Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0001418 (adenocarcinoma)
 68,496 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A human pancreatic cancer cell line, PSN-1, was established from pancreatic adenocarcinoma tissue that had been stored for 1.5 years at -80 degrees C without any special treatment. The stored tissues were first transplanted into nude mice, and from the xenograft, the PSN-1 cell line was established. The original primary tumor and two metastatic lymph nodes were previously found to have 50-fold amplification of c-myc and also 3- to 6-fold amplification of activated c-Ki-ras with a point mutation from GGT to CGT at codon 12. PSN-1 cells are unique in that amplifications of both c-myc and activated c-Ki-ras are present in the same degree as the original tumors. These cells were also found to contain increased amounts of c-myc and c-Ki-ras transcripts.
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PMID:Establishment of a human pancreatic adenocarcinoma cell line (PSN-1) with amplifications of both c-myc and activated c-Ki-ras by a point mutation. 377 42

DNA isolated from a lymph node with metastasis from pancreatic adenocarcinoma in a Japanese male patient transformed NIH3T3 cells upon transfection by the calcium-phosphate precipitation technique. Analysis of DNA from the transformant revealed the presence of an activated human c-Ki-ras gene, which is considered to be responsible for the transformation of the NIH3T3 cells.
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PMID:Activation of c-Ki-ras gene in human pancreatic cancer. 393 75

We have identified a case of serous cystadenocarcinoma of the ovary in which the tumor cells display an amplification (from 10- to 20-fold) of the cellular oncogene K-ras. Normal cells purified from the malignant ascites did not show such amplification. Five consecutive samples were obtained by paracentesis over a 9-month period during which the patient received chemotherapy and underwent clinical progression. The level of c-K-ras amplification in the tumor cells did not change during this period. In studies of the tumors of 6 additional patients with adenocarcinoma of the ovary and 5 cell lines of the same histology, we have detected no other example of significant c-K-ras amplification.
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PMID:Stability of c-K-ras amplification during progression in a patient with adenocarcinoma of the ovary. 402 28

DNA sequences capable of inducing oncogenic transformation of NIH3T3 mouse cells are found in a number of human tumour cell lines. When DNAs of these cell lines are applied to monolayer cultures of the mouse fibroblasts, foci of transformed cells are observed 2-3 weeks later. DNA from cells of such primary foci can be used in turn to induce foci in a second cycle of gene transfer. The human DNA sequences responsible for transformation have been called oncogenes, the best characterized of which is closely related to the Harvey murine sarcoma virus oncogene. Here we present a characterization of an oncogene which we found originally to be present in DNA of the SW480 colon carcinoma cell line. We indicate its structural outlines and demonstrate, in extension of reported results, its presence in an activated form in the genome of several types of human tumour cell lines as well as in biopsy tissue from an adenocarcinoma of the large bowel. We identify this tumour oncogene with c-Ki-ras2, one of two known members of the Kirsten ras family of human proto-oncogenes, extending a series of recent reports which have demonstrated homologies between human oncogenes and those of Harvey and Kirsten murine sarcoma viruses. The c-Ki-ras2 oncogene of several tumour cell lines is shown to be amplified.
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PMID:Characterization of a human colon/lung carcinoma oncogene. 629 38

A human colonic adenocarcinoma transforming gene, recently identified as a cellular homolog of the Kirsten sarcoma gene (v-ras), was used to assign the human cellular Kirsten ras2 gene to chromosome 12 by the Southern hybridization method. A single 640 base-pair Eco RI--Hind III fragment of the transforming gene, isolated by DNA transfection and molecular cloning, can detect a single Eco RI fragment (2.9 kilobase pairs) of DNA from phenotypically normal cells. The data suggest a constant chromosomal location of c-Ki-ras2.
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PMID:Human c-Ki-ras2 proto-oncogene on chromosome 12. 682 69

This is the first description of the detection of pancreatic adenocarcinoma peritoneal metastasis by established radiolabeled polymerase chain reaction (PCR) based Ki-ras mutational analysis. The present study evaluates both routine cytology and Ki-ras mutational analysis in the detection of peritoneal micrometastases in 24 subjects with pancreatic adenocarcinoma compared to seven control cases of chronic pancreatitis and seven control cases of cholecystitis. Locoregional extension, vascular invasion, and distal metastases were confirmed in 21/24 (88%) of the subjects with pancreatic adenocarcinoma by compute tomography, angiography, endosonography, or laparoscopy. The most common site of histologically confirmed extrapancreatic involvement was the vasculature (29%), followed by the liver (25%), duodenum (17%), peritoneum (17%), and lymph nodes (12%). Peritoneal lavage cytology was positive in 3/24 (12%) cases of pancreatic carcinoma while Ki-ras codon 12 mutational analysis was positive in 2/24 (8%). Two histologically confirmed cases of peritoneal metastases were not detected by either methodology, while peritoneal lavage cytology detected malignant cells in one case with histologically confirmed lymph node metastasis.
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PMID:Peritoneal exfoliative cytology and Ki-ras mutational analysis in patients with pancreatic adenocarcinoma. 749 64

A total of 124 specimens of prostate tissue (25 normal prostate, 41 benign prostatic hyperplasia, 58 adenocarcinoma) was immunostained for ras p21 using a commercially available monoclonal antibody directed against a peptide sequence conserved among all members of the ras gene family. Of normal prostate specimens, 76% showed no staining while the remainder showed only weak epithelial (glandular) staining. No significant stromal staining was noted in any normal prostate specimen. In contrast most benign prostatic hyperplasia specimens showed abundant staining. Epithelial staining was observed in 88% and stromal staining in 73% of specimens. A majority of prostate carcinoma specimens also stained, with 62% and 36% showing epithelial and stromal staining, respectively. No association was noted between staining and either tumor grade or clinical stage. These data argue against any clinical usefulness of immunostaining for ras p21 in the diagnosis or grading of prostate cancer.
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PMID:Immunohistochemical staining of ras p21: staining in benign and malignant prostate tissue. 752 5

In the present study we used monoclonal antibodies to investigate the expression of phosphotyrosine, c-myc and c-Ha-ras proteins along the crypt continuum of normal and transformed rat colon tissue. Colon cancer was induced by administration of dimethylhydrazine. Particular attention was focused on the immunohistochemical pattern of murine colon mucosa during preneoplastic stages so as to permit the identification of putative changes in the expression/location of the oncoproteins prior to frank neoplasia. The immunohistochemical analysis of tyrosinephosphorylated proteins in the normal rat indicated that positive staining was mostly restricted to the lower colonic crypt zones. The carcinogenetic insult altered the magnitude and positional profile of phosphotyrosine along the colon crypt axis during the preneoplastic period. An intense positive reaction was observed in the upper crypt regions. Four weeks following the last DHM administration, viz. before tumor appearance, positive staining was evident in invasive adenocarcinoma tissue. In contrast to phosphotyrosine, the feeble c-myc immunohistochemical staining of normal rat colonic did not exhibit a focal topology. However, following DMH administration and prior to frank neoplasia, a substantial increase in the staining intensity for c-myc was noted, confined mostly to the supranuclear region of luminal cells. Invasive adenocarcinomas displayed intense cytoplasmic c-myc immunoreactivity. p21 c-Ha-ras expression and location along the colon crypt axis showed a different pattern when compared to p62 c-myc and phosphotyrosine. The p21 c-Ha-ras protein was prominently expressed in surface epithelium of normal and DMH-treated rats. Midcrypt colonocytes exhibited moderate p21 ras staining; in contrast, proliferating colonic cells resident in the lower crypt regions were consistently negative. These results suggest that c-Ha-ras gene product plays an important contributory role in determining the differentiated phenotype of the colonic cell.
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PMID:Phosphotyrosine, p62 c-myc and p21 c-Ha-ras proteins in colonic epithelium of normal and dimethylhydrazine-treated rats: an immunohistochemical analysis. 753 85

The observation that the proteins encoded by ras genes play a central role in the signalling pathways used by cells to respond to growth factors and the fact that mutated ras proteins are constantly promoting cell division have led to a PCR-based hunt for additional clinical information. In the present study, K-ras analysis draws the following conclusions: (1) K-ras point mutation frequency was higher in the surgery group (10 of 24 patients) than in the chemotherapy-surgery group (3 of 20 patients). (2) Mutated K-ras was predominantly observed at codon 12 but five mutations appeared at codon 61. (3) Mutations were identified in the squamous cell carcinoma histological NSCLC subtype except in four cases corresponding to adenocarcinoma. (4) A multifarious pattern of substitutions, especially at codon 12, were noted with aspartic K 12 substitutions more prone to develop bone metastases. (5) Although a genotypic K-ras classification of NSCLC may not yet be formulated, our accumulated data (unpublished) suggest a trend toward it. (6) Patients with mutated K-ras tumors in the surgery group had no different survival than those with normal K-ras. However our pooled data as well as other authors' results assert that mutated K-ras constitute an additional prognostic datum that deserves to be included together with TNM classification. In the design of new preoperative (neoadjuvant) chemotherapy trials, stratification of tumors by K-ras status deserves to be further investigated in order to correlate with response, relapse and survival. Mutated K-ras genotype merits further research. Finally, the paradigm of uneven histological distribution and mutated K-ras spectra among researchers should serve as a stimulus to search for further contributions in this field.
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PMID:Mutated K-ras gene analysis in a randomized trial of preoperative chemotherapy plus surgery versus surgery in stage IIIA non-small cell lung cancer. 755 35

With the aim of detecting the timing of p53 and Ki-ras gene alterations in the gastric adenoma-carcinoma sequence, 19 early gastric adenocarcinomas arising from adenomas were studied. Immunohistochemically, 5 adenocarcinomas were positive for p53; 3 focally and 2 diffusely. The p53 point mutations were detected in a focal area with p53 immunoreactivity in 2 of the 5 p53-positive adenocarcinomas. This indicated that p53 point mutations may play a less crucial part in malignant conversion of adenoma to adenocarcinoma in the stomach than in the colon. No Ki-ras gene mutations at codons 12 and 13 were detected in any lesion. These results suggest that the adenoma-carcinoma sequence in the stomach has a different mechanism from that in the colon.
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PMID:Gastric adenoma-carcinoma sequence with special reference to p53 and Ki-ras gene alterations. 758 40


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