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Madeline Churchill's Discussion Page

Bad Luck and Cancer

1) Based on the observation in the paper that Glioblastomas are consistent with the correlation of increased cell replication and incidence of cancer, it makes sense(Figure 3 from the 2017 paper) that a huge percentage of cancer in the brain is derived from replicative risk. However there are other glioblastoma cancers (which effect the same type of brain cell as the one reported) that only effect young children (age 5 to 10). Does this fit the model proposed in the paper discussed?

2) Should another category regarding the immune system be added into the 3 categories of cancer? (i.e hereditary, repetitive and environmental) or would this fit under the three already established catagories as proposed by the paper?

3) How likely do you think that cancers that are termed by the paper as replicative errors are possibly just caused by genes mutations or environmental effects that are unknown at this point?

Identifiers for the 21st century: How to design, provision, and reuse persistent identifiers to maximize utility and impact of life science data

How would you envision optimizing the standards for identifiers?

Should database companies have a standard for archival capabilities in case the company goes in? Who would enforce this?

What standards should be put into place in regard to differential naming of genes and future discoveries?

TZAP protein controls telomere trimming process

1) How would you take advantage of this TZAP function to increase aging?

2) Could this be a viable therapeutic target for treating "aging" in the future?

3) How would you translate these conclusions made in an in vitro study design into animal models?

Heterochromatin dependent transcription drives piRNA

1) How do you feel about the use of describing transposons as a parasite?

2) Are all transposons deleterious?

3) what experiment done in the paper showed that hetereochromatin is transcribed

Disruptions of topological chromatin domains cause pathogenic rewiring of Gene-Enhancer Interactions

1) What mechanisms do you think affect enhancer specificity to binding sites that are further downstream?

2) I think it is interesting that depending on what modification of DNA (i.e inversion, duplication) that occurred within the WNT6/IHH, it didn't affect both genes, just one.

3) In figure 3, the change in RNA expression profiles due to mutation were interesting. In particular, the DBF mutation resulted in aberrant expression in the forelimb which resulted in "stubby" fingers. Why do you think that is?

  • Maureen 14:35, 6 November 2017 (PST)How come I didn't hear the answer to question #3? Or the question?

HSP90 Shapes the Consequences of Human Genetic Variation

1) Do you think that there is another chaperone that could have a similar role as Hsp90?

2) I think it is interesting that the twins discussed in the paper that although they had the same mutations, the disease manifested differently (i.e blood phenotype).

3) Do you think that Hsp90 along with TADs could help explain patients with a variance of unknown significance?

Competing memories of mitogen and p53 signaling in control cell-cycle entry

Highly recommend to read in color.

1) In figure 1C, I think it is interesting that the first cell has a different percentage of CDK high/CDK low compared to the other cells shown. Why do you think that is?

2) In Figure 2D, I thought it was interesting that depending on when the double stranded break was initiated, there was a variable effect on the probability of proilferation. Why do you think that is?

3) I think this data has interesting implications if true on cancer progression. In particular, since tyrosine kinases activate RAS, any mutation that would result in increased tyrosine kinase activity would cause a bias of cdk2 compared to p21 and this could explain why tyrosine kinases have been implicated in many different cancers.