| To inquiry into the significance of the mitochondrial DNA (mtDNA) alterations in pancreatic cancer coexisting with chronic pancreatitis and cancer-mimmicking pancreatitis. The entire mitochondrial genomes in 12 tumor samples,11 cancer-mimicking pancreatitis, and their paired normal tissues from the same patients were amplified using 58 pairs of overlapping primers. The mtDNA common alterations was studied by polymerase chain reaction. Somatic point mutations and sequence variants of mitDNA were searched for tumors, pancreatitis, and their normal part by direct sequencing of the mitochondrial genome. By BLAST different banding patterns between normal and tumor, normal and chronic pancreatitis were detected in DNA fragments. mtDNA were sequenced to identify the mutations. 12 of 12 tumors displayed at least one somatic mtDNA mutation, including one tumor with heteroplasmy. 185 somatic mutations were found in pancreatic cancer coexisting with chronic pancreatitis, mutations occurred in the D-loop region (n=11), COI(n=7), ATPase(n=7}, NDl(n=6), COII(n=6), ND2(n=4), COIII(n=4), ND4L(n=4), ND3(n=3), ND4(n=3), ND5(n=2), ND6(n=2), 12sANA (n=2), 16sMA fa=2), respectively, 9of 11 cancer mimicking pancreatitis had totally 70 spots of homoplasmic mutions, the involved mutated gene included D-loop region(n=6), COI(n=4}, ATPase(n=4), NDl(n=2), COII(n=S), COIII(n=l), ND4L (n=l), ND3(n=3), ND5(n=l), 12sANA (n=2), 16sRNA (n=3). Asignificantly higher prevalence of D-Joopregion, ATPase, complex I and COI-III sequence variants were detected in pancreatic cancer and cancer-mimicking pancreatitis. Carcinomas did not carried an unique significantly prevalence of point mutations of genes than pancreatitis. We can conclude that mtDNA gene mutations can be detected in any diseases ,or we can saydifferent pathological stages of any diseases behave different mtDNA gene mutations. Usefulness and status of mtDNA gene mutations are contradictive , either the mutation indicates a preneoplastic condition, or cancer at an early stage, and progressive cancer. mtDNA gene mutations status can only be identified as a clonal expansion in these lesions. Therefore disclosure of mtDNA gene mutations in chronic pancreatitis seems not sufficiently predictive of malignant transformation, and its detection in combination with clinical and morphological follow-up should not be recommended at this time for screening pancreatic cancer, The finding of mtDNA mutations in cytology or biopsy samples from pancreatic mass can not specifically confirm the diagnosis of pancreatic cancer. Only raises the possibility for early surgical intervention if these patients are at high risk of developing pancreatic cancer in the future. Further studies are needed to define the value of mtDNA mutations screening in patients with other evidences suggesting the presence of pancreatic cancer. Chronic pancreatitis may be positive for the mutations in the absence of cancer, and pancreatic cancer does not necessarily have the mutations. The ultimate gole is to detect pancreatic cancer at a early stage and avoid unnecessary pancreaticoduodenectomies for chronic pancreatitis.Part twoAbstractTo evaluate the significance of insertion of ND4 gene into nuclear genome in pancreatic cancer. 12 pathological slice of pancreatic cancer coexisting with chronic pancreatitis ,11 pathological slice cancer-mimicking pancreatitis , and their paired normal tissues from the same patients, two frozen slice were assessed with a mitochondrial ND4 gene probe, nuclear suspensions of these tissues were evaluated by fluorescent in situ hybridization (FISH). all tumors showed evidence of ND4gene sequence localization within the nuclei, but none could be found in chronic pancreatitis and corresponding normal tissues. Positive of FISff of two frozen slice were diagnosed as pancreatic cancer post operation. We concluded that evidence of ND4gene sequence localization within the nuclei can be used as a identification tumor marker of pancreatic cancer...
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