PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “RECTAL NEOPLASMS”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 415 records · Page 23Linked to original sources
PubMed1988

Hepatic metastases from colorectal cancer: resection or not.

This review evaluates the available evidence dealing with the natural history of hepatic metastases in patients with colorectal cancer. Methods of detection of such metastases are discussed and the factors influencing survival after surgical resection are reviewed.

Colonic Neoplasms↗
PubMed1988

Growth rate of hepatic metastases in colorectal carcinoma.

The rates of growth of 29 hepatic metastases from 15 patients with primary colorectal carcinoma were studied using serial computed tomography (CT). Eleven metastases were found by the surgeon at laparotomy (overt metastases); the remaining eighteen were not evident to the surgeon at laparotomy, but were detected by CT scan during the immediate postoperative period (occult metastases). An estimate of tumour volume doubling time was obtained from a semi-logarithmic plot of tumour cell number against time. The mean doubling time for the overt metastases was 155 +/- 34 days (+/- s.e.m.) compared with 86 +/- 12 days (P less than 0.05) for the occult metastases. The age of the metastases at the time of surgery was estimated by extrapolation of the observed growth curve assuming Gompertzian kinetics. The mean age of the overt metastases was 3.7 +/- 0.9 years (+/- s.e.m.) The corresponding age of the occult metastases was 2.3 +/- 0.4 years.

Cell Division↗
PubMed1977

A modified leukocyte adherence inhibition test in the laboratory investigation of gastrointestinal cancer.

A modification of the leukocyte adherence inhibition (LAI) technique has been used to test 60 hospital patients with gastrointestinal symptoms, for specific immunoreactivity against extracts of tumours of colon, pancreas and stomach. The modified technique employed mononuclear cells and soluble tumour extracts in glass test tubes, the non-adherent cells being enumerated in an electronic counter. Laboratory tests were completed before the eventual diagnosis was known. Groups of patients with adenocarcinoma of colon or rectum (11), carcinoma of pancreas (3) and adenocarcinoma of stomach (6) were clearly distinguished from each other and from patients with non-malignant diseases or with neoplasms of different histological type.

Adenocarcinoma↗
PubMed1978

Isolation of a sulfated glycopeptidic antigen from human gastric tumors: its localization in normal and cancerous gastrointestinal tissues.

A sulfated glycopeptidic antigen (SGA) was purified from papain-digested cancerous human gastric mucosa. The amino acid composition of this antigen was characterized by a high percentage of threonine and proline. Serine was present in small quantities and aromatic amino acids were absent. The amount of sulfate present was evaluated at 7.5%. Fucose, galactose, N-acetyl glucosamine, N-acetyl galactosamine and sialic acid were found to be present in the molar ratio 1:4.6:3.0:6.2:5.0. With immunofluorescence techniques, a rabbit antiserum against the sulfated glycopeptide stained adult gastric mucosa when this tissue had intestinal metaplasia and stained the goblet cells of the intestinal tract (small and large intestines). About 50% of colonic carcinomas and some gastric carcinomas contained SGA. This sulfated antigen was present in well-differentiated tumors and there was a good correlation between tumoral acid mucous secretory activity and the SGA positivity.

Amino Acids↗
PubMed1980

Patterns of gastro-intestinal cancer in European migrants to Australia: the role of dietary change.

Cancers of the stomach, pancreas, colon and rectum are increasingly regarded as being diet-influenced. Migrants to Australia from England, Scotland, Ireland, Poland, Yugoslavia, Greece, and Italy have come from countries with varied dietary backgrounds and gastrointestinal cancer risks. Age-standardized cancer death rates in migrrants, by country of origin, sex, age, and duration of residence in Australia (less than or equal to 16 years and greater than 16 years), have been calculated for 1962-76, and compared with those of the Australian-born population. All seven migrant source countries, in 1970, had higher rates of stomach cancer than Australia, and the corresponding migrants groups, which initially reflected those higher rates, experienced an approximately 25% risk reduction with increased duration of residence. For cancer of the pancreas, migrants initially had rates well above their "native" rates; with longer stay, the risks generally converged upon that of the Australian-born population. The four "continental" (European) migrant groups, whose native risk of colon cancer is about half that of the Australian population, showed an increased risk with increasing duration of stay. The increase was greater in men than in women, perhaps reflecting their greater dietary acculturation. By contrast, Scottish migrants, with an initially high risk of cigrants showed even larger increases than colon cancer, while in British migrants there was a marked decline towards the "Australian-borne" risk. These various changes in cancer risk are discussed with reference to inter-country dietary differences.

Adolescent↗
PubMed1983

Endotoxin-induced in vitro release of interleukin-1 by cancer patients' monocytes: relation to stage of disease.

The in vitro release of IL-1 by monocytes in response to endotoxin was subnormal in many patients with breast cancer, malignant melanoma or colorectal cancer but not in patients with benign tumors of the breast or colon. In each of these groups, IL-1 release was low in patients with early cancer, normal in patients with regional metastases, and low in patients with disseminated cancer.

Adult↗
PubMed1986

Imbalance of sex chromosomes, with gain of early-replicating X, in human solid tumors.

An imbalance of sex chromosomes was observed in several cases of solid tumors: colorectal, anal canal and breast carcinomas. Replication studies, using BUdR incorporation, show that in males there is a tendency towards a gain of early-replicating X and a deficiency of Y chromosomes. In females, there is a tendency towards a gain of early-replicating X and a loss of late-replicating X chromosomes. Although almost no replication studies have been published in the literature, making it impossible to distinguish between late- and early-replicating Xs, it is likely that a similar situation exists for several solid tumors other than those we have studied. A possible consequence of this imbalance is briefly discussed.

Anus Neoplasms↗
PubMed1989

Time trends in cancer mortality in the Federal Republic of Germany: progress against cancer?

In accordance with a previous analysis of US cancer mortality, this report also indicates that cancer mortality in the FRG over the last 3 decades (1952-1985) has not shown any decline commencing in a given period and prevailing in all age groups. If present, such effects could have been interpreted as a manifestation of improvements associated with cancer treatment. The absence of such an effect, derived by using data up to 1985 and age-specific mortality rates, supports the view expressed in the US analysis that improvements in cancer treatment are unlikely to have an impact on overall cancer mortality statistics and that efforts toward prevention may be more rewarding.

Age Factors↗
PubMed1991

Monoclonal antibodies to glutathione S-transferase pi-immunohistochemical analysis of human tissues and cancers.

Mouse monoclonal antibodies (MAb) have been generated against the anionic isozyme of human glutathione S-transferase (GST pi). MAb AGST I can inhibit 50-70% of GST pi enzymatic activity and reacts with a 3-dimensional epitope which includes a putative glutathione binding site on GST pi. A sandwich enzyme-immunoassay established using MAb AGST I and a polyclonal antibody displayed a sensitivity of 0.5 ng/ml. Immunohistochemical analysis of human tissues demonstrated marked increases in GST pi levels in cancers of the brain, cervix, endometrium, colon, rectum and testis and in fibro- and chondrosarcomas.

Antibodies, Monoclonal↗
PubMed1994

Haemopoietic progenitor and myeloid cell kinetics in humans treated with interleukin-3 and granulocyte/macrophage colony-stimulating factor in combination.

Patients with advanced adenocarcinoma of the colon, rectum or pancreas were entered into trials for evaluation of treatment with sequential doses of IL-3 and GM-CSF. They received 0.25 to 5 micrograms IL-3/kg/d for up to 7 days, followed by 1 microgram GM-CSF/kg/day for a maximum of 10 further days. We assessed the kinetics of bone-marrow cell proliferation and of blood production using tritiated thymidine labelling in vitro and in vivo. Megakaryocytic-CFC were unaffected but proliferation rates of GM-CFC and BFU-E were increased. Progenitor cells were mobilized (12-fold over baseline) into the peripheral blood. The proliferative activity of maturing cells in the marrow was increased (cell-cycle times were reduced by at least 30%). This translated into amplified blood cell production (WCC approximately 30 x 10(9)/l), a 2.2-fold increase in platelet counts and significant eosinophilia. Newly generated neutrophils appeared in the circulation at the normal time and their peripheral half-life was also normal. The calculated 3.2-fold amplification in neutrophil production required nearly 2 extra divisions in the marrow, shared between the progenitors and the proliferating granulocytic cells. The results were compared with those of a previous trial using GM-CSF only, although at a 10-fold higher dose level. Comparable levels of peripheral neutrophils were obtained in both trials but significant ineffective granulopoiesis developed in the earlier study. This was overcome in the present study, the priming dose of IL-3 apparently giving the latitude to utilize lower doses of GM-CSF with less risk of complications.

Adenocarcinoma↗