Disease relevance of Ccdc132

• Mutations in BLM give rise to Bloom syndrome, a disease that is characterized by an elevated rate of crossovers and increased cancer susceptibility [1].
• The differential effects (BLM) on cycling and noncycling cells were investigated with a mouse ascites tumor in vivo [2].
• Thus, the pulmonary fibrosis seen with i.t. BLM administration may reflect the high initial content of unmetabolized drug achieved in the lungs [3].
• Mice bearing transplanted glioma received 0.9% NaCl, 0.1 mg of BLM, or 200-250 microCi of 111In-BLM (0.1 mg BLM) daily for 5 days intraperitoneally [4].
• However, it was evidenced in the present report that tranilast suppressed BLM-induced fibrosis in WBB6F1-W/Wv mice [5].

Psychiatry related information on Ccdc132

• Further evidence for the dependence of the action of this drug upon the proliferative state of the cell population is derived from time-response studies after single doses of BLM [6].

High impact information on Ccdc132

• Accumulating evidence points to telomeres as targets of WRN and BLM, but the importance in vivo of the proteins in telomere biology has not been tested [7].
• However, the fact that percentage of cells in mitosis versus time after the administration of BLM showed two peaks indicates the possibility that another cause of the increase in mitotic figures might be a relative increase of cycling cells due to higher sensitivity of noncycling cells to the agent [2].
• Hence BLM may be cell cycle nonspecific, and the BLM-induced decrease in cell number, i.p., may stimulate some nondividing cells to reenter the division cycle [2].
• An i.p. injection of 37.0 or 111.1 mug BLM per g caused a decrease in tumor cell number but an increase in percentage of tumor cells in mitosis [2].
• There are no significant differences between the percentage labeled mitoses at various times after pulse labeling by tritiated thymidine of BLM-treated tumor cells and by that of an untreated control, except that the height of the second peak was significantly lower in the treated cells [2].

Chemical compound and disease context of Ccdc132

• In the present paper, we evidenced that pulmonary fibrosis could be induced in genetically mast cell-deficient WBB6F1-W/Wv mice as well as WBB6F1-(+/+) mice having mast cells normally by the treatment with bleomycin (BLM, 5 mg/kg, i.v., 10 days), and there was not much difference in the histological changes of lungs between the two strains [5].
• Increases in the number of mast cells and in histamine content of the lung, which were widely reported in the lungs of BLM-treated mice, may be the result of fibrosis [5].

Biological context of Ccdc132

• Single intravenous injections of BLM into tumor-bearing mice result in single- and double-stranded cleavage of episomes that are dose related and occur within 1 min [8].
• DNA damage induced by UV mimetic mutagens MMS and MNU, and X-ray mimetic mutagen BLM was observed just after treatment, crosslinking agent MMC-induced DNA damage was detected 21 h after treatment, and 6-MP as an inhibitor of DNA synthesis did not induce DNA damage at any sampling time [9].
• In DNA analysis, the percentages of cells in the G2/M-phases increased after exposure to BLM and particularly to (111)InBLMC in all three cell lines [10].
• Chromosome instability and tumor predisposition inversely correlate with BLM protein levels [11].
• The tissue distributions in glioma-bearing mice given injections of [111In]bleomycin (BLM) indicated that tumor concentrations and ratios of tumor to blood, muscle and brain for [111In]BLM-B2 and -A2 were higher than those for unfractionated [111In]BLM [12].

Anatomical context of Ccdc132

• The BLM results now demonstrate that there are chemicals that can induce specific-locus mutations in spermatogonia without testing positive in postspermatogonial stages [13].
• cDNA cloning of mouse BLM gene, the homologue to human Bloom's syndrome gene, which is highly expressed in the testis at the mRNA level [14].
• Tranilast may act through suppressing BLM-induced activation of lymphoid cells including macrophage and neutrophil [5].
• Tranilast neither suppressed the cytotoxic activity of BLM against KB cells and L-929 cells in vitro, nor inhibited the antitumor activity of BLM against Sarcoma-180 transplanted subcutaneously into ICR mice [5].

Associations of Ccdc132 with chemical compounds

• In particular, BLM and G418 survival data demonstrate that, inserted into the pR plasmid, the ble and neo genes of the Tn5 transposon express themselves [15].
• Dominant-lethal tests [P.D. Sudman, J.C. Rutledge, J.B. Bishop, W.M. Generoso, Bleomycin: female-specific dominant lethal effects in mice, Mutat. Res. 296 (1992) 205-217] had suggested that Bleomycin sulfate (Blenoxane), BLM, might be a female-specific mutagen [13].
• This fact implies a peculiar response to (BLM) treatment with Bleomycin, a drug which appears to be proliferation-dependent [6].
• Those with 5-FU, BLM or CDDP of 10 micrograms/ml exhibited ciliary swelling after 2 hr, but the morphological changes of 5-FU were more remarkable than those of BLM or CDDP [16].

Analytical, diagnostic and therapeutic context of Ccdc132

• MATERIALS AND METHODS: In an animal experiment, 10 SCC-xenografted mice were used, two for demonstrating targeting in gamma-camera images, eight for intraperitoneally receiving NaCl, BLM, or (111)InBLMC as therapy [10].
• After intratumor injection of a total dose of 0.1 mg of BLM/gm tumor weight, or of 1 mCi/gm tumor weight of 111In-BLM (carried by 0.1 mg of BLM/gm tumor weight), the tumor size decreased in the 111In-BLM group more than in the BLM group [4].

References