Defective recognitive immunity in family aggregates of colon carcinoma.

Cancer-free individuals from family agregates of seemingly hereditary colon carcinoma were studied to determine the nature of their cell-mediated immune capacities in miexed leukocyte culture. Members of families who demonstrated no evidence of a precancerous condition such as polyposis coli did demonstrate substantial cellular immunopathology. Of these, 44% showed a decreased responsiveness of their peripheral mononuclear cells to allogeneic stimuli, and in a number of these individuals this deficiency clearly manifested itself as an inappropriate suppression of potentially normal lymphocyte blastogenic capacities by an adherent population of mononuclear leukocytes. This in vitro defect of recognitive immunity appears to be the same type of defect that has already been described for individuals with established maligancies. The pattern of phenotypic expression of this immunopathology within these families is not inconsistent with an hereditary disorder. Individuals from families with a known hereditary somatic precancerous condition usually did not demonstrate this immunopathology. It is appropriate to speculate that the defect of recognitive immunity in the former families could be contributory to the genesis of the colon carcinoma.

[1]  E. Thorsby,et al.  Identification of five lymphocyte activating determinants in man. , 2008, Tissue antigens.

[2]  Good Ra,et al.  Concomitant immunopathology with squamous cell carcinomas of the head and neck regions. , 1976 .

[3]  R. Good,et al.  Facilitation or attenuation of mixed leukocyte culture responsiveness by adherent cells , 1976, Nature.

[4]  C. Nathan,et al.  Isolation of a subpopulation of adherent peritoneal cells with anti-tumour activity , 1976, Nature.

[5]  C. Nathan,et al.  Differential stimulation of murine lymphoma growth in vitro by normal and BCG-activated macrophages , 1975, The Journal of experimental medicine.

[6]  W. Blattner,et al.  Varied manifestations of a familial lymphoproliferative disorder. , 1975, The American journal of medicine.

[7]  E. Unanue,et al.  Two biological activities regulating cell proliferation found in cultures of peritoneal exudate cells , 1975, Nature.

[8]  H. Lynch Familial cancer prevalence spanning eight years. Family N. , 1974, Archives of internal medicine.

[9]  F. Bach Normal histocompatibility antigens as a model for tumors. , 1974, American journal of clinical pathology.

[10]  I. Ly,et al.  Separation of mouse spleen cells by passage through columns of sephadex G-10. , 1974, Journal of immunological methods.

[11]  W. Catalona,et al.  Cellular immunity in cured cancer patients , 1974 .

[12]  J. Fraumeni,et al.  Familial gastric cancer and immunologic abnormalities , 1973, Cancer.

[13]  J. Kersey,et al.  Primary immunodeficiency diseases and cancer: The immunodeficiency‐cancer registry , 1973, International journal of cancer.

[14]  Z. Bentwich,et al.  Human lymphocyte-sheep erythrocyte rosette formation: some characteristics of the interaction. , 1973, Clinical immunology and immunopathology.

[15]  J. Twomey,et al.  An adaptation of the mixed leukocyte culture test for use in evaluating lymphocyte and macrophage function. , 1972, Journal of Immunology.

[16]  H. Takita,et al.  Impaired lymphocyte response to allogeneic cultured lymphoid cells in patients with lung cancer. , 1972, The New England journal of medicine.

[17]  H. Lynch,et al.  Cancer family “G” revisited: 1895‐1970 , 1971, Cancer.

[18]  M. Swift Fanconi's Anaemia in the Genetics of Neoplasia , 1971, Nature.

[19]  A. Knudson Mutation and cancer: statistical study of retinoblastoma. , 1971, Proceedings of the National Academy of Sciences of the United States of America.

[20]  A. Laughter,et al.  Cellular requirements for the mitotic response in allogeneic mixed leukocyte cultures. , 1970, Journal of immunology.

[21]  V. McKusick,et al.  Gardner's syndrome: Formal genetics and statistical analysis of a large Canadian kindred , 1970 .

[22]  J. Fraumeni,et al.  Familial chronic lymphocytic leukemia. , 1969, Annals of internal medicine.

[23]  J. Cleaver,et al.  Xeroderma pigmentosum: a human disease in which an initial stage of DNA repair is defective. , 1969, Proceedings of the National Academy of Sciences of the United States of America.

[24]  W. B. Taylor,et al.  The Nevoid Basal Cell Carcinoma Syndrome: Autopsy Findings , 1968 .

[25]  S. Soukup,et al.  Bloom's syndrome. , 1968, American journal of diseases of children.

[26]  H. Lynch,et al.  Heredity and adenocarcinoma of the colon. , 1967, Gastroenterology.

[27]  P. Peltokallio,et al.  Relationship of familial factors to carcinoma of the colon , 1966, Diseases of the colon and rectum.

[28]  V. McKusick Genetic factors in intestinal polyposis. , 1962, JAMA.

[29]  J. Despres,et al.  Malignant tumors of the central nervous system associated with familial polyposis of the colon , 1959 .

[30]  D. Savage A FAMILY HISTORY OF UTERINE AND GASTRO‐INTESTINAL CANCER , 1957, British medical journal.

[31]  G. Deshors,et al.  Bloom's syndrome. , 1995, Dermatologic clinics.

[32]  T. Waldmann,et al.  Immunodeficiency in the Wiskott-Aldrich syndrome. , 1975, Birth defects original article series.

[33]  B. Dupont,et al.  Lymphocyte transformation in vitro in patients with immunodeficiency diseases: use in diagnosis, histocompatibility testing and monitoring treatment. , 1975, Birth defects original article series.

[34]  D. Rosenstreich,et al.  THE MECHANISM OF ACTION OF MACROPHAGES IN THE ACTIVATION OF T-LYMPHOCYTES IN VITRO BY ANTIGENS AND MITOGENS , 1975 .

[35]  C. Heath,et al.  Lymphoreticular malignancies and immunologic abnormalities in a sibship. , 1971, The American journal of medicine.

[36]  H. Kunkel,et al.  Lymphocytes in human immunodeficiency states: a study of membrane‐associated immunoglobulins , 1971, European journal of immunology.