Postby StDrogo » Tue May 08, 2018 4:40 am
With the current state of genomics, there's not much to interpret. KRAS (which controls cell proliferation) mutations generally have an unfavorable prognosis (which is obvious on the face of it since the cell has lost the ability to switch off multiplication, which is really bad for a eukaryotic organism), particularly in more advanced stages. TP53 is a tumor suppressor that regulates over/irregular proliferation and is putatively part of the cascade of genomic mutations that leads to the development of a carcinoma. Amer1 is a transcription activator—not really sure how it's involved in carcinogenesis, but it's commonly implicated. The APC gene regulates APC protein, which is, in essence, a tumor suppressor; this mutation is present in the vast majority of colon cancers. Likewise PGEN, which is commonly also implicated in the carcinogenic cascade. I am really unclear about the role of the REL gene in cancer, but I'm now very interested.
In summary, the only currently clinically relevant mutation you have at the moment is KRAS.
Wife Age 33
02/17 dx Ovarian mass, ascites, pleural effusions
03/17 Resection of 16 x 20 cm ovarian mass; CEA = 10, CA125 = 180, CA19-9 = 36
04/17 Emergency surgery, diastatic perforation, purulent peritonitis, extended right hemicolectomy, well-differentiated adenocarcinoma in splenic flexure, 1/16 lymph
11/17 CT = NED, CEA < 1
12/17 CRS (peritoneal nodules of foreign body giant cell reaction, no evidence of malignancy; liver resection—1 cm FBGCR and .5 cm focal nodular hyperplasia), HIPEC