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M R Berger

Publications and source records attributed to M R Berger.

153 records · Page 9Linked to original sources
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Quantification of liver metastases from LS174T human colorectal cancer cells in nude rats by PCR.

Liver metastasis of colorectal cancer is a challenging problem and associated with poor prognosis. Appropriate experimental models based for example on xenografts of human colorectal cancer (HCRC) cells may help to find new therapeutic options. To establish an orthotopic liver metastasis model, 9 HCRC cell lines (HDC8, HDC63, HDC101, Isreco-1, Isreco-2, Isreco-3, SW480, SW620, LS174T) were tested for their appropriateness after subcutaneous (s.c.), intrasplenic, intrahepatic and intraportal injection into rnu-rats. The growth curve of the most appropriate cell line (LS174T) was established in a subsequent experiment. For early tumor detection, a quantitative nested PCR-assay using an internal standard was developed. The detection limit of the assay was 10 HCRC cells/mg liver tissue, which was 100-1000 fold more sensitive than histological examination. LS174T cells showed an exponential, but somewhat irregular growth in the liver of nude rats within the observation period of 6 weeks. The model will be useful for future therapeutic studies.

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Efficacy of new ruthenium complexes against chemically induced autochthonous colorectal carcinoma in rats.

SD rats bearing acetoxymethylmethylnitrosamine-induced colorectal carcinomas were treated by i.v. administration of trans-imidazolium-bisimidazoletetrachlororuthenate (III) ImH(RuIm2Cl4), bisbenzimidazolium-benzimidazolepentachlororuthenate (III) (BzImH)2(RuBzImCl5) and trans-indazolium-bisindazoletetrachlororuthenate (III) In-dH(ruInd2Cl4). The dose levels used were 0.022 mmol/kg body weight administered twice weekly over ten weeks for all compounds and, additionally, 0.015 mmol/kg for ImH(RuIm2Cl4). All compounds caused a tumor growth inhibition exceeding 90%; differences were found with regard to toxicity: ImH(RuIm2Cl4 and (BzImH)2(RuBzImCl5) caused dose-related decreases in body weight and increases in mortality as shown by 21% and 29% body weight loss compared to controls as well as 10% and 45% mortality for the two dosages of the first compound, and 9% body weight loss compared to controls as well as 7% mortality for the latter compound. In contrast, equimolar administration of IndH(RuInd2Cl4) was not related to any symptoms of toxicity as evidenced by 2% body weight gain compared to controls as well as 0% mortality. Since this latter drug obviously showed remarkable activity in a highly resistant type of tumor at negligible toxicity, it certainly deserves special attention.

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Morton's neuroma.

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Foot Diseases↗
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Frozen shoulder.

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Humans↗
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Dinaline inhibits amino acid transport and proliferation of colon carcinoma cells in vitro.

The human colon carcinoma cell line SW707 was incubated with different concentrations (7 microM - 540 microM) of the novel antineoplastic drug 4-amino-N(2'-aminophenyl)benzamide (GOE1734, dinaline) to study the effects on 3H-alpha-aminoisobutyric acid (AIB) - and 14C-methionine uptake as well as on 3H-thymidine incorporation into DNA. Additionally, adenine nucleotide pools were determined by high performance liquid chromatography (h.p.l.c.), and cell cycle distribution by flow cytometry. 24 h exposure to low concentrations of dinaline caused mild cell proliferation which turned into a cytostatic effect within a further 24 h without drug exposure. High concentrations of dinaline, however, were found to be cytostatic and then cytotoxic after corresponding time intervals. Dinaline caused a concentration-dependent decrease in sodium-dependent AIB uptake. Immediately after exposure the effect ranged from 67%-36% of control uptake. One day later an incomplete recovery not exceeding 70% of control was found for the three highest concentrations. This differed significantly from sodium-dependent methionine uptake which was initially decreased by 24%-36% but recovered within one hour and was enhanced one day after exposure. Significant differences were also measured for sodium-independent AIB uptake and sodium-independent methionine uptake immediately, 1 and 4 h after exposure. Adenine nucleotide pools were mildly increased immediately and 4 h after exposure. Thymidine incorporation into DNA was decreased by 70% to 84% immediately after exposure, and no full recovery was seen in the subsequent observation period. Cell cycle analyses revealed a block at the S phase entrance. Changes in thymidine incorporation and S phase fraction were highly correlated. The inhibition of the sodium-dependent uptake of AIB might indicate interaction of dinaline with cell membrane functions at low concentrations, the increase in methionine uptake points to enhanced protein synthesis following drug withdrawal and the impaired thymidine incorporation into DNA results from the cytostatic effect of dinaline. Taken together, the results show that SW707 colon carcinoma cells exposed to dinaline demonstrate distinct but reversible changes in amino acid transport, protein metabolism, DNA synthesis and cell proliferation, thus giving a correlation with observations in vivo.

Adenine Nucleotides↗
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Hexadecylphosphocholine inhibits invasion of mouse T-cell lymphoma cells in two different invasion assays.

Hexadecylphosphocholine (HePC), an ether lipid analogue, is a new antineoplastic drug which has been shown to exert a remarkable antiproliferative effect in vitro and in vivo. The signal transduction pathway and the phospholipid synthesis are thought to be the main putative molecular targets of HePC, yet the exact mechanism of action is still unclear. To investigate the antiinvasive activity of HePC on a mouse T-cell lymphoma cell line (BW-O-Li1), we used a type I collagen gel and devitalized dermis as substrate to evaluate the migration of BW-O-Li1 after exposure to HePC. BW-O-Li1 cells were exposed for 24 h to a non-cytotoxic (10 microM) as well as to cytotoxic concentrations of HePC. Afterwards, BW-O-Li1 cells were seeded on top of a reconstituted collagen gel layer or pippeted into a steel ring placed on the dermal site of a devitalized dermis. Lymphoma cells, which invaded the collagen layer were counted by light microscopy, invasion into devitalized dermis was measured by an image analysis system. Compared to unexposed cells, invasion into the collagen gel differed significantly even at 10 microM HePC, whereas the absolute number of invading cells, independently of the HePC concentration, showed no difference in the amount of counted cells. Migration into devitalized dermis was significantly reduced for 10 microM and 40 microM HePC. These data show that complementary information can be obtained by application of the two invasion assays and that the antiinvasive effect of HePC emerges at non-cytotoxic concentrations of the substance.

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