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A Hammann

Publications and source records attributed to A Hammann.

30 records · Page 2Linked to original sources
PubMed1992

Effect of gut-associated lymphoid tissue on cellular proliferation in proximal and distal colon of the rat.

In previous studies, chemically induced colonic carcinomas were found to originate preferentially from crypts adjacent to lymphoid tissue. Proliferative parameters and mucosecretion were analyzed in proximal and distal rat colon in relation to the proximity of lymphoid patches. Animals received an intraperitoneal pulse of bromodeoxyuridine 1-hr before death. In both proximal and distal colon, crypts located at the immediate proximity of the lymphoid formations contained fewer mucous cells (P less than 0.001), but a higher percentage of proliferative epithelial cells (P less than 0.001) than the crypts far from lymphoid formations. The labeling index was higher in crypts adjacent to lymphoid patches compared to crypts distant from lymphoid patches only in the lower third of the crypts. The association of an increased proliferative activity and a decrease in differentiated mucosecreting cells in colonic crypts adjacent to lymphoid patches could be related to the particular sensitivity of these crypts cells to the effects of mutagens and carcinogens.

Animals↗
PubMed1992

Histological reactivity of a monoclonal antibody against rat colon cancer cells on human and rat normal gut and colonic tumours.

A monoclonal antibody, F11C, was raised against rat colon cancer cells. Its immunoreactivity on normal human and rat gut as well as human and rat colonic tumours was studied by the avidin-biotin-peroxidase complex technique. In both normal rat and human gastrointestinal tract, F11C stained surface epithelial cells from the fundus to distal colon, mainly as supranuclear vesicles. These vesicles appeared to be part of the Golgi apparatus on electron microscopy with immunogold labelling. Twenty primary rat colon tumours and 28 of 43 human colon tumours were also stained, with a heterogeneous pattern but much more strongly than the normal colonic mucosa. Biochemical purification suggested that in rat tumours F11C epitope was carried by a high molecular weight glycoprotein. Absorption experiments with synthetic oligosaccharides showed that F11C monoclonal antibody reacted with blood group A-related oligosaccharides. Nevertheless, F11C reactivity on human tissues was not related to the individual ABO or Lewis phenotype.

1,2-Dimethylhydrazine↗
PubMed1991

Growth characteristics and metastatic potential of seven intestinal carcinoma lines serially passaged in syngeneic rats.

Transplantable tumour lines were obtained from one duodenal carcinoma induced by N-methyl-N'-nitro-N-nitrosoguanidine in the Lewis rat and from six colonic carcinomas induced by 1,2 dimethylhydrazine in BDIX or Fisher rats. The tumours were serially transplanted by the subcutaneous route into homologous syngeneic rats. The seven tumours differ from one another in their histological structure, five of them being well or moderately differentiated adenocarcinomas, and in their capacity to produce neutral or acidic mucins. The seven tumours also differ in their growth rate. The seven lines produced metastases; the metastatic potential and the location of the metastases differed from one line to another. The seven lines kept their original differentiation characteristics through multiple passages, representing several years of transplantation into syngeneic hosts. These tumours represent a useful and diversified model of metastatic intestinal carcinoma, available for basic research and therapeutic trials.

Animals↗
PubMed1989

Histoimmunological characterization of the cellular reaction to liver metastases induced by colon cancer cells in syngeneic rats.

Artificial liver metastases were produced by injecting in vitro cultivated colonic cancer cells into the mesenteric vein of syngeneic rats. An immunohistologic study of the inflammatory host cells infiltrating the tumors was carried out from 1 to 46 days after tumor cell injection, using a set of monoclonal antibodies labelling tumor cells, macrophages or lymphoid cells subpopulations. In small metastases, 3-7 days after tumor cell injection, tumor cell foci were surrounded by a dense corona of inflammatory cells, predominantly T lymphocytes and NK cells. This inflammatory corona regressed when metastases grew larger and completely disappeared around the large metastases found more than 28 days after cell injection. Inside the metastases, the tumor cells were mixed with a small number of cells with the characteristic labelling of macrophages (KiM2R+, W3/25+); however, the inside macrophages are OX8+ in contrast to macrophages found in normal liver and in the peritumoral corona. The progressive disappearance of the coronal inflammatory cells suggests that cancer cells are able to produce or to induce other cells to produce anti-inflammatory agents inhibiting the accumulation of macrophages and lymphoid cells around the tumors.

Animals↗
PubMed1987

Effects of a single injection of anti-asialo GM1 serum on natural cytotoxicity and the growth of a regressive colonic tumor in syngeneic rats.

The REGb tumor cell line is a cloned variant of the DHD-K12 cell line, established from a colon carcinoma chemically induced in the rat. Unlike the parent DHD-K12 cell line, or other clones, which give progressive tumors when inoculated to the syngeneic rat, REGb cells produce tumors which regress in 3 to 5 weeks and never cause metastasis. In order to explore the role of natural killer (NK) cells in REGb tumor regression, each rat was given one injection of anti-asialoGM1 (anti-asGM1) serum, a known inhibitor of NK activity. This injection was done 24 hr before REGb cell challenge. This injection significantly depressed the in vitro cytotoxicity of peripheral blood lymphocytes on REGb cells for 2 weeks. REGb tumors grew larger and regressed later in the treated animals than those in the controls. Furthermore, a progressive or recurrent tumor was observed in 4 out of 10 treated rats, giving lung and/or lymph-node metastases in 2 cases. Immuno-histological study of the cells infiltrating the REGb tumors in control and treated animals showed a decrease number of asGM1+ and OX8+ lymphocytes, presumably NK cells, after anti-asGM1 treatment. An increase in number of macrophages was demonstrated in the progressive tumors of treated animals. These results suggest that NK cells play an important role in the initial stage of the regression TSb tumors in untreated syngeneic rats.

Animals↗
PubMed1987

An immunohistological study of cells infiltrating progressive and regressive tumors induced by two variant subpopulations of a rat colon cancer cell line.

In order to understand the mechanisms leading up to progression or regression, tumors resulting from the s.c. inoculation of progressive or regressive variants of a cell culture established from a chemically-induced rat colonic carcinoma were subjected to sequential histological study. As immunological factors have been previously described in this system of progressive or regressive tumors, special interest was given to inflammatory cells, T and B lymphocytes and macrophages, located inside and outside the tumor. Immunohistological methods using monoclonal or polyclonal antibodies and enzyme histology were performed to identify different populations of infiltrative cells. In both variants of tumors an accumulation of these cells were seen at the periphery of the tumor, surrounding the nodules. In contrast, very few inflammatory cells, macrophages or T lymphocytes were seen inside the clumps of tumor cells where cytolytic cells could have a contact-dependent tumoricidal effect. Only small differences were found between progressive and regressive tumors in the density of the various populations of T helper, T cytotoxic/suppressor, B lymphocytes or macrophages inside or around the tumor nodules. On the other hand, progressive and regressive tumors clearly differ in the relationship between tumor cells and the fibroblastic reaction they induce. Regressive tumors were rapidly encircled by a fibroblastic reaction isolating them from the peripheral tissues. The fibroblastic reaction was less dense around the progressive tumor cells which were able to migrate and invade the periphery. This suggests that immunological factors leading to tumor progression or regression could act indirectly through a control of the fibroblastic reaction, rather than through a direct cytotoxic effect on the tumor cells.

Animals↗
PubMed1986

Gut-associated lymphoid tissue and 1,2-dimethylhydrazine intestinal tumors in the rat: an histological and immunoenzymatic study.

The association between chemically-induced intestinal carcinoma and gut lymphoid patches was studied in 20 male Sprague-Dawley rats 7 months after the first of 16 weekly injections of 1,2 dimethylhydrazine (DMH). The lymphoid patches of DMH-treated rats and of 14 untreated control animals were systematically studied histologically on sections of "swiss-rolled" whole intestine. It was found that 78% of the small-intestine carcinomas and 73% of the colorectal carcinomas were associated with intestinal lymphoid patches. Furthermore, misplaced and often atypical glandular crypts were often found in the parafollicular or interfollicular areas of lymphoid patches, in treated as well as in control animals. These glands could be the origin of the lymphoid-patch-associated carcinoma. Immunohistological staining with monoclonal antibodies (MAbs) against T-lymphocyte antigens or anti-IgM serum labelling B lymphocytes clearly localized early carcinoma and atypical glands in the T-dependent, interfollicular and parafollicular area of lymphoid follicles. An MAb directed against la-antigen stained some well-differentiated carcinomas and some atypical glands found in control rats. On the other hand, lymphoid patches, when not invaded by a carcinoma, were not modified in their number, size, morphology or cellular composition in DMH-treated rats as compared to control animals.

1,2-Dimethylhydrazine↗
PubMed1986

Amiodarone-induced enhancement of doxorubicin and 4'-deoxydoxorubicin cytotoxicity to rat colon cancer cells in vitro and in vivo.

The mechanisms of the resistance of intestinal cancer to anthracyclines were studied on an experimental model of rat colon cancer cells. The accumulation of anthracyclines in the nucleus of living cancer cells was observed by fluorescence microscopy. This accumulation depended on both the capacity of anthracyclines to penetrate into the cell and the activity of an efflux mechanism extruding the drug from the cell. We found that 4'-deoxydoxorubicin was superior to 4 other anthracyclines in its capacity to penetrate into confluent colon cancer cells. Amiodarone, an antiarrhythmic agent used in cardiology, inhibited the efflux mechanism efficiently and increased the toxicity of anthracyclines to the colon cancer cells. Association of amiodarone and 4'-deoxydoxorubicin was able to cure 5 of 13 rats that had been inoculated i.p. previously with syngeneic colon cancer cells. This association could be of interest in the treatment of human colon cancer.

Adenocarcinoma↗
PubMedDate not supplied

P27KiP1 overexpression inhibits the growth and doxorubicin sensitivity of HT29 human colon cancer cells in vivo.

We have previously shown that p27KiP1 plays a role in the tumor cell resistance of HT29 confluent monolayers to cytotoxic drugs in vitro. To determine whether p27KiP1 was a resistance factor to cytotoxic drugs in vivo we tested the effect of doxorubicin on p27KiP1-overexpressing HT29 tumors in nude mice. In this study we show that ectopic overexpression of p27KiP1 in HT29 human colon cancer cells decreases their tumorigenicity in vivo in nude mice. This decreased tumor growth was associated with increased p27KiP1 protein expression, studied by Western blotting in tumor extracts. Interestingly, the overexpressing-p27KiP1 tumors were significantly more resistant to intraveneous doxorubicin treatment than the control tumors. These results indicate that p27KiP1, which delays tumor growth could also increase tumor resistance to cytotoxic drugs in vivo.

Animals↗
PubMedDate not supplied

Use of a specific monoclonal antibody for studying the liver metastatic invasion of a rat colon cancer.

A simple model for liver metastasis from colon cancer resulted from the intraportal injection of 2 x 10(7) highly tumorigenic DHD/K12/PROb cells into syngeneic BDIX rats. Early detection and development of cancer invasion were studied by conventional microscopy and immunoenzymatic staining using a specific monoclonal antibody. Metastases developed either from isolated cancer cells early disseminated in sinusoid network or from intraportal microthrombi. An intense immune reaction developed until day 15 after injection but decreased and disappeared at the latest stages of evolution.

Animals↗