camptothecin/atrofia

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Increased susceptibility of spinal muscular atrophy fibroblasts to camptothecin is p53-independent.

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BACKGROUND Deletion or mutation(s) of the survival motor neuron 1 (SMN1) gene causes spinal muscular atrophy (SMA). The SMN protein is known to play a role in RNA metabolism, neurite outgrowth, and cell survival. Yet, it remains unclear how SMN deficiency causes selective motor neuron death and

Increased susceptibility of spinal muscular atrophy fibroblasts to camptothecin-induced cell death.

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Spinal muscular atrophy (SMA) is a neuromuscular disease caused by deletions or mutations in the telomeric copy of the survival motor neuron (SMN1) gene. Although the SMN protein has been implicated in the biogenesis of ribonucleoprotein complexes and RNA processing, it is not clear how these

DNA structural alterations induced by bis-netropsins modulate human DNA topoisomerase I cleavage activity and poisoning by camptothecin.

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Bis-netropsins (bis-Nts) are efficient catalytic inhibitors of human DNA topoisomerase I (top I). These DNA minor groove binders are considered to serve as suppressors of top I-linked DNA breaks, which is generally believed to be related to their affinity to DNA. In this study, it was found that

Neurotoxic activity of a topoisomerase-I inhibitor, camptothecin, in cultured cerebellar granule neurons.

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DNA Topoisomerase-I (Topo-I) is an enzyme involved in DNA rearrangements, transcription and replication and is a potential target for cancer chemotherapy. Camptothecin is one of the chemotherapeutic agents inhibiting the catalytic activity of Topo-I through the formation of single-strand protein-DNA

4-Week repeated intravenous dose toxicity study of a new camptothecin anticancer agent CKD-602 in dogs.

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CKD-602 is a new camptothecin derivative antitumor agent with a formula (7-[2-(N-isopropylamino)ethyl]-(20S)-camptothecin) developed by Chong Kun Dang Pharmaceutical Company in Korea. In the present study, the subacute toxicity of CKD-602 was investigated after 4-week repeated intravenous

Reproductive toxicity evaluation of a new camptothecin anticancer agent, CKD-602, in pregnant/lactating female rats and their offspring.

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CKD-602 is a camptothecin anticancer agent that was recently developed by the Chong Kun Dang Pharmaceutical Co. (Seoul, Korea). This study examined the potential adverse effects of CKD-602 on pregnancy, delivery, and lactation in female Sprague-Dawley rats as well as on the pre- and postnatal

Evaluation of the toxic potentials of a new camptothecin anticancer agent CKD-602 on fertility and early embryonic development in rats.

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This study examined the potential adverse effects of a new camptothecin anticancer agent, CKD-602, on the fertility and early embryonic development of Sprague-Dawley rats. Ninety-six rats of each gender were divided into four groups: three treatment groups and a control group. CKD-602 was

Regression of human colon cancer xenografts in SCID mice following oral administration of water-insoluble camptothecins.

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Gastrointestinal cancers pose major public health problems worldwide, in part because little progress has been made in the treatment of colorectal cancers. The present study explored the potential use of natural product topoisomerase I inhibitors, 10-hydroxycamptothecin (HCPT) and camptothecin

Disc degeneration in the rabbit: a biochemical and radiological comparison between four disc injury models.

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METHODS A biochemical and radiologic comparison of 4 disc injury models to produce disc degeneration in the rabbit was carried out in 2 experiments. OBJECTIVE To develop a reliable animal model of intervertebral disc degeneration. BACKGROUND In order to study various interventions for retarding or

Subacute toxicity evaluation of a new camptothecin anticancer agent CKD-602 administered by intravenous injection to rats.

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The subacute toxicity of a new camptothecin anticancer agent, CKD-602, was investigated after 4-week repeated intravenous administration of the chemical in Sprague-Dawley rats. The test chemical was administered intravenously to rats at dose levels of 0, 0.003, 0.013, or 0.067 mg/kg/day for males

Adipose mesenchymal stem cells protect chondrocytes from degeneration associated with osteoarthritis.

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Our work aimed at evaluating the role of adipose stem cells (ASC) on chondrocytes from osteoarthritic (OA) patients and identifying the mediators involved. We used primary chondrocytes, ASCs from different sources and bone marrow mesenchymal stromal cells (MSC) from OA donors. ASCs or MSCs were

Identification of the gene encoding DNA topoisomerase I from Candida albicans.

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A gene encoding a type I topoisomerase (TOP1) was isolated from Candida albicans, sequenced, and expressed in Saccharomyces cerevisiae. The TOP1 gene was identified from a C. albicans genomic library by hybridization with the product of a polymerase chain reaction with degenerate primer sets

Downregulation of free ubiquitin: a novel mechanism of p53 stabilization and neuronal cell death.

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Neuronal death through activation of the p53 stress response pathway has been implicated in the pathogenesis of neurodegenerative disorders. The mechanisms regulating p53 accumulation and function in neurons are poorly understood. Recent evidence has demonstrated that Mdm2 is a major inhibitor of

Topoisomerase I action on the heterochromatic DNA from the brine shrimp Artemia franciscana: studies in vivo and in vitro.

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The genomes of higher eukaryotes contain various amounts of tandem repeated DNA sequences (satellite DNA) typically located in the constitutive heterochromatin, the most highly condensed region of interphase chromosomes. We have previously demonstrated that an AluI DNA family of repeats is the major

Neurotoxin-induced DNA damage is persistent in SH-SY5Y cells and LC neurons.

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Degeneration of the noradrenergic neurons has been reported in the brain of patients suffering from neurodegenerative diseases. However, their pathological characteristics during the neurodegenerative course and underlying mechanisms remain to be elucidated. In the present study, we used the

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