TAMU BIOL 213 - Cancer (7 pages)

Previewing pages 1, 2 of 7 page document View the full content.
View Full Document

Cancer



Previewing pages 1, 2 of actual document.

View the full content.
View Full Document
View Full Document

Cancer

481 views


Lecture number:
25
Pages:
7
Type:
Lecture Note
School:
Texas A&M University
Course:
Biol 213 - Molecular Cell Biol
Edition:
1
Unformatted text preview:

BIOL 213 1st Edition Lecture 25 Outline of Last Lecture I Eukaryotic cell cycle a Four phases II III IV V b Regulation was discovered by observing mitosis of Xenopus frog eggs Cyclin and Cdks control progression through the cell cycle a M cyclin binds to Cdk to create an M Cdk b The sharp decrease in levels of M cyclin after M phase is due to degradation of cyclin by proteasomes S Phase DNA replication G1 phase arrest due to DNA damage a Outline If DNA damage is detected p53 will be activated which will initiate transcription of the p21 gene The p21 protein a Cdk will bind to the active SCdk and inactivate it so that S phase cannot be initiated Apoptosis programmed cell death a It s mediated by an intracellular proteolytic cascade that cuts the cell up into nice little pieces b High stress to the p53 protein causes the p53 to induce apoptosis Outline of Current Lecture I The hallmarks of cancer II Discovery of oncogenes III Properties of cancer cells IV Activate motility pathways to invade tissues V Activate telomerase VI Genome instability VII Resist apoptosis VIII Kinds of genes that when they get mutations can cause cancer a Oncogenes b Tumor suppressor genes IX Recruit blood vessels a Angiogenesis X Cancer treatment a Traditional treatments These notes represent a detailed interpretation of the professor s lecture GradeBuddy is best used as a supplement to your own notes not as a substitute b Developing treatments Current Lecture I II The hallmarks of cancer a Sustained proliferation signaling i The pathways that initiate proliferation are on even if there s no proliferation signal b Evade growth suppressor signaling c Activate motility pathways to invade tissues d Activate telomerase i To keep the telomeres long so that the cell can keep dividing without worrying whether or not some of the chromosome will be lost e Genome instability f Resist apoptosis g Recruit blood vessels h Deregulated cell energetics i Tumor cells usually only go through glycolysis and not the rest of cellular respiration ii Because of this they use a lot of glucose and essentially starve the other cells around the tumor Discovery of oncogenes a Oncogenes mutated genes that cause cancer b A retrovirus was studied i This virus normally has three genes 1 Gag for the protein coat 2 Pol for reverse transcriptase 3 Env for envelope around the virus ii These genes are transcribed from single strand RNA to cDNA by reverse transcriptase and inserted into the host s DNA iii The virus proteins are synthesized by the cell and the viruses emerge from the host cell c The Rous Sarcoma virus was found to cause tumor growth in chicken muscles i They looked at its genome and found that it had an extra gene SRC ii When they took this gene out of the genome the virus stopped causing tumor growth iii When they added this gene to other viruses these viruses started to cause tumor growth iv They found that this SRC gene closely resembled an important gene in chicken muscle cells v They determined that this gene was the cause of the tumor growth III IV V Properties of cancer cells a These traits are heritable b When a cell divides without normal constraints it becomes a tumor i Benign tumor just a big mass of fatty tissue that doesn t invade any other tissue ii Malignant tumor forms metastases that invade other tissue c Cancer cells arise from the accumulation of mutations i A lot of mutations have to accumulate in the same cell for it to turn into a cancer cell ii The chance of cancer increases with age because the cells have had more time to accumulate mutations 1 However there is a higher chance of childhood leukemia at a young age a When a fetus is growing there is a gene that causes extremely fast proliferation b Once the baby is born this gene is usually turned of c Sometimes a really active promoter like those found in immunoglobulin genes can be transposed to the proliferation gene d This causes a lot of uncontrolled proliferation which can lead to leukemia Activate motility pathways to invade tissues a In epithelial cells cancerous cells start growing on the surface b As they grow and divide they ll accumulate more mutations becoming more cancerous and a tumor arises c The growing mass penetrates the surface and grows into the tissue to look for a blood source i They break through the basal lamina d Once they reach a blood vessel they can metastasize and spread cancerous cells to other tissue Activate telomerase a Some cells like those lining the intestines have active telomerase because they need to frequently divide because the food is scrapping them away b Therefore there are epithelial stem cells c These divide into one stem cell and one other daughter cell i The stem cell is important for future divisions and has active telomerase d The other daughter cell goes through a series of divisions until it s completely diferentiated e Its telomerase is then inactivated because it doesn t need to divide any more f A mutation can occur in the stem cell i This is bad because the stem cell has active telomerase therefore it will keep dividing and the mutation will spread VI VII VIII g A mutation can occur in the other daughter cell i This isn t as bad because its telomerase will be inactivated ii BUT if the mutation turns on the telomerase and other hallmarks of cancer this can lead to cancer Genome instability a Normal cells have nicely packed and organized chromosomes i All of the DNA that belongs in chromosome 1 is packaged only in chromosome 1 b In cancerous cells the chromosomes are rearranged so that the DNA of chromosome 1 is spread throughout other chromosomes the same is true for all the other chromosomes they re not neatly organized i This is a result of double strand DNA breaks and fusion with other DNA strands ii This is also a result of inactive p53 1 In a normal cell if the DNA scanning proteins saw how messed up the DNA was they would activate p53 and the p53 would cause the cell to either stop dividing until the problem was fixed or go through apoptosis Resist apoptosis a Mutations in genes can cause the cell to not go through apoptosis like it should when the cell is damaged i Ex p53 Kinds of genes that when they get mutations can cause cancer a Signaling genes these mutated proteins are stuck in the on position so that they re always telling the cell to divide even when there s no signal i Ex mutation in Ras proteins leads to uncontrolled proliferation 1 A single amino acid is changed so that GTP is


View Full Document

Access the best Study Guides, Lecture Notes and Practice Exams

Loading Unlocking...
Login

Join to view Cancer and access 3M+ class-specific study document.

or
We will never post anything without your permission.
Don't have an account?
Sign Up

Join to view Cancer and access 3M+ class-specific study document.

or

By creating an account you agree to our Privacy Policy and Terms Of Use

Already a member?