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Condition: Faconi Anemia

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Total 16 results found since Jan 2013.

An Ensemble Strategy to Predict Prognosis in Ovarian Cancer Based on Gene Modules
Conclusion Considering the heterogeneity and complexity of ovarian cancer, we demonstrated a new method to predict the prognosis of ovarian cancer based on the clustering information and gene co-expression network in each subtype of cancer patients. We divided the ovarian cancer data into three subtypes by clustering analysis and we found that the survival risks in these three subtypes were significantly different. We mined the important communities based on the co-expression networks in each subtype. There are 50, 73, and 92 communities in the first, second and third subtype, respectively. Next, we constructed a new ense...
Source: Frontiers in Genetics - April 23, 2019 Category: Genetics & Stem Cells Source Type: research

hnRNP U and DDX47 Are Novel FANCD2 Interactors That May Help to Resolve R-Loops during Mild Replication Stress
Conclusion: We suggest that FANCD2 protects genome stability by recruiting RNA processing enzymes, including hnRNP U or DDX47, to resolve or prevent accumulation of R-loops induced by transcription-replication collisions during mild replication stress. Thus, our study may provide a novel insight to understand the mechanism of bone marrow failure and leukemogenesis in Fanconi anemia patients.DisclosuresTakaori-Kondo: Bristol-Myers Squibb: Honoraria; Pfizer: Honoraria; Celgene: Honoraria, Research Funding; Novartis: Honoraria; Janssen Pharmaceuticals: Honoraria.
Source: Blood - November 21, 2018 Category: Hematology Authors: Okamoto, Y., Abe, M., Itaya, A., Tomida, J., Takaori-Kondo, A., Taoka, M., Isobe, T., Takata, M. Tags: 508. Bone Marrow Failure: Poster I Source Type: research

Blockade of Deubiquitylating Enzyme USP1 Inhibits DNA Repair and Triggers Apoptosis in Multiple Myeloma Cells.
CONCLUSIONS: Our preclinical studies provide the framework for clinical evaluation of USP1 inhibitors, alone or in combination, as a potential novel MM therapy. PMID: 28270494 [PubMed - as supplied by publisher]
Source: Clinical Cancer Research - March 6, 2017 Category: Cancer & Oncology Authors: Das DS, Das A, Ray A, Song Y, Samur MK, Munshi NC, Chauhan D, Anderson KC Tags: Clin Cancer Res Source Type: research

The FA/BRCA Pathway Identified as the Major Predictor of Cisplatin Response in Head and Neck Cancer by Functional Genomics
Patients with advanced stage head and neck squamous cell carcinoma (HNSCC) are often treated with cisplatin-containing chemoradiation protocols. Although cisplatin is an effective radiation sensitizer, it causes severe toxicity and not all patients benefit from the combination treatment. HNSCCs expectedly not responding to cisplatin may better be treated with surgery and postoperative radiation or cetuximab and radiation, but biomarkers to personalize chemoradiotherapy are not available. We performed an unbiased genome-wide functional genetic screen in vitro to identify genes that influence the response to cisplatin in HNS...
Source: Molecular Cancer Therapeutics - March 1, 2017 Category: Cancer & Oncology Authors: Martens-de Kemp, S. R., Brink, A., van der Meulen, I. H., de Menezes, R. X., te Beest, D. E., Leemans, C. R., van Beusechem, V. W., Braakhuis, B. J. M., Brakenhoff, R. H. Tags: Companion Diagnostics and Cancer Biomarkers Source Type: research

The functional status of DNA repair pathways determines the sensitization effect to cisplatin in non-small cell lung cancer cells
Conclusions Our results indicate that the functional status of DNA repair pathways determine the sensitivity of NSCLC cells to cisplatin. Direct targeting of the pathway that is involved in cisplatin resistance may be an effective strategy to surmount cisplatin resistance in NSCLC.
Source: Cellular Oncology - July 28, 2016 Category: Cancer & Oncology Source Type: research

Ranking novel cancer driving synthetic lethal gene pairs using TCGA data.
In this study, we propose an efficient and comprehensive in-silico pipeline to rank novel SL gene pairs by mining vast amounts of accumulated tumor high-throughput sequencing data in The Cancer Genome Atlas (TCGA), coupled with other protein interaction networks and cell line information. Our pipeline integrates three significant features, including mutation coverage in TCGA, driver mutation probability and the quantified cancer network information centrality, into a ranking model for SL gene pair identification, which is presented as the first learning-based method for SL identification. As a result, 107 potential SL gene...
Source: Oncotarget - July 21, 2016 Category: Cancer & Oncology Tags: Oncotarget Source Type: research

Abstract A164: The small molecule UAE inhibitor TAK-243 (MLN7243) prevents DNA damage repair and reduces cell viability/tumor growth when combined with radiation, carboplatin and docetaxel
Clinical results of VELCADE® (bortezomib) For Injection have prompted evaluation of other enzymes within the ubiquitin proteasome system (UPS) as druggable targets for human cancer. We have identified a first in class investigational drug, TAK-243 (MLN7243), which targets the ubiquitin activating enzyme, UAE (UBA1), an essential cellular enzyme responsible for activating > 99% of all cellular ubiquitin. Ubiquitin is involved in multiple cellular processes including ubiquitin-dependent protein turnover, cell cycle progression, regulation of apoptosis, protein localization and response to DNA damage. Experiments combi...
Source: Molecular Cancer Therapeutics - January 7, 2016 Category: Cancer & Oncology Authors: Milhollen, M. A., Shi, J., Traore, T., Huck, J., Sappal, D., Duffy, J., Lightcap, E., Ishii, Y., Ciavarri, J., Fleming, P., Bence, N., Hyer, M. L. Tags: Therapeutic Agents: Other: Poster Presentations - Proffered Abstracts Source Type: research

RNA interferences targeting the Fanconi anemia/BRCA pathway upstream genes reverse cisplatin resistance in drug-resistant lung cancer cells
Conclusion: Knockdown of FANCF, FANCL, or FANCD2 by RNAi could synergize the effect of cisplatin on suppressing cell proliferation in cisplatin-resistant lung cancer cells through inhibition of FA/BRCA pathway.
Source: Journal of Biomedical Science - September 18, 2015 Category: Biomedical Science Authors: Chun-Hua DaiJian LiPing ChenHe-Guo JiangMing WuYong-Chang Chen Source Type: research

Abstract 1656: MK-1775 (WEE1 inhibition) lacks efficacy against DNA repair deficient pancreatic cancer cells
Conclusions: These results support a paradigm in which identified high risk FA/BRCA2-mutated patients would not benefit from WEE1 inhibitor monotherapy; and thus, would most likely respond better to conventional DNA damaging agent-based therapies (e.g., oxaliplatin or MMC).Citation Format: Shruti Lal, Saswati N. Chand, Emanuela Dylgjeri, Charles J. Yeo, Jordan M. Winter, Jonathan R. Brody. MK-1775 (WEE1 inhibition) lacks efficacy against DNA repair deficient pancreatic cancer cells. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Phi...
Source: Cancer Research - August 2, 2015 Category: Cancer & Oncology Authors: Lal, S., Chand, S. N., Dylgjeri, E., Yeo, C. J., Winter, J. M., Brody, J. R. Tags: Experimental and Molecular Therapeutics Source Type: research

Abstract 3012: The Snm1B/Apollo DNA nuclease functions in resolution of replication stress and maintenance of genome stability
A critical aspect of normal cellular processes is the maintenance of genomic stability. Defects in cellular responses to DNA damage can lead to an accumulation of unrepaired or misrepaired lesions and ultimately, increased genome instability. Genomic DNA is constantly damaged through exposure to exogenous agents as well as during endogenous processes, including DNA replication. Progression of the replication fork can be impaired by structural or physical blocks leading to fork stalling. If stalled forks are not properly restarted or repaired, they can collapse, leading to chromosomal damage including breaks, deletions, and...
Source: Cancer Research - August 2, 2015 Category: Cancer & Oncology Authors: Das, I., Mason, J., Sekiguchi, J. Tags: Molecular and Cellular Biology Source Type: research

Abstract 3027: Investigating the function of NONO, a novel double strand break repair factor, and exploring its potential role as a biomarker for melanoma
We investigated the in vivo function of NONO, a protein that has been shown to promote a distinct sub-pathway of nonhomologous end joining (NHEJ) repair in vitro and in cultured cells. We used a gene trap strategy to create a null mutant for Nono, the mouse homolog of the human NONO gene. We investigated hematopoietic stem cells (HSCs), which are known to be sensitive to deficiencies in other DNA repair proteins. Nono-deficient mice showed reduced bone marrow and spleen cellularity. HSCs from Nono-deficient mice showed severe impairment in competitive repopulation assays in primary and secondary recipients. HSCs from Nono-...
Source: Cancer Research - August 2, 2015 Category: Cancer & Oncology Authors: Li, S., Shu, F., Khan, M. K., Pollack, B. P., Li, Z., McLemore, M., Dynan, W. S. Tags: Molecular and Cellular Biology Source Type: research

BRCA/Fanconi anemia pathway implicates chemoresistance to gemcitabine in biliary tract cancer
The BRCA/Fanconi anemia (FA) pathway plays a key role in the repair of DNA double strand breaks. We focused on this pathway to clarify chemoresistance mechanisms in biliary tract cancer (BTC). We also investigated changes in the CD24+/44+ population that may be involved in chemoresistance, as this population likely includes cancer stem cells. We used three BTC cell lines to establish gemcitabine (GEM)‐resistant (GR) cells and evaluated the expression of BRCA/FA pathway components, chemoresistance, and the effect of BRCA/FA pathway inhibition on the CD24+/44+ population. FANCD2 and CD24 expression were evaluated in 108 re...
Source: Cancer Science - April 22, 2015 Category: Cancer & Oncology Authors: Shinsuke Nakashima, Shogo Kobayashi, Hiroaki Nagano, Akira Tomokuni, Yoshito Tomimaru, Tadafumi Asaoka, Naoki Hama, Hiroshi Wada, Koichi Kawamoto, Shigeru Marubashi, Hidetoshi Eguchi, Yuichiro Doki, Masaki Mori Tags: Original Article Source Type: research

BRCA/Fanconi Anemia Pathway Implicates Chemo‐resistance to Gemcitabine in Biliary Tract Cancer
This article is protected by copyright. All rights reserved.
Source: Cancer Science - March 3, 2015 Category: Cancer & Oncology Authors: Shinsuke Nakashima, Shogo Kobayashi, Hiroaki Nagano, Akira Tomokuni, Yoshito Tomimaru, Tadafumi Asaoka, Naoki Hama, Hiroshi Wada, Koichi Kawamoto, Shigeru Marubashi, Hidetoshi Eguchi, Yuichiro Doki, Masaki Mori Tags: Original Article Source Type: research

Abstract 820: Inhibition of Rad6 sensitizes triple negative breast cancer cells to platinum-based therapy
Treatment of triple negative breast cancers (TNBCs) poses a clinical challenge because they are not treatable with therapies targeting estrogen receptor and Her2/neu as they lack expression of estrogen, progesterone, and Her2/neu receptors. Since TNBCs share several histologic features with BRCA1-related breast cancer, and these breast cancers have aberrant DNA repair, DNA repair pathways are thought to play a role in TNBC development and drug response. Platinum (Pt)-based compounds induce toxic interstrand DNA crosslinks (ICL), the repair of which requires activities of BRCA/Fanconi anemia (FA) network and Rad6 postreplic...
Source: Cancer Research - September 30, 2014 Category: Cancer & Oncology Authors: Haynes, B., Sanders, M., Shekhar, M. Tags: Experimental and Molecular Therapeutics Source Type: research

Abstract 2380: Separate but important roles of {alpha}SpII and FANCD2 in the FA pathway after DNA interstrand crosslink damage
Fanconi anemia (FA) is a genetic disorder characterized by bone marrow failure, an increased incidence of cancer, genomic instability, congenital abnormalities and a defect in ability to repair DNA interstrand crosslinks (ICLs). We have previously shown that FA cells have a deficiency in the structural protein, nonerythroid alpha spectrin (SpII), which is critical for repair of DNA ICLs and binds to crosslinked DNA. The FA protein, FANCD2, after monoubiquitination (FANCD2-Ub), has also been shown to be critical for ICL repair. However, the relationship between SpII and FANCD2 and whether they are involved in the same steps...
Source: Cancer Research - September 30, 2014 Category: Cancer & Oncology Authors: Lambert, M. W., Sridharan, D., Zhang, P. Tags: Molecular and Cellular Biology Source Type: research