PubMed HealthSearch

PubMed · 205963

Circulating immune complexes in patients following clinically curative resection of colorectal cancer.

Abstract

Sixty-nine patients have been followed prospectively after curative resection of Dukes-Kirklin B-2 or C colorectal cancer. Serial plasma samples were studied in selected patients to determine changes in circulating immune complex concentrations (CIC) following primary tumor resection, and to compare serial plasma CIC and carcinoembryonic antigen (CEA) levels. CIC was determined in an average of seven serial samples per patient by inhibition of antibody-dependent cell-mediated cytotoxicity (ADCC). CEA assays were performed by the Hanson Z-gel method. Two distinct patterns of serial CIC have emerged. In seven patients with no known tumor recurrences, serial CEA levels and CIC oscillated regularly and were inversely related. In seven of eight patients whose tumors recurred, both CEA and CIC rose together. In three patients with elevated plasma CEA levels due to inflammatory bowel disease, serial Ag-Ab complex concentrations did not vary, nor did separated Ag or Ab fractions inhibit ADCC. These data suggest that, in patients following curative resection of colorectal cancer, serial changes in circulating immune complexes may discriminate between transient CEA elevations which occur despite no known tumor recurrence and tumor recurrence which is beyond the capacity of adequate host antitumor defense.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

G Steele, S Sonis, P Stelos, R Rittgers, N Zamcheck, D Finn, J Maltz, R Mayer, J Lokich, R E Wilson. 1978. Circulating immune complexes in patients following clinically curative resection of colorectal cancer.. https://pubmed.ncbi.nlm.nih.gov/205963/

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

Interaction of Galpha 12 and Galpha 13 with the cytoplasmic domain of cadherin provides a mechanism for beta -catenin release.

The G12 subfamily of heterotrimeric G proteins, comprised of the alpha-subunits Galpha12 and Galpha13, has been implicated as a signaling component in cellular processes ranging from cytoskeletal changes to cell growth and oncogenesis. In an attempt to elucidate specific roles of this subfamily in cell regulation, we sought to identify molecular targets of Galpha12. Here we show a specific interaction between the G12 subfamily and the cytoplasmic tails of several members of the cadherin family of cell-surface adhesion proteins. Galpha12 or Galpha13 binding causes dissociation of the transcriptional activator beta-catenin from cadherins. Furthermore, in cells lacking the adenomatous polyposis coli protein required for beta-catenin degradation, expression of mutationally activated Galpha12 or Galpha13 causes an increase in beta-catenin-mediated transcriptional activation. These findings provide a potential molecular mechanism for the previously reported cellular transforming ability of the G12 subfamily and reveal a link between heterotrimeric G proteins and cellular processes controlling growth and differentiation.

Adenocarcinoma

Bone metastases from breast cancer treated with calcitonin. Case report.

A case of bone metastases from breast cancer is reported. After 6 months of therapy with calcitonin, the skeletal radiological examination showed an evident change in the roentgenographic pattern of a large metastasis of the left femur. A possible relationship between the calcitonin treatment and the radiological change is discussed.

Adenocarcinoma

A case of hyperthyroidism due to metastasis of a thyroid carcinoma.

A case of hyperthyroidism, which developed in a patient affected by thyroid carcinoma a few days after thyroidectomy, is described. The symptomatology was caused by a bone metastasis at the left ischiopubic branch, which had a high iodine-uptake capacity and was sensitive to metabolic radiotherapy. Pulmonary metastases were also present; they had a distinct low affinity for iodine and showed no response to repeated administrations of 131I. The case is evaluated on the basis of the evolution of the clinical picture and the hormone dosages administered in a follow-up period of 3 years.

Adenocarcinoma