42 - MCB 142 Professor Georjana Barnes 12/3/07 Lecture 42...

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12/3/07 Lecture 42 ASUC Lecture Notes Online (formerly Black Lightning) is the only authorized note-taking service at UC Berkeley. Please do not share, copy or illegally distribute these notes. Our non-profit, student-run program depends on your individual subscription for its continued existence. These notes are copyrighted by the University of California and are for your personal use only. Sharing or copying these notes is illegal and could end note taking for this course REVIEW Last Friday we covered three points about cancer. There are many different phenotypes; cancer cells look different from normal cells. While cancer cells may not have all the phenotypes we discussed, they do have a large number of them. More than one mutation needs to accumulate in a normal cell in order for it to become cancerous. Cancer cells are clonal descendants of a single somatic cell. Most cancers arise by chance in somatic cells over time as a result of mutations. I mentioned that we will look at chemical and environmental mutations and different kinds of viruses that can cause tumors. Then we looked at the evidence that most cancers are sporadic. Siblings do not tend to get the same types of cancers. But there are some cancers that seem like they’re inherited – or predispositions for cancers – and those do have a genetic basis. But more needs to happen than just that one mutant gene being passed on to the offspring. Interpreting all this evidence we talked about last week gives you this kind of a figure, which is 19.21 in the book, which shows you a model for the statement that cancer arises by successive mutations in a clone of proliferating cells. You have a normal cell at the top and it grows through cell cycle and produces two cells. Now that offspring cell may have a mutation in it; it doesn’t necessarily have to be a cancerous mutation. Then it goes on to divide and so does its sister cell and now you have daughter cells that are either like itself or have a second mutation. Over time, you get an accumulation of mutations; eventually enough will accumulate in a cell’s genome so that it becomes malignant. You can see that all of these cells might be together in a group of cells, but they all have a single somatic cell as an origin. The rest of the cells in this organism won’t be contributing to this one malignant cell. ONCOGENES AND MUTANT TUMOR SUPPRESSOR GENES Mutations that cause cancer create two different types of alleles. Mutations can give you dominant alleles and those are called oncogenes. Mutations can also give you recessive alleles, relative to wild-type function, and these types of mutants are called mutant tumor suppressor genes. The dominant alleles improperly activate genes – that is, you might get too much of the wt protein product. They are wt in the sense that the sequence hasn’t changed, but they are not wt in terms of expression. Another way to activate a gene is to mutate a gene product and then have it have a function that is no longer regulatable. Such a
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This note was uploaded on 04/04/2008 for the course MCB 142 taught by Professor Slatkin during the Fall '08 term at University of California, Berkeley.

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42 - MCB 142 Professor Georjana Barnes 12/3/07 Lecture 42...

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