Journal of cancer biology & research最新文献

Assessment of Breast Cancer Treatment Delay Impact on Prognosis and Survival: a Look at the Evidence from Systematic Analysis of the Literature. 乳腺癌治疗延迟对预后和生存影响的评估:基于文献系统分析的证据

Journal of cancer biology & research Pub Date : 2015-01-01 Epub Date: 2015-12-04

Faustine Williams

{"title":"Assessment of Breast Cancer Treatment Delay Impact on Prognosis and Survival: a Look at the Evidence from Systematic Analysis of the Literature.","authors":"Faustine Williams","doi":"","DOIUrl":"","url":null,"abstract":"Introduction: Breast cancer has remained the most commonly diagnosed disease among women globally. Despite the advancement in biomedical sciences leading to improve survival outcomes, some patients endure longer wait periods prior to initiation of treatment.Objective: To elucidate the impact of treatment delay on breast cancer patient's quality of life and survivorship. Second was to determine the optimal length of time (delay) between breast cancer diagnosis and start of first treatment in order to improve prognosis and general health and well-being of survivors.Methods: Systematic search of the literature was conducted across five electronic databases: Pub Med, EMBASE, CINAHL, Scopus and Science Direct as well as the reference list of all articles retrieved.Results: A total of 33 articles were included in the evidence based systematic review, which comprised of 255,366 observations. The results of the studies were categorized under five main themes as: study characteristics, cancer staging and classification, treatment delay time definition and interval, treatment regimen classification and delay impact on quality of life and survival. Analyzed wait times from diagnosis to the initiation of first therapy ranged from 7 days to a period of over 180 days. Combinations of standardized treatment including loco-regional radiotherapy, systemic chemotherapy surgery as well as hormonal therapy were examined. Even though some of the studies showed mixed results, overall, findings indicated that early detection, diagnosis and initiation of treatment within 90 days increase survival.Conclusions: Evidence revealed that delaying the initiation of treatment for breast cancer more than 90 days after diagnosis has a detrimental effect on disease free and overall well-being of survivors.","PeriodicalId":90581,"journal":{"name":"Journal of cancer biology & research","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2015-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8274552/pdf/nihms-1607067.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39183552","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Cross-Phosphorylation and Interaction between Src/FAK and MAPKAP5/PRAK in Early Focal Adhesions Controls Cell Motility. Src/FAK和MAPKAP5/PRAK在早期局灶粘连中的交叉磷酸化和相互作用控制细胞运动。

Journal of cancer biology & research Pub Date : 2014-05-14

Sheila Figel Dwyer, Irwin H Gelman

{"title":"Cross-Phosphorylation and Interaction between Src/FAK and MAPKAP5/PRAK in Early Focal Adhesions Controls Cell Motility.","authors":"Sheila Figel Dwyer, Irwin H Gelman","doi":"","DOIUrl":"","url":null,"abstract":"P38-regulated and activated kinase (PRAK/MAPKAPK5) is a serine/threonine kinase which lies downstream of the p38 and ERK3/4 MAP kinase pathways. PRAK plays diverse roles in the processes of cell growth, nutrient starvation response, programmed cell death, senescence and motility. PRAK has been shown to both promote and inhibit cell motility in different contexts. The pro-motility functions of PRAK are attributed mainly to cytoskeletal rearrangement occurring downstream of its phosphorylated substrate HSP27; however, it was recently shown that PRAK is required for motility in endothelial cells upstream of Focal adhesion kinase (FAK). Along with Src, FAK functions as a mediator of motility signaling through the phosphorylation of substrates in focal adhesions. Here, we show that PRAK, initially identified as a FAK substrate in an in situ/ kinase overlay assay, is a Src substrate, the phosphorylation of which directs PRAK to focal adhesions. Focal adhesion localization of PRAK was not found to affect cell motility, however transient over expression of PRAK inhibited motility in HeLa cells. This effect requires PRAK kinase activity and proceeds through an impairment of FAK activation via phosphorylation on Y861. Our studies demonstrate for the first time that PRAK is regulated by tyrosine phosphorylation, localizes to focal adhesions, and interacts physically with and can phosphorylate FAK/Src. Further we provide a novel mechanism for the inhibition of motility downstream of PRAK.","PeriodicalId":90581,"journal":{"name":"Journal of cancer biology & research","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2014-05-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4450445/pdf/nihms693479.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"33361358","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Multiple Mechanisms Contribute To Telomere Maintenance. 多种机制有助于端粒维护。

Journal of cancer biology & research Pub Date : 2013-11-19

Tammy A Morrish, Dulat Bekbolysnov, David Velliquette, Michelle Morgan, Bryan Ross, Yongheng Wang, Benjamin Chaney, Jessica McQuigg, Nathan Fager, Ira P Maine

{"title":"Multiple Mechanisms Contribute To Telomere Maintenance.","authors":"Tammy A Morrish, Dulat Bekbolysnov, David Velliquette, Michelle Morgan, Bryan Ross, Yongheng Wang, Benjamin Chaney, Jessica McQuigg, Nathan Fager, Ira P Maine","doi":"","DOIUrl":"","url":null,"abstract":"The unlimited growth potential of tumors depends on telomere maintenance and typically depends on telomerase, an RNA-dependent DNA polymerase, which reverse transcribes the telomerase RNA template, synthesizing telomere repeats at the ends of chromosomes. Studies in various model organisms genetically deleted for telomerase indicate that several recombination-based mechanisms also contribute to telomere maintenance. Understanding the molecular basis of these mechanisms is critical since some human tumors form without telomerase, yet the sequence is maintained at the telomeres. Recombination-based mechanisms also likely contribute at some frequency to telomere maintenance in tumors expressing telomerase. Preventing telomere maintenance is predicted to impact tumor growth, yet inhibiting telomerase may select for the recombination-based mechanisms. Telomere recombination mechanisms likely involve altered or unregulated pathways of DNA repair. The use of some DNA damaging agents may encourage the use of these unregulated pathways of DNA repair to be utilized and may allow some tumors to generate resistance to these agents depending on which repair pathways are altered in the tumors. This review will discuss the various telomere recombination mechanisms and will provide rationale regarding the possibility that L1 retrotransposition may contribute to telomere maintenance in tumors lacking telomerase.","PeriodicalId":90581,"journal":{"name":"Journal of cancer biology & research","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2013-11-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4181876/pdf/nihms628633.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"32722320","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

The Potential Role of BRCA1-Associated ATM Activator-1 (BRAT1) in Regulation of mTOR. BRCA1-Associated ATM Activator-1 (BRAT1)在mTOR调控中的潜在作用

Journal of cancer biology & research Pub Date : 2013-07-01

Eui Young So, Toru Ouchi

引用次数: 0

Roles of DNA Damage Response Proteins in Mitogen-Induced Thp-1 Differentiation into Macrophage. DNA损伤反应蛋白在丝裂原诱导Thp-1向巨噬细胞分化中的作用。

Journal of cancer biology & research Pub Date : 2013-07-01

Eui Young So, Martin Kozicki, Toru Ouchi

引用次数: 0