Influence of 1 and 25 Hz, 1.5 mT magnetic fields on antitumor drug potency in a human adenocarcinoma cell line.

The resistance of tumor cells to antineoplastic agents is a major obstacle during cancer chemotherapy. Many authors have observed that some exposure protocols to pulsed electromagnetic fields (PEMF) can alter the efficacy of anticancer drugs; nevertheless, the observations are not clear. We have evaluated whether a group of PEMF pulses (1.5 mT peak, repeated at 1 and 25 Hz) produces alterations of drug potency on a multidrug resistant human colon adenocarcinoma (HCA) cell line, HCA-2/1(cch). The experiments were performed including (a) exposures to drug and PEMF exposure for 1 h at the same time, (b) drug exposure for 1 h, and then exposure to PEMF for the next 2 days (2 h/day). Drugs used were vincristine (VCR), mitomycin C (MMC), and cisplatin. Cell viability was measured by the neutral red stain cytotoxicity test. The results obtained were: (a) The 1 Hz PEMF increased VCR cytotoxicity (P < 0.01), exhibiting 6.1% of survival at 47.5 microg/ml, the highest dose for which sham exposed groups showed a 19.8% of survival. For MMC at 47.5 microg/ml, the % of survival changed significantly from 19.2% in sham exposed groups to 5.3% using 25 Hz (P < 0.001). Cisplatin showed a significant reduction in the % of survival (44.2-39.1%, P < 0.05) at 25 Hz and 47.5 microg/ml, and (b) Minor significant alterations were observed after nonsimultaneous exposure of cells to PEMF and drug. The data indicate that PEMF can induce modulation of cytostatic agents in HCA-2/1(cch), with an increased effect when PEMF was applied at the same time as the drug. The type of drug, dose, frequency, and duration of PEMF exposure could influence this modulation.

Physical map and characterization of transcripts in the candidate interval for familial chondrocalcinosis at chromosome 5p15.1.

The gene for familial chondrocalcinosis (MIM 118600; gene symbol CCAL2) has been localized to a 0.8-cM interval on the short arm of chromosome 5, between the polymorphic microsatellite markers D5S416 and D5S2114. We have undertaken the physical and transcript mapping of this interval, as well as regions telomeric to the interval, in an attempt to define ultimately the gene for this disorder. The physical map is composed of YAC, BAC, PAC, and cosmid resources and spans a physical distance of approximately 0.3 Mb. Using cDNA selection, we have identified eight novel transcripts in and around the interval; two of the selected transcripts reside in the candidate interval. We have also more precisely placed several expressed sequence tags (ESTs) that were previously mapped by radiation hybrid analysis and were reported to reside in or near the candidate interval. Two of the ESTs analyzed overlap with the selected cDNAs that reside in the candidate interval. All of the selected cDNAs are expressed partial transcripts, as determined by Northern blot analysis, and using RT-PCR analysis, we have determined that the cDNAs that reside in the candidate interval are expressed in cartilage and synovium, tissues that are presumably relevant to the chondrocalcinosis phenotype.