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Query: UMLS:C0699790 (colon cancer)
 28,837 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The prevalence, rate of correct clinical diagnosis and mortality of cancer were analyzed in 4,894 consecutive autopsies at the Tokyo Metropolitan Geriatric Hospital from 1972 to 1990. average age and standard deviation of patients was 78.1 +/- 9.1 years. Cancer was found in 45.5% of patients of 60 years and over, and in 49.1% in men and 41.9% in women (p < 0.001). Cancer prevalence decreased with advance in age; 50.0% in the sixties, 47.9% in the seventies, 43.2% in the eighties and 39.3% in the nineties and over. Multiple cancer was found in approximately 12% of patients of 70 years and over. The top three cancer incidences were gastric cancer, 15.0%, lung cancer, 10.7% and colon cancer, 5.9% in both genders. In men, prostate cancer was next common, followed in orderly hepatic cancer, esophageal cancer, gall bladder-bile duct cancer, pancreas cancer, renal cancer and urinary bladder cancer. In women, the following order of frequency was gall bladder-bile duct cancer, uterus cancer, pancreas cancer, hepatic cancer, breast cancer, thyroid cancer, esophageal cancer, renal cancer and urinary bladder cancer. The prevalence of gastric cancer, lung cancer, hepatic cancer and esophageal cancer was significantly higher in men, while that of gall bladder-bile duct cancer was higher in women. The age-related tendencies varied among cancers of different organs. Gastric cancer increased up to the sixties in men and up to the seventies in women and leveled off after those ages. Lung cancer revealed peak prevalence in the sixties and seventies and decreased after the age of eighty.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Prevalence, rate of correct clinical diagnosis and mortality of cancer in 4,894 elderly autopsy cases]. 847 26

Using data from a case-control study in the United States (the Selected Cancers Study), we examined the relationship between non-Hodgkin's lymphoma (NHL) and family history of different cancers. Cases were 1,511 men aged 31 to 59 years and diagnosed pathologically with non-Hodgkin's lymphoma during 1984-88. Controls were men, frequency-matched to cases by age range and cancer registry (n = 1,910). All study subjects with acquired immunodeficiency syndrome were excluded from analyses. Our results showed that the risk of NHL is associated with a history of lymphoma (odds ratio [OR] = 3.0, 95 percent confidence interval [CI] = 1.7-5.2) and hematologic cancer (OR = 2.0, CI = 1.2-3.4) in first-degree relatives after adjustment for age, ethnic background, and educational level. Further analyses were performed for the subgroups defined by age at diagnosis (younger than 45 years cf 45 years or older). The association of NHL with a family history of lymphoma and hematologic cancer was found primarily among men aged 45 and older (OR = 4.1, CI = 1.9-8.8 for lymphoma and OR = 2.3, CI = 1.3-4.0 for hematologic cancer). The association among men aged 45 and older did not vary by whether or not there were any familial patients diagnosed at the age of 45 or older. No significant associations could be found for a family history of lung cancer, breast cancer, prostate cancer, colon cancer, skin cancer, liver cancer, stomach cancer, brain cancer, thyroid cancer, or myeloma. This study suggests that the familial risk of NHL is influenced primarily by hematolymphoproliferative malignancies rather than other cancers. The familial effects of hematolymphoproliferative malignancies may be stronger for men aged 45 to 59, compared with those aged 31 to 44.
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PMID:Non-Hodgkin's lymphoma and family history of malignant tumors in a case-control study (United States). 948 66

We have been investigating the mathematical nature of intercancer linkage that underlies the mutual regulation of cancer risks between any 2 tumors in their variations in time and space. Applications of both sequential regression test and topological manipulation of age-adjusted incidence rate (AAIR) data set enabled us to prepare the oncogene (Onc) activation profile and the tumor suppressor gene (TSG) inactivation profile for each tumor. The purpose of this study was to investigate the relation between the changes of 2 cancer gene profiles and the sex discrimination of cancer risk in 7 human neoplasias. Results obtained are as follows: i) The sex discrimination of cancer risk could better be defined by the use of log-transformed AAIR data rather than of untransformed AAIR data. ii) The sex discrimination of cancer risk, as calculated with the AAIR data of 47 population units of the world, is as follows: a) breast cancer (Br), M:F=1:120.2; b) thyroid cancer (Thy), M:F=1:2. 64; c) colon cancer (Co), M:F=1.18:1; d) liver cancer (Li), M:F=2. 63:1; e) lung cancer (Lu), M:F=3.66:1; f) esophageal cancer (Eso), M:F=3.68:1; g) laryngeal cancer (Lar), M:F=7.26:1. iii) Female-dominant cancers were associated with inversion (Br) or defectiveness (Thy) of male oncogene profile, whereas male-dominant cancers were associated with inversion (Lar) or defectiveness (Li, Lu and Eso) of female Onc profiles. Sex-indifferent cancer, Co, was distinguished from other tumors by the emergence of defectiveness in the TSG profiles of both sexes. TSG defectiveness was also detectable in female (Br, Thy) and bisexual (Lu) tumors. iv) The Onc vs TSG interaction, as assessed in terms of r value of the reciprocal regression analysis, was increasing in its positivity rate from the top of the female-dominant family (Br) through the sex-indifferent tumor (Co) to the bottom of the male-dominant family (Lar). In conclusion, the emergence of sex discrimination of cancer risk was positively correlated to the extent of integrity of oncogene activation in the dominant gender relative to the recessive gender. Findings with 6 sex-discriminant tumors are discussed in their relevancy to tumorigenesis from the point of view of endocrinological epidemiology.
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PMID:Relation between the changes of oncogene versus tumor suppressor gene interaction and the transition of cancer risk from female dominance through no sex discrimination to male dominance, as investigated by the reciprocal regression analysis of 5 human neoplasias. 968 28

To determine the role of the Wilms' tumor gene WT1 in tumorigenesis of solid tumors, expression of the WT1 gene was examined in 34 solid tumor cell lines (four gastric cancer cell lines, five colon cancer cell lines, 15 lung cancer cell lines, four breast cancer cell lines, one germ cell tumor cell line, two ovarian cancer cell lines, one uterine cancer cell line, one thyroid cancer cell line, and one hepatocellular carcinoma cell line) by means of quantitative reverse transcriptase-polymerase chain reaction. WT1 gene expression was detected in three of the four gastric cancer cell lines, all of the five colon cancer cell lines, 12 of the 15 lung cancer cell lines, two of the four breast cancer cell lines, the germ cell tumor cell line, the two ovarian cancer cell lines, the uterine cancer cell line, the thyroid cancer cell line, and the hepatocellular carcinoma cell line. Therefore, of the 34 solid tumor cell lines examined, 28 (82%) expressed WT1. Three cell lines expressing WT1 (gastric cancer cell line AZ-521, lung cancer cell line OS3, and ovarian cancer cell line TYK-nu) were further analyzed for mutations and/or deletions in the WT1 gene by means of single-strand conformation polymorphism analysis. However, no mutations or deletions were detected in the region of the WT1 gene ranging from the 3' end of exon 1 to exon 10 (the WT1 gene consists of 10 exons) in these three cell lines. Furthermore, when AZ-521, OS3, and TYK-nu cells were treated with WT1 antisense oligomers, the growth of these cells was significantly inhibited in association with a reduction in WT1 protein levels. Furthermore, constitute expression of the transfected WT1 gene in cancer cells inhibited the antisense effect of WT1 antisense oligomer on cell growth. These results indicated that the WT1 gene plays an essential role in the growth of solid tumors and performs an oncogenic rather than a tumor-suppressor gene function.
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PMID:Expression of the Wilms' tumor gene WT1 in solid tumors and its involvement in tumor cell growth. 1018 90

The occurrence of multiple primary cancers in the aerodigestive tract is a well known phenomenon that has been explained by the concept of 'field carcinogenesis'. Metachronous or synchronous esophageal cancer has usually been identified in patients with head and neck cancer, gastric cancer or colon cancer. The incidence of multiple primary cancers of the esophagus and thyroid gland is very low. We treated four patients with synchronous cancers of the cervical esophagus and the thyroid gland. Histologically, all of the esophageal cancers were squamous cell carcinomas. Thyroid cancers were evaluated as papillary carcinoma or follicular carcinoma. Both the esophageal cancer and the thyroid cancer frequently metastasized to lymph nodes. All patients had multiple lymph nodes metastasis from the esophageal or the thyroid cancer. In one patient, both the esophageal and the thyroid cancers were detected in the same lymph node. Three of four patients died from recurrence of esophageal cancer. The prognosis of these patients was poor. In the treatment of esophageal carcinoma, cancers of other organs including the thyroid gland should be carefully investigated.
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PMID:Multiple primary cancers of the esophagus and thyroid gland. 1047 Jun 60

The N-terminal amino acid sequence of TA02 (molecular weight 35.0 kDa, isoelectric point 5.29), which is associated with primary lung adenocarcinoma, was determined and a fragment peptide was used to generate mouse monoclonal antibodies (mAbs) against TA02. The amino acid sequence suggested that TA02 might be homologous with napsin A, a new type of aspartic proteinase. In this context, we confirmed the expression of napsin A in primary lung adenocarcinoma using reverse-transcription polymerare chain reaction (RT-PCR) and showed that the TA02 mAbs reacted with glutathione-S-transferase (GST)-napsin A fusion protein. We concluded that TA02 is the same molecule as napsin A, and showed immunohistochemically that it is distributed mainly in type II pneumocytes, alveolar macrophages, renal tubules and exocrine glands and ducts in the pancreas. In particular, type II pneumocytes and alveolar macrophages showed high expression of TA02 among human normal tissues. In primary lung adenocarcinoma, 47 out of 58 (81.0%) primary lesions were positive. All well-differentiated adenocarcinomas except those of goblet cell type showed high expression of TA02. In addition, two out of seven (28.6%) large cell carcinomas showed low expression of TA02. The other histopathological types of primary lung cancer did not express TA02 at all. A few cases of renal cell cancer, pancreatic cancer, breast cancer, thyroid cancer, colon cancer and ovarian cancer showed low expression, but the staining patterns were completely different from that of primary lung adenocarcinoma, which showed a granular staining pattern. Our novel mAbs should be valuable for immunochemical detection of TA02/napsin A.
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PMID:Human tissue distribution of TA02, which is homologous with a new type of aspartic proteinase, napsin A. 1105 Apr 72

Background and Purpose: [F-18]FDG has long been used for detection of the malignant tumors and assessment of the metabolic activity of the tumors. However, there are several drawbacks of FDG including hyperglycemic effect, nonspecific uptake on inflammation, sink phenomenon due to high accumulation of FDG in urinary tract, and physiologic uptake of FDG in the bowels and muscles, which may cause false positive as well as false negative results. [C-11]acetate, as a metabolic substrate of beta-oxidation, precursors of amino acid, fatty acid and sterol, has been proved useful in detecting various malignancies. The aim of this study is to assess the feasibility of clinical application of [C-11]acetate in oncology.Methods: High quality whole body images could be obtained by using large dosage (20 mCi) of [C-11]acetate and modern PET scanner. In the recent years, [C-11]acetate PET studies have been performed in 513 patients with various malignancies.Results: The results showed that [C-11]acetate is more accurate in detecting meningioma (accuracy 97%), glioma (91%), nasopharyngeal cancer (93%), lymphoma (85%), non-small cell cancer (81%), colon cancer (78%), renal cell cancer (80%), ovarian cancer (76%), than in detecting small cell cancer of lung, thyroid cancer, and pancreas cancer. The advantages of [C-11]acetate are less time consuming (whole procedure completed within 45 min after injection), no hyperglycemic effect and no sink phenomenon. The disadvantages are increased uptake in salivary glands, pancreas, and sometimes the bowels, which may cause either false positive or false negative results, and on-site-cyclotron dependent.Conclusion: In summary, [C-11]acetate is clinically useful in detecting various malignant tumors clinically and may play a complementary role to FDG.
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PMID:31. Clinical Application of 1115 Jul 88

A single founder allele of the CHEK2 gene has been associated with predisposition to breast and prostate cancer in North America and Europe. The CHEK2 protein participates in the DNA damage response in many cell types and is therefore a good candidate for a multisite cancer susceptibility gene. Three founder alleles are present in Poland. Two of these result in a truncated CHEK2 protein, and the other is a missense substitution of an isoleucine for a threonine. We ascertained the prevalence of each of these alleles in 4,008 cancer cases and 4,000 controls, all from Poland. The majority of the common cancer sites were represented. Positive associations with protein-truncating alleles were seen for cancers of the thyroid (odds ratio [OR] 4.9; P=.0006), breast (OR 2.2; P=.02), and prostate (OR 2.2; P=.04). The missense variant I157T was associated with an increased risk of breast cancer (OR 1.4; P=.02), colon cancer (OR 2.0; P=.001), kidney cancer (OR 2.1; P=.0006), prostate cancer (OR 1.7; P=.002), and thyroid cancer (OR 1.9; P=.04). The range of cancers associated with mutations of the CHEK2 gene may be much greater than previously thought.
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PMID:CHEK2 is a multiorgan cancer susceptibility gene. 1549 28

The cribriform-morular variant (CMV) of papillary thyroid carcinoma (PTC) is a rare histologic subtype of PTC that shows a combination of growth patterns including cribriform and spindle cell areas. The thyroid cancer with this unique histology was originally reported in patients with familial adenomatous polyposis (FAP), although it was later found in patients without polyposis as well. Because of its rarity, its clinical features are not clear. We reviewed seven patients with CMV-PTC who were found among 4194 patients with PTC in our pathology files between June 1991 and March 2003. The prevalence of CMV was 0.16% among all PTCs. We invited these patients to our hospital so we could obtain a detailed family history and recommend colonoscopic examination and germline APC gene analysis. Two patients without subjective symptoms had polyposis of the colon and colon cancers. Germline APC gene mutations were found in both patients. The father of a patient who refused the invitation was revealed to have undergone surgery for colon polyposis. In the remaining four patients, neither polyposis nor APC gene mutation was found. Common clinical features included a young age (mean 25 years), predominance of females, circumscribed tumors, negative node metastasis, and no recurrence of the thyroid cancer after surgery. Two of the three patients with colon polyposis had bilateral multiple thyroid tumors, whereas the remaining four (without polyposis) had a solitary tumor. The histopathology of CMV in patients with PTC should arouse a suspicion of FAP, especially if there are multiple tumors. This finding can lead to early detection of colon cancer.
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PMID:Cribriform-morular variant of papillary thyroid carcinoma: clue to early detection of familial adenomatous polyposis-associated colon cancer. 1559 62

The clinical diagnosis of primary thyroid cancer is uncommon, constituting 1.5% of all cancers in the United States. Clinically diagnosed metastatic cancer to the thyroid gland is rare. Colon cancer is one of the most common cancers in the United States, with a high propensity to metastasize; 30% to 40% of patients have metastatic disease at the initial diagnosis. The most common sites of metastasis from colon cancer are the regional lymph nodes, the liver, the lung, and the peritoneum. Colon cancer metastasis to the thyroid gland is rare, with only a few reported cases, mainly in the pathology literature. These cases describe metastasis from colon cancer to the thyroid gland that became apparent years after the initial diagnosis of colon cancer and were usually associated with dissemination to the liver, the lung, or both. We report a case of colonic adenocarcinoma metastatic to the thyroid gland and lung without involvement of the liver. A review of the literature is also included.
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PMID:Colon cancer metastatic to the lung and the thyroid gland. 1641 18


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