[Cystic dilatation of the common bile duct. Echotomographic findings].
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to F Calvo.
Explore the source record for details and available documents.
A monoclonal antibody (7B10) which displays differential reactivity with breast carcinomas compared to benign lesions or normal breast tissue was selected by fusion of spleen cells from BALB/c mice immunized with the T47D human mammary carcinoma cell line. The antigen, recognized by 7B10 on T47D cells, appeared to be both surface and cytoplasm localized, as demonstrated by indirect immunofluorescence, immunoperoxidase, and electron microscopy studies. This antibody (IgG1) bound with four human breast cancer cell lines (T47D, MCF7, ZR-75-1, and HSL53) which express estrogen receptors. No binding was observed with cancer cell lines of other origin or with normal cells. In vivo, by immunoperoxidase staining of frozen sections of normal breast, the antigen recognized by 7B10 appeared to be located on epithelial cell membranes, whereas in benign and malignant mammary disorders, staining also involved the cytoplasm, as confirmed by electron microscopy on fresh cancer tissue. On formalin-fixed, paraffin-embedded sections, cytoplasmic staining was detected in breast cancer, but no immunostaining was observed with benign lesions or normal breast. In paraffin sections, most normal tissues investigated did not react with 7B10 antibody. However, ducts in the parotid gland, tubules in the kidney and some biliary ducts, and apocrine glands in the skin showed irregular, diffuse weak staining. 7B10 was unreactive with adenocarcinomas of origin other than breast, except for some cells in ovarian clear cell carcinoma. No reactivity was observed with squamous carcinomas, lymphomas, or melanomas. The antigen recognized by 7B10 appeared to be a Mr 32,000 protein, as identified by immunoprecipitation from extracts of T47D after labeling with [35S]methionine. Since the antigen was present only on the membrane of differentiated normal mammary epithelial cells, and was also expressed in the cytoplasm of tumor cells, it may be of interest in immunological studies of mammary epithelial cell differentiation. Moreover, since in formalin-fixed tissues immunostaining is virtually confined to mammary carcinomas, monoclonal antibody 7B10 may have diagnostic applications in breast cancer.
H466-B and T47-D breast carcinoma cell lines were treated with recombinant gamma interferon (r gamma IFN) to study major histocompatibility complex (MHC) class I and class II antigen responses. Untreated H466-B cells released B2 microglobulin (B2M) into the culture medium and expressed B2M and class I heavy chain on 100% of the cells. The expression of class II antigens (DR) was limited to 8 +/- 4% of the cells. This subpopulation was isolated by cell sorting and labelled with 35S methionine. Protein extracts were immunoprecipitated with anti-DR antibody and subjected to two dimensional non-equilibrium pH gradient electrophoresis (2D-PAGE). A normal pattern of expression of invariant, alpha and beta chains was shown. The MHC antigenic expression of H466-B parental cell line was not modified by interferon treatment. Untreated T47-D cells did not release B2M into the culture medium, expressed B2M and class I heavy chain on 100% of the cells but did not express class II molecules using radio-immunoassay or 2D-PAGE. As early as 24 h after r gamma IFN addition, T47-D cells released B2M into the medium, B2M and class I heavy chain were significantly greater than that of untreated cells, and class II antigenic expression was found, all these in a dose dependent manner. 2D-PAGE analysis of class II antigens revealed the profile of human DR molecules but this expression seemed incomplete since only single alpha and beta spots were detected suggesting a possible defect in the sialilation of DR molecules. These results show a heterogeneity in MHC antigenic responses to r gamma IFN and suggest that synthetized class II molecules may be incompletely processed.
We have examined the expression of several myeloid cell associated antigens, some of which are involved in myelomonocyte adhesion, in seven well characterized human breast cancer cell lines, since common properties of adhesiveness and migration are found in haemopoietic cells and epithelial cancer cells. Five of these cell lines were of metastatic origin and two were derived from primary breast carcinoma. Antigenic expression was evaluated by immunofluorescence (IF), flow cytometry (FCM), radioimmunoassay on live cells (RIA) and immunoperoxidase staining. None of these cell lines expressed T or B lymphoid specific antigens. Myeloid antigens My4, MO1, and MOF11 (derived from the hybridization of mouse X63 - Ag8 cells with spleen cells from Balb/c mice immunized with purified human monocytes) were expressed in the 7 cell lines. Leu M1, Leu M3, My9, and MO2 antigens were expressed in some of the cell lines. Leu M2 and My7 antigens were not expressed or at very low levels. The expression of these myeloid antigens was also tested by immunoperoxidase staining, and found on frozen sections of normal mammary gland, fibroadenoma of the breast, primary breast cancer, and lymph node and skin metastases of breast tumours. This common expression in epithelial breast cells and in myeloid cells might be related to common biological functions such as interaction with extracellular matrix which precedes cell migration, a normal function of macrophages and an abnormal function expressed or amplified in human cancer epithelial cells.
Explore the source record for details and available documents.
The effect of 1,25-dihydroxycholecalciferol [1,25(OH)2D3], the active form of vitamin D3, on cell growth, clonogenicity, and cyclic adenosine monophosphate (cAMP) production was examined in human breast cancer cell line T47D. 1,25(OH)2D3 markedly inhibited proliferation of T47D cells in a time- and concentration-dependent manner. 1,25(OH)2D3 5 X 10(-7) reduced to 70% [3H]thymidine incorporation into DNA. Specific high affinity nuclear receptors for 1,25(OH)2D3 were present in this cell line. The cAMP produced by T47D cells was measured during 10 min stimulation by effectors (prostaglandin E1 or forskolin). Without effector, T47D cells produced similar amounts of cAMP in control and 1,25(OH)2D3-treated cells. After 3 days in the presence of 1,25(OH)2D3, cAMP production was significantly increased compared to control cells when stimulated by 10(-4) M prostaglandin E1 or 5 X 10(-7) M forskolin (3.2- and 2.4-fold increase, respectively). This cAMP increase was concentration dependent within the same range that inhibited cell growth and clonogenicity. These results suggest that 1,25(OH)2D3 may indirectly affect cAMP production by modulating the target cell response to stimulatory agents of cAMP production.
In vitro differentiating agents causing little bone marrow aplasia have been proposed as a specific therapy of myelodysplastic syndromes with excess of blasts. A critical review of the published data is presented. The preliminary results of a cooperative protocol using very low dosage of cytosine arabinoside (3mg/m2/twice daily) with or without androgens are given.
Two mouse hybridomas, producing the monoclonal antibodies 7B10 and 1BE12 which react with membrane antigens of a metastatic human breast tumor cell line were selected. One of them, 7B10, is directed against a mammary gland antigenic determinant and selectively stain mammary carcinoma on histologic sections after fixation and paraffin embedding.
Among 10 human mammary tumor cell lines analyzed for transforming genes by transfection of NIH 3T3 cells, one carcinoma cell line, H-466B, established from an ascitic effusion of a woman with an adenocarcinoma of the breast was scored as positive. The transforming gene was identified as the K-ras2 oncogene. Nucleotide sequencing of exons 1 and 2 of the activated gene revealed two adjacent G----T transversions at the first and second position in codon 12 leading to the replacement of the normally encoded glycine by a phenylalanine. Since the phenylalanine substitution had never been observed in any type of tumor, this raises the question about the frequency as well as the cell type specificity of this K-ras2 activation in mammary tumors.
A total of 32 patients with acute myelomonocytic leukemia and abnormal bone marrow eosinophils (LAM4 Eo) have been treated at this Institute since 1977. Abnormalities of chromosome 16 have been noted in 14 of 22 evaluable cases. After a median follow-up of 4 years, median duration of complete remission was 46 months and median duration of survival had not been reached; 8 patients have been receiving no therapy for between 1 and 6 years. These results compare favorably with LAM4 without abnormal bone marrow eosinophils (median duration of complete remission: 12 months; median duration of survival: 14 months). LAM4 Eo constitute a particular entity, with a special hematological presentation, the incidence of abnormalities of chromosome 16, and a particularly good prognosis.
We report 5 cases of peripheral T cell lymphoma (PTCL) which initially presented as angioimmunoblastic lymphadenopathy (AIL). In 4 cases, the delay between the 2 phases was less than 1 year, and 3 patients were under corticosteroid therapy when the second biopsy was performed. Clinical and biological features were very similar during the 2 phases. The initial disease was morphologically characterized by a high cellular pleomorphism with immunoblasts, plasma cells, eosinophils and lymphoid cells of various size with abundant venules; this pleomorphism then regressed, emphasizing the T cell nature of the lymphoma, as proven by immunological staining with monoclonal antibodies raised against T cell subpopulations. In 4 cases, T cell proliferation bore T helper (CD4) and T cytotoxic/suppressor (CD8) antigens and, in 1 case only, CD4 antigen. The entity of AIL and the role of corticosteroid therapy is discussed; the short interval between the 2 diagnose suggests that T cell proliferation was present initially, but was masked by reactive B lymphocytes.
The experience with 59 patients affected by diverticular disease who underwent surgery after failure of medical treatment, is reported. 40 patients showed one or more postoperative complications, 19 none. The operations performed were: in 46 cases one-stage resection with anastomosis, Hartmann's operation in 8 and other procedures in 5. Six patients died: 3 after Harmann's operation, 2 after colostomy and one after anastomosis. The mean stay in bed for complicated cases was 24 days after anastomosis and 36 after Hartmann's operation. Therefore anastomosis is preferred in all cases including those with stenosis, fistula or abscess provided that peritonitis is not present. The anastomosis is performed away from the site of abdominal sepsis. In cases with peritonitis the selected surgical procedure is usually Hartmann's operation.
Two hundred and fifty patients (mean age 39 years) were involved in a multicentric pilot trial aimed at evaluating the effectiveness of a piperacillin (P) + amikacin (A) combination in severe neutropenic patients (less than 500 PNN/microliters). In patients who failed to improve under this combination vancomycin (V) was added. Two hundred and thirty-five patients were assessable for response to P + A. The infection was microbiologically undocumented in 148 of them (63%) and documented in 87 (37%). Response rates were 64% and 53% respectively, rising to 73% in both groups after addition of vancomycin. Thirty p. 100 of the patients had bacteremia. The most frequently encountered pathogens were staphylococci, enterobacteria, streptococci and Pseudomonas aeruginosa. Sixty-six p. 100 of gram-negative and staphylococcal infections responded to the P + A combination, while the response rate of staphylococcal infections was 23%. Fifty-seven p. 100 of staphylococci resistant to P + A were controlled by P + A + V. Fifteen (6.4%) patients died of infection, 5 of them of fungal infection. Toxicity was mild, with 3% renal toxicity. The P + A combination is effective as first line therapy in febrile neutropenic patients. These results and epidemiological data suggest that this combination plus vancomycin would be a suitable second line therapy for patients who did not improve.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Platelets may promote the development of metastasis, and tumor cells that aggregate platelets are believed to be more malignant. We studied three different human mammary carcinoma cell lines, which had different interactions with human platelet-rich plasma (PRP). The MCF-7 and the T47-D cell lines induced an adenosine diphosphate (ADP)-mediated platelet aggregation. The third cell line, MDA-MB 231 did not induce any platelet aggregation. On the contrary, this cell line inhibited ADP- and arachidonic acid-induced platelet aggregation. This inhibiting activity is mainly adenosine-mediated. The mechanism by which platelets may contribute to the dissemination of cancer could be related to platelet growth factors. MCF-7 and T47-D cell lines induced a release of platelet-derived growth factor (PDGF). On the contrary, the MDA-MB 231 cell line did not induce any platelet release. The role of these platelet growth factors in tumor cell growth is discussed.
Thirty-two patients with advanced colorectal carcinoma were treated with cisplatin (100 mg/m2) by infusion over 24 hours on Day 1 and 5-FU (1000 mg/m2/day) by infusion over 24 hours on Days 2-6 every 28 days. Ten of the 32 patients had received prior chemotherapy consisting of either 5-FU alone or 5-FU combination regimens. Objective response was observed in 13 patients (two complete and 11 partial responses). Another 11 patients had stabilization of disease. The overall median survival time in this study was 9.53 months. Toxicity was generally mild and tolerable. The response rate found in this study indicated that continuous infusion of cisplatin-5-FU administered at this dose and schedule was moderately active in advanced colorectal carcinoma.
Explore the source record for details and available documents.