ORCID Profile
0000-0002-1738-9863
Current Organisations
University of Rome Tor Vergata
,
University of Sydney
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Publisher: Elsevier BV
Date: 03-2013
DOI: 10.1016/J.BBRC.2013.02.032
Abstract: Ionizing radiation can induce DNA strand breaks' formation both through direct ionization and through induction of oxidative stress. The resistance to radiation is mostly associated with the efficacy of DNA repair system. The ionizing radiation damage response of human topoisomerase IB, that is the selective target of c tothecin and derivatives widely used for various cancers often in association of radiotherapy, has been investigated treating with 30 Gy of X-rays a Saccharomyces cerevisiae strain in which the endogenous topoisomerase IB, not essential in this organism, has been deleted and a similar strain which overexpresses the human enzyme. The results show that before irradiation the genetic damage is significantly lower in cells containing human topoisomerase, but soon after irradiation the amount of DNA breaks in these cells is larger than in cells not containing the enzyme. Kinetic analysis of DNA repair rate as well as colonies growth demonstrate that cells containing human topoisomerase display a more efficient rescue. Finally, ionizing radiation induces in the Saccharomyces cells an increase of enzymatic activity and of the amount of the enzyme bound to the DNA indicating a direct role of topoisomerase IB in the mechanism of nucleic acid repair.
Publisher: American Association for Cancer Research (AACR)
Date: 03-04-2023
DOI: 10.1158/1541-7786.22515163
Abstract: Figure S1, related to Figure 1: Expression and correlation of CHK1 and CIP2A in multiple glioma cohorts. Figure S2, related to Figure 1: Overall survival and mRNA expression of PP2A subunits in glioma patients. Figure S3, related to Figure 1: Role of CHK1-CIP2A in Glioma Stem cell lines. Figure S4, related to Figure 3: Effect of CHK1 or CIP2A expression on GBM cells. Figure S5, related to Figure 5: Depletion of CIP2A induces senescence in GBM cells. Figure S6, related to Figure 6: Regulation of CIP2A expression by CHK1 and STAT3.
Publisher: American Association for Cancer Research (AACR)
Date: 03-04-2023
DOI: 10.1158/1541-7786.22515163.V1
Abstract: Figure S1, related to Figure 1: Expression and correlation of CHK1 and CIP2A in multiple glioma cohorts. Figure S2, related to Figure 1: Overall survival and mRNA expression of PP2A subunits in glioma patients. Figure S3, related to Figure 1: Role of CHK1-CIP2A in Glioma Stem cell lines. Figure S4, related to Figure 3: Effect of CHK1 or CIP2A expression on GBM cells. Figure S5, related to Figure 5: Depletion of CIP2A induces senescence in GBM cells. Figure S6, related to Figure 6: Regulation of CIP2A expression by CHK1 and STAT3.
Publisher: MDPI AG
Date: 14-07-2021
Abstract: MSH3 gene or protein deficiency or loss-of-function in colorectal cancer can cause a DNA mismatch repair defect known as “elevated microsatellite alterations at selected tetranucleotide repeats” (EMAST). A high percentage of MSI-H tumors exhibit EMAST, while MSI-L is also linked with EMAST. However, the distribution of CpG island methylator phenotype (CIMP) within the EMAST spectrum is not known. Five tetranucleotide repeat and five MSI markers were used to classify 100 sporadic colorectal tumours for EMAST, MSI-H and MSI-L according to the number of unstable markers detected. Promoter methylation was determined using methylation-specific PCR for MSH3, MCC, CDKN2A (p16) and five CIMP marker genes. EMAST was found in 55% of sporadic colorectal carcinomas. Carcinomas with only one positive marker (EMAST-1/5, 26%) were associated with advanced tumour stage, increased lymph node metastasis, MSI-L and lack of CIMP-H. EMAST-2/5 (16%) carcinomas displayed some methylation but MSI was rare. Carcinomas with ≥3 positive EMAST markers (13%) were more likely to have a proximal colon location and be MSI-H and CIMP-H. Our study suggests that EMAST/MSI-L is a valuable prognostic and predictive marker for colorectal carcinomas that do not display the high methylation phenotype CIMP-H.
Publisher: American Association for Cancer Research (AACR)
Date: 05-2020
DOI: 10.1158/1541-7786.MCR-19-0934
Abstract: High expression of CIP2A in gliomas is maintained by a CHK1-dependent pSTAT3–CIP2A recursive loop interrupting CIP2A induces cell senescence and slows GBM growth adding impetus to the development of CIP2A as an anticancer drug target.
Location: Australia
No related grants have been discovered for Zeenat Jahan.