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Sister chromatid exchange assay as a predictor of tumor chemoresponse.

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TLDR
A critical appraisal of the SCEs-assay as an important biomarker used for predicting cancer chemo-response as well as a summary of the key findings from several studies published within the last 20 years in this field is performed.
Abstract
Sister Chromatid Exchanges (SCEs) are known to enhance as a consequence of exposure to various mutagenic agents and appear to indicate DNA damaging effects and/or subsequent repair by homologous recombination (HR). DNA damage plays an interesting role in the majority of mechanisms underlying the effects of antitumor drugs, since the genetic activity of the plethora of these agents is due to their ability to damage the DNA. The DNA-effects of antitumor agents towards normal cells (genotoxicity) are great drawbacks of antitumor therapy and are connected to important adverse health effects in cancer patients undergoing chemotherapy. On the other hand, failure of chemotherapy in many cases is due to the DNA repair ability which cancer, like normal cells, also possess. As both DNA repair and genotoxic exposure are expected to vary among patients, correlating SCEs frequencies with only individual repair capacity may be feasible to predict. Cancer risk has not been observed to be associated with high SCEs levels. Since the administration of effective antitumor drugs with limited adverse effects is of great importance in the success of anticancer therapy, a lot of interest has been directed toward the development of methods and approaches that would enable the correct selection of appropriate drugs prior to the initiation of therapy on an individual basis. To this effect, more than 30 years ago, an investigation of the ability of the in vitro and the in vivo SCEs-assay to predict the in vitro and in vivo sensitivity of tumor cells to newly synthesized drugs or to those already in use began. In this short review a critical appraisal of the SCEs-assay as an important biomarker used for predicting cancer chemo-response as well as a summary of the key findings from several studies published within the last 20 years in this field is performed.

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Synthetic lethality in malignant pleural mesothelioma with PARP1 inhibition.

TL;DR: Surprisingly, it was found that all MPM cell lines examined, regardless of BAP1 status, were addicted to PARP1-mediated DNA repair for survival, and this data demonstrate that thePARP1 inhibitors could be effective in the treatment of MPM, for which little effective therapy exists.
Journal ArticleDOI

Evaluation of the cytotoxic and genotoxic effects of mycotoxin fusaric acid.

TL;DR: It is pointed out that being exposed to FA at high concentrations show cytotoxicity, and no genotoxic effects were seen in human lymphocytes in vitro using CA, SCE and MN assays.
Journal ArticleDOI

Potential chromosome damage, cell-cycle kinetics/and apoptosis induced by epoxiconazole in bovine peripheral lymphocytes in vitro.

TL;DR: Electrophoretic analysis confirmed the epoxiconazole potential to induce ladder-like patterns of DNA fragments that are a hallmark of apoptosis.
Journal ArticleDOI

RBMX is required for activation of ATR on repetitive DNAs to maintain genome stability.

TL;DR: It is identified that RBMX is an ssDNA binding protein that orchestrates a novel pathway to activate ATR on repetitive DNAs, a new ssDNA-RBMX-TopBP1 pathway that is specifically required for activation of ATR in response to replication stress.
Journal ArticleDOI

Investigation of in vitro genotoxic effects of an anti-diabetic drug sitagliptin.

TL;DR: It was concluded that higher concentration of sitagliptin had genotoxic effects in the human lymphocytes in vitro and this compound increased the MN at only the highest concentration compared with the solvent control.
References
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Journal Article

Chromosomal aberrations in lymphocytes predict human cancer: A report from the European study group on cytogenetic biomarkers and health (ESCH)

TL;DR: The present study further supports the previous observation on the cancer predictivity of the CA biomarker, which seems to be independent of age at test, gender, and time since test, and Cox's proportional hazards models gave no evidence that the effect of CAs on total cancer incidence/mortality was modified by gender, age attest, or timeSince test.
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Inactivation of Human MAD2B in Nasopharyngeal Carcinoma Cells Leads to Chemosensitization to DNA-Damaging Agents

TL;DR: In this paper, the authors investigated whether MAD2B played a key role in cellular sensitivity to DNA-damaging anticancer drugs by suppressing its expression using RNA interference in nasopharyngeal carcinoma cells.
Journal Article

Antineoplastic and cytogenetic effects of complexes of Pd (II) with 4N-substituted derivatives of 2-acetyl-pyridine-thiosemicarbazone.

TL;DR: Among these compounds, the compound Bis(3-hexamethyleneiminyl-2-acetylpyridine-thisemicarbazonato++ +) palladium (II) was found to be distinctly effective against Leukemia P388, in inhibiting incorporation of 3H-thymidine into DNA and in inducing SCEs and cell division delays.
Journal Article

Enhancement of Cytogenetic Damage and of Antineoplastic Effect by Caffeine in Ehrlich Ascites Tumor Cells Treated with Cyclophosphamide in Vivo

TL;DR: The in vivo antitumor effect by CP in conjunction with caffeine appears to correlate well with the in vivo synergistic effect on cytogenetic damage caused by the combined CP plus caffeine treatment.
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