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M Lacroix

Publications and source records attributed to M Lacroix.

153 records · Page 9Linked to original sources
PubMedDate not supplied

A low-density DNA microarray for analysis of markers in breast cancer.

Breast cancer remains a major cause of death in women from Western countries. In the near future, advances in both nucleic acids technology and tumor biology should be widely exploited to improve the diagnosis, prognosis, and outcome prediction of this disease. The DNA microarray, also called biochip, is a promising tool for performing massive, simultaneous, fast, and standardized analyses of multiple molecular markers in tumor samples. However, most currently available microarrays are expensive, which is mainly due to the amount (several thousands) of different DNA capture sequences that they carry. While these high-density microarrays are best suited for basic studies, their introduction into the clinical routine remains hypothetical. We describe here the principles of a low-density microarray, carrying only a few hundreds of capture sequences specific to markers whose importance in breast cancer is generally recognized or suggested by the current medical literature. We provide a list of about 250 of these markers. We also examine some potential difficulties (homologies between marker and/or variant sequences, size of sequences, etc.) associated with the production of such a low-cost microarray.

Breast Neoplasms↗
PubMedDate not supplied

The aspirin metabolite salicylate inhibits breast cancer cells growth and their synthesis of the osteolytic cytokines interleukins-6 and -11.

Some epidemiological studies have suggested that aspirin could be a chemopreventive agent against breast cancer. We tested the effects of the aspirin metabolite salicylate (SA) on four (Hs578T, MCF-7, MDA-MB-231, and T-47D) breast cancer cell (BCC) lines in vitro. Two features were studied: the proliferation of BCC and their production of the osteolytic cytokines interleukins-6 (IL-6) and -11 (IL-11) since BCC frequently metastasize to bone and induce tumor-induced osteolysis. SA, from 0.5 to 5 mM, caused BCC growth inhibition by up to 70% (IC50 range 2.54 to 4.28 mM). At high concentrations, the drug induced apoptosis only (MDA-MB-231), or both apoptosis and primary necrosis (MCF-7). SA, as well as indomethacin (INDO), reduced the synthesis of IL-6 and -11, at both the protein and mRNA levels, in the two cell lines producing these cytokines (MDA-MB-231 and Hs578T). This latter effect seemed to be mediated by PGE2 since SA and INDO reduced PGE2 levels in MDA-MB-231 and Hs578T cells, PGE2 was not detected in MCF-7 and T-47D cells and exogenous PGE2 increased IL-6 and -11 expression by MDA-MB-231 cells. Collectively, our results suggest that SA could reduce the growth of breast tumors and inhibit to some extent the ability of BCC to induce osteoclast recruitment and osteolysis. These data indicate the need for further epidemiological and experimental studies.

Breast Neoplasms↗
PubMedDate not supplied

Effect of physical training on the oxidation of an oral glucose load at rest: a naturally labeled 13C-glucose study.

UNLABELLED: This study aimed at investigating, in six healthy, non obese, young (25 +/- 1 years) male volunteers, with strictly normal oral glucose tolerance, the influence of a six week physical training period (60 min bicycling 5 days/week at 30-40% of their individual VO2 max) on the hormonal and metabolic response to a 100 g oral 13C-naturally labeled glucose load given at rest before and 36 h after the last training session. Exogenous glucose oxidation was derived from 13CO2 measurements on expired air. Training resulted in: a 29% increase in VO2 max (2 p less than 0.002), a 27% decrease in plasma triglycerides (2 p less than 0.02). No changes were observed concerning weight, total body K, skinfold tolerance, which was strictly normal before training, remained unchanged, but the insulin response to the oral glucose load decreased by 24% (2 p less than 0.025). Exogenous glucose oxidation was similar before and after training, averaging 35.9 +/- 2.1 and 37.4 +/- 2.0 g/7 h respectively. IN CONCLUSION: a 6 week training period, performed on strictly healthy young males, studied at rest, induced an increase in VO2 max, a decrease in plasma triglycerides and a lower insulin response to oral glucose while glucose tolerance and exogenous glucose oxidation remained unchanged.

Adult↗