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SCIENCE AGAIN
Dec. 1st, 2006 10:03 am*Sigh*
This week's been another week of 13-hour days, grappling with the crappy rail network and feeling like a hermit.
I did manage to go clubbing Weds (the club flooded, hilarity ensued), and there is a mate's birthday outing tonight. Still reeling a bit from being politely told on Monday that the next phase of my PhD experiments is totally impractical. It'd take me at least six months work to probably get a confusing answer.
I'm beginning to see why pancreatic cancer has a mortality rate equivalent to it's morbidity rate. Genetically, it's as broken as can be. Not only does the cell line I am working with have a chromosome number of 56 to 80-odd (normal number is 46) but: "The most common partial or whole-arm gains involved 5p, 7q, 12p, 1q, 7p, 5q, 9p, 9q and 11p. The most common partial or whole-arm losses affected 9p, 11q, 18q, 3p, 2q and 1p, as well as the short arms of the acrocentric chromosomes. Spectral karyotyping allowed us to identify a number of recurrent structural aberrations, all of them unbalanced: most frequently i(5)(p10), del(11)(q23), i(12)(p10), i(1)(q10), del(7)(q22) and del(10)(p11)". (Professor Denise Sheer, ICMS) It's not like leukaemia or something where you have ONE chromosomal translocation. I'm not sure how the hell one is supposed to find ANY kind of pattern in it when even a single cell division is unlikely to give rise to daughter cells with the same number of chromosomes, let alone the same functional genes.
However, the tumour still functions, so I'm not giving up, so there.
This week's been another week of 13-hour days, grappling with the crappy rail network and feeling like a hermit.
I did manage to go clubbing Weds (the club flooded, hilarity ensued), and there is a mate's birthday outing tonight. Still reeling a bit from being politely told on Monday that the next phase of my PhD experiments is totally impractical. It'd take me at least six months work to probably get a confusing answer.
I'm beginning to see why pancreatic cancer has a mortality rate equivalent to it's morbidity rate. Genetically, it's as broken as can be. Not only does the cell line I am working with have a chromosome number of 56 to 80-odd (normal number is 46) but: "The most common partial or whole-arm gains involved 5p, 7q, 12p, 1q, 7p, 5q, 9p, 9q and 11p. The most common partial or whole-arm losses affected 9p, 11q, 18q, 3p, 2q and 1p, as well as the short arms of the acrocentric chromosomes. Spectral karyotyping allowed us to identify a number of recurrent structural aberrations, all of them unbalanced: most frequently i(5)(p10), del(11)(q23), i(12)(p10), i(1)(q10), del(7)(q22) and del(10)(p11)". (Professor Denise Sheer, ICMS) It's not like leukaemia or something where you have ONE chromosomal translocation. I'm not sure how the hell one is supposed to find ANY kind of pattern in it when even a single cell division is unlikely to give rise to daughter cells with the same number of chromosomes, let alone the same functional genes.
However, the tumour still functions, so I'm not giving up, so there.