKs) on the cell surface and causes the RTKs to dimerize and become active, thereby initiating an intracellular signaling cascade that stimulates cell division and inhibits apoptosis. Many cancer cells secrete high levels of VEGF and increased VEGF expression in a tumor is correlated with a poor medical outcome for the patient. You work for a biotechnology company that seeks to create anti-cancer drugs that prevent growth of tumors and/or cause tumors to shrink, while leaving normal cells relatively untouched. Your company has purchased the rights to therapeutic uses of VEGF derived proteins as anti-tumor drugs. You have found that the VEGF protein has 2 domains, one involved in receptor binding, the other is required for dimerization of VEGF. You propose to make mutant versions of the protein that will act as antagonists of the receptor to be given to patients as an IV treatment as a way to inhibit the endogenous VEGF secreted by the tumor.

a.Which of the 2 domains should you mutate (receptor binding or dimerization)?

b. How do you expect the introduction of the mutant protein into the bloodstream of patients to block tumor progression (in other words, why did you change the domain in part a)?

peachmoose600

Tasmanian devils (Sarcophilus harrisii), the worldâs largest carnivorous marsupials, are facing extinction. Not from hunting, or habitat loss, but from within; a transmissible cancerous derivative of Schwann cells, responsible for devil facial tumour disease (DFTD). First seen in 1996, the disease has spread widely though the population, and is now estimated to be present in 80% of the population. With the grim prognosis of ~100% mortality in 12-18 months, animals that once went through multiple breeding cycles are now lucky to reproduce once before death, resulting in a 70% decline in their population over the past decade. The cancer is transmitted by biting (a common ritual used by these animals to establish and maintain social position), with cancer cells from one animal (the biter) being implanted in the wound inflicted on the other animal. Equally common in both sexes, the disease itself is more prevalent in animals higher on the social scale, presumably reflecting higher levels of social interaction (biting). The cancer is usually first evident as facial tumors, from which metastasis to cervical lymph nodes occurs, often followed by dissemination to other organ systems. Cause of death is by organ failure or by malnutrition in those with facial tumors large enough to prevent feeding. Based on what we have covered regarding the Major Histocompatibility Complex, you would expect the passage of a cancer from one individual to another* to be a rare event (to see just how rare, read the accompanying popular press piece from the New York Times). Here are some things that you already know: *Yes, some viruses can cause cancer (example: Hepatitis B virus and liver cancer), and you can transmit a virus from one individual to another; but that is not the same thing as passing the cancer itself. v Almost all nucleated cells express high levels of class I MHC proteins on their surface. v Class I MHC proteins collect peptides produced from endogenous proteins and display them at the cell surface. v Different Class I MHC proteins bind and display different peptides. v Developing cytotoxic T-cells that recognize self-antigens are eliminated. v Mature cytotoxic T-cells conduct surveillance by scanning the peptides displayed by class I MHC proteins. v Mature cytotoxic T-cells that recognize an antigen on a cell will kill that cell (recall that cytotoxic T cell activity is important in rejection of tissue transplants).

Before the questions:
v Tasmanian Devils are not immunosuppressed.
v Tasmanian Devil cytotoxic T-cells are not broken, they can kill cells.
So neither of those should be part of your answers.
This is an ongoing research topic with large gaps in our knowledge; we really donât fully understand how this works
and so there is no âcorrectâ answer. Your job is to provide a logical argument, with some research and details to
support your contention. Note that in questions 1 & 2 class I MHC should be part of your answer, but not in
question 3.

Questions:
1.) Acquiring DFTD is basically like receiving a transplant that is not rejected. How can that be? Suggest a possible
way this could occur. Be sure to explain why you think this would work, and then explain how you would test
that model to determine if it were correct. (10 point question).
2.) Canine Transmissible Venereal Tumor (CTVT) is the other know transmissible cancer in mammals. Unlike
DFTD, CTVT does not usually result in death. Do a little research on this disease and summarize how it is
different from DFTD. Provide an explanation as to why one is lethal and the other is generally not. (10 point
question).
3.) Recently, researchers at Washington State University determined that some Tasmanian devils had developed
resistance to this cancer. By scanning partial genome sequences of resistant and susceptible animals (a
complete devil genome has yet to be assembled) they identified a set of genes where mutations appeared to
enhance resistance. Speculate as to the function of the proteins these genes encode, and explain why that
might provide for resistance (note: they were NOT MHC genes).

Mainly need guidance/ideas for #1's 1 and 3!

1) The studies in cell sorting and affinity demonstrated

A	the epidermis has a tighter affinity that the nueraltissue

B	the mesoderm is never capable of resorting as the outter layerof a re-sorted tissue

C	all of the above

D	mesoderm actually requires input from both the ectoderm andendoderm to "know" it's middle location

E	there is no mechanism in which cells known their properlocation identity within a developing embryo

2) The extracellular matrix

A	provides a structure for cells to crawl over

B	contains multiple signaling proteins to guide/repel cells sothey progress in the correct direction

C	interacts with the transmembrane proteins on the cells toproduce a response

D	all of the above

3) EMT is required

A	for mammary glad formation

B	for progression of cancer from single tumor to metastaticcancerous cells roaming throughout the body

C	for neural crest cell formation which provides the cells forinternal organs

D	all of the above

E	for the initiation of gastrulation in birds and mammals becausethey form as a disc and not a ball of cells

4) Permissive induction

A	allow for species to change their genetic fate due to thesignals recieved from surrounding tissue

B	describes regions of specificity hotspots within the developingembryo

C	describes when cells that no indication towards their fate dueto having the proper signalling/surroundings

D	none of the above

5) Classical Cadherins (those dependent on calcium for properfunction)

A	all have the same sequence identity (~98%) on the intracelluarside acroos multipe species

B	are all regulated by the same 3 catenin proteins to regulatestability and cytoskeletal regulation

C	Require calcium for a conformational change to present theirbinding site

D	are very specific to which other cadherin on the neighboringcell it is interested in binding to

E	all of the above

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MDSA01H3 Lecture Notes - Lecture 10: Retina, Retinoblastoma Protein, Oncogene

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