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

Circulating carcinoembryonic antigen (CEA) and alpha fetoprotein (AFP) levels were measured by radioimmunoassay in 53 patients with carcinoma of the ovary, 16 patients with other malignant genital tumors, and 31 women with nonmalignant diseases of the genital tract. The serum CEA concentration was elevated (greater than 5 ng/ml) in 11 patients with ovarian cancer, 2 patients with endometrial cancer, 1 patient with carcinoma of the cervix, and 1 patient with a benign embryonal cystic teratoma. Elevated CEA levels were found only in patients with advanced malignant disease, while early stages were associated with normal CEA concentrations. AFP levels were normal in all but 1 patient. Both CEA and AFP levels were markedly raised in a case of advanced genital carcinoma arising probably from the ovary. Ascitic fluid of another patient with ovarian cancer contained a high concentration of CEA, giving an identical reaction in immunodiffusion with CEA from colon cancer. The present results indicate that while the increased expression of carcinofetal components takes place in some malignant tumors of the female genital tract, it is usually a late phenomenon.
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PMID:Carcinoembryonic antigen and alpha fetoprotein in malignant tumors of the female genital tract. 4 62

This study was designed to answer the question, do molecules with carcinoembryonic antigen (CEA) activity from colon, breast, and ovarian cancer differ? Extracts of two breast and three ovarian cancers with CEA activity were compared to three colon cancer CEA preparations and to the related antigen, colon carcinoma antigen-III, in terms of lectin- and antiserum-binding properties. With the use of Farr-type radioimmunoassays with the lectins, concanavalin A and wheat germ agglutinin, the iodinated colon CEA and CEA-like preparations from breast and ovarian cancer all showed distinctly different patterns of binding. Specificity of binding was confirmed by inhibition studies with the relevant monosaccharides. Similarly, with antisera prepared against colon CEA, colon carcinoma antigen-III, or breast CEA, it was shown that, although all preparations shared some antigens, unique antigenic determinants were also present on all preparations. These data are consistent with the concept of a series of closely related CEA and CEA-like molecules with distinct characteristics for each tissue source of CEA.
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PMID:Evidence for common and distinct determinants of colon carcinoembryonic antigen, colon carcinoma antigen-III, and molecules with carcinoembryonic antigen activity isolated from breast and ovarian cancer. 6 90

A radioimmunoassay for a plancental glycoprotein, beta1SP1, capable of detecting 2 microgram/l of the glycoprotein in serum was used to measure concentrations of beta1,SP1 in patients with choriocarcinoma, teratoma, colonic cancer, breast cancer, and ovarian cancer. 12 out of 94 (13%) healthy men and health non-pregnant women had detectable serum-beta1SP1 concentrations. Concentrations up to 50 000 microgram/l were found in the sera of patients with hydatidiform mole, invasive mole, choriocarcinoma, and malignant teratoma. beta1-glycoprotein concentrations were generally much lower than corresponding concentrations of chorionic gonadotrophin which is the most reliable marker for trophoblastic tumours. In a few cases, however, beta1-glycoprotein measurements may be useful in the detection of minimal residual tumour. The slightly raised values found in some patients with carcinoma of the colon, breast, or ovary seem unlikely to be useful for diagnostic purposes of for monitoring the course of these cancers.
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PMID:Serum-SP1-pregnancy-specific-beta-glycoprotein in choriocarcinoma and other neoplastic disease. 7 23

A clinical trial of the oral form of VP 16-213 (NSC-141540), a semisynthetic podophyllotoxin, was undertaken. In 20 patients, treatment was started at 200 mg/day p.o. for 5 days; courses were repeated after a rest period of 16 days. Five patients were treated at the same dose, repeated with only 9-day rest periods. Subsequently, 65 patients were given 300-400 mg/day for 5 days, with rest periods of 9 days between courses. The side effects encountered included anorexia, nausea and vomiting, stomatitis, diarrhea, leukopenia, thrombocytopenia, alopecia, and pruritus. Substernal discomfort with or without palpitations was reported by 18 patients; no explanation for this symptom could be found. No complete remissions (CR) were observed. Parital remissions (PR) and improvement (IMP) were seen as follows: small cell carcinoma, lung (10 patients)--2 PR, 3 IMP; adenocarcinoma, lung (4 patients)--1 PR; alveolar cell carcinoma, lung (1 patient)--1 IMP; mesothelioma (4 patients)--1 IMP; ovarian cancer (12 patients)--3 PR, 3 IMP; breast cancer (20 patients)--4 IMP; colon cancer (8 patients)--2 IMP; bladder cancer (4 patients)--2 IMP; histiocytic lymphoma (7 patients)--2 PR, 3 IMP; chronic myeloid leukemia (1 patient)--1 IMP.
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PMID:A clinical trial of the oral form of 4'-demethyl-epipodophyllotoxin-beta-D ethylidene glucoside (NSC 141540) VP 16-213. 16 75

Follow-up surveys of patients with ovarian cancer revealed an increased risk of second primary cancers of the uterine corpus, colon, bladder, breast, and hematopoietic system. The excess risk or uterine corpus cancer was independent of therapy. The risk of colon cancer was increased in all treatment groups but was especially high among patients receiving radiation or chemotherapy. The predisposition to other neoplasms was limited to certain treatment groups: bladder cancer to irradiation, leukemia to chemotherapy, and lymphoma to either modality. The pattern of second neoplasms following ovarian cancer appears to be influenced by therapy as well as by common etiologic factors.
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PMID:Second primary neoplasms following ovarian cancer. 28 Jul 6

Human peripheral-blood mononuclear cells, separated by Isopaque-Ficoll flotation and E-rosette formation, were tested by the fluorescein fluorescence polarization method of Cercek & Cercek (the SCM test). The response to stimulation with PHA or cancer tissue leads to a decreased polarization value TP). The responding cells were present in the T-cell fraction (E-rosette-forming cells), which contained less than 10% macrophages and less than 1% cells with surface-bound Ig. Control experiments with the non-T-cell fraction gave different response patterns. The response of T cells from apparently healthy donors and patients with and without cancer were compared. All of the group of 16 healthy persons had a polarization value (P) which decreased (mean +/- s.e. = 23% +/- 2) after PHA stimulation, compared with no or little decrease after stimulation with cancer tissue, giving cancer indices (P cancer/PPHA) of 1.15--1.56. In 13 patients with carcinoma of the colon, stimulation with PHA produced little decrease of polarization, while stimulation with colonic cancer tissue decreased the polarization in all cases (mean +/- s.e. = 25% +/- 2). The corresponding cancer indices were 0.61--0.86. Seven of 10 colonic-cancer patients tested against ovarian cancer tissue did not respond, whilst 3 patients in this group responded and had a cancer index less than 1.0. Three patients with non-malignant diseases had response patterns similar to those of healthy persons, except for the lack of PHA response in the patient with ulcerative colitis. This method seems to open up new possibilities for evaluation of cancer patients, although further studies including many more patients are needed before any conclusion can be drawn as to the validity of the test.
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PMID:Response of T lymphocytes to phytohaemagglutinin (PHA) and to cancer-tissue-associated antigens, measured by the intracellular fluorescence polarization technique (SCM test). 38 60

Lipotropin (LPH) has been evaluated as a potential tumor marker using a sensitive beta melanocyte-stimulating hormone (beta MSH) radioimmunoassay. All 79 acetic acid extracts of carcinomas of lung, colon, stomach, esophagus and breast contained LPH in concentrations greater than blood; 61 of 79 extracts contained LPH in larger amounts than control tissues from patients without cancer. In a blind prospective study, plasma LPH was quantified in 107 patients admitted for work-up because of an abnormality on a chest roentgenogram. Thirty-one of 33 patients subsequently diagnosed as having benign lesions had plasma LPH within the 95 per cent confidence limits of normal subjects whereas 28 (36 per cent) of the 74 patients subsequently diagnosed histologically as having primary lung carcinoma had elevated levels. In control studies, 13 of 100 patients with chronic obstructive pulmonary disease had elevated plasma LPH levels; three of the 13 with elevated levels and four with normal levels have been diagnosed, during the two years of follow-up, as having lung carcinoma. In control studies of 23 patients with granulomatous lung disease, 22 had normal levels of LPH. In those with carcinoma of the colon elevated plasma LPH levels were observed in two of 21 untreated patients and in 11 of 61 patients receiving noncurative chemotherapy. Elevated plasma LPH levels were also observed in 10 of 59 patients with breast cancer, eight of 28 with pancreatic cancer, eight of 22 with gastric or esophageal cancer, six of 16 with renal cancer, four of eight with prostatic cancer, one of seven with cervical cancer and one of six with ovarian cancer. We conclude, an elevated LPH level is frequently observed in blood and tumor tissue from patients with various types of carcinoma.
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PMID:Ectopic production of lipotropin by cancer. 43 67

To seek explanations for the geographic variation of breast cancer across the continental United States, we calculated the correlations between mortality rates for premenopausal and postmenopausal women and demographic data for the 3,056 U.S. counties. The northern predominance of this tumor was primarily among postmenopausal women, whereas mortality among premenopausal women was distributed almost uniformly across the country. Socioeconomic status (particularly income), German ethnicity, and colon cancer mortality were strong indicators of the rates for postmenopausal women, but only partly explained the northern excess and latitudinal gradient. In contrast, fertility patterns and ovarian cancer mortality were more closely linked to breast cancer among premenopausal women. The geographic peculiarities of this tumor in older women suggest extrinsic risk factors that remain to be identified, whereas the patterns for younger women point to the primary role of reproductive and genetic determinants.
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PMID:Geographic patterns of breast cancer in the United States. 90

Peritoneal effusion recurrence is one of the most important problem in the palliative management of patients with gastrointestinal malignancies and ovarian cancer. Ten patients with recurrent malignant ascites (three with ovarian cancer, two with pancreas cancer, two with gastric adenocarcinoma and one affected by colon cancer, one patient with peritoneal carcinomatosis, one subject with pleural mesothelioma surgically treated that after three years showed a peritoneal metastases and ascites), were treated with intraperitoneal beta interferon. In all patients a Tenckoff's catheter for peritoneal dialysis was introduced and peritoneal effusion extracted and measured. Three millions of beta interferon in saline solution was infused in peritoneal cavity every three days for nine days. Successively twenty millions every three days for nine days. In the 50% of patients a significant reduction of peritoneal effusion was observed. The locoregional therapy with beta interferon is proposed in palliative management of malignant ascites.
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PMID:[The locoregional treatment of neoplastic ascites with interferon-beta]. 150 25

Tumorigenesis is a multistep process involving mutations of dominantly acting proto-oncogenes and mutations and loss-of-function mutations of tumor suppressor genes. Some of these mutations may be inherited, but most of them are acquired. Models for the sequential steps of the genetic changes involved in tumor development have been proposed for certain cancers, such as colon cancer. In the case of ovarian cancer, relatively little is known about the genetic events associated with the initiation or subsequent progression and metastases of the tumor. Cytogenetic analysis has revealed a high incidence of both structural and numerical chromosome changes, and the extent of these changes seems to increase with tumor progression. Oncogene activations of the proto-oncogenes K-ras, c-myc and c-erbB-2 have been found more frequently in aggressive ovarian tumors and may be associated with poor survival. Tumor-specific allele loss involving putative tumor suppressor genes has been observed for loci at chromosomes 11p, 17p, and 17q,--loci commonly deleted in other cancers too. A relatively high incidence of allelic loss on chromosome 6q appears to be specific to ovarian carcinoma. Familial breast/ovarian cancer has been suggested to map to chromosome 8q. Recently we have found a germ-line mutation in the tumor suppressor gene p53 in a family with breast- and ovarian cancers, indicating that this is the predisposing gene in this family. Genetic changes important for the etiology of ovarian cancers seem to involve both somatic mutations of oncogenes and somatic or germ-line inactivation of tumor suppressor genes.
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PMID:Oncogenesis in ovarian cancer. 150 89


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