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https://www.readbyqxmd.com/read/28993779/natural-killer-cell-response-to-chemotherapy-stressed-cancer-cells-role-in-tumor-immunosurveillance
#1
REVIEW
Alessandra Zingoni, Cinzia Fionda, Cristiana Borrelli, Marco Cippitelli, Angela Santoni, Alessandra Soriani
Natural killer (NK) cells are innate cytotoxic lymphoid cells that actively prevent neoplastic development, growth, and metastatic dissemination in a process called cancer immunosurveillance. An equilibrium between immune control and tumor growth is maintained as long as cancer cells evade immunosurveillance. Therapies designed to kill cancer cells and to simultaneously sustain host antitumor immunity are an appealing strategy to control tumor growth. Several chemotherapeutic agents, depending on which drugs and doses are used, give rise to DNA damage and cancer cell death by means of apoptosis, immunogenic cell death, or other forms of non-apoptotic death (i...
2017: Frontiers in Immunology
https://www.readbyqxmd.com/read/28969871/alternative-lengthening-of-telomeres-dna-repair-pathways-converge
#2
REVIEW
Alexander P Sobinoff, Hilda A Pickett
Telomeres shorten during each cellular division, with cumulative attrition resulting in telomeric damage and replicative senescence. Bypass of replicative senescence precipitates catastrophic telomere shortening or crisis, and is characterized by widespread genomic instability. Activation of a telomere maintenance mechanism (TMM) is necessary to stabilise the genome and establish cellular immortality through the reconstitution of telomere capping function. The alternative lengthening of telomeres (ALT) pathway is a TMM frequently activated in tumors of mesenchymal or neuroepithelial origin...
September 29, 2017: Trends in Genetics: TIG
https://www.readbyqxmd.com/read/28966990/a-crispr-view-of-gene-regulation
#3
Budhaditya Banerjee, Richard I Sherwood
Due to plummeting costs, whole genome sequencing of patients and cancers will soon become routine medical practice; however, we cannot currently predict how non-coding genotype affects cellular gene expression. Gene regulation research has recently been dominated by observational approaches that correlate chromatin state with regulatory function. These approaches are limited to the available genotypes and cannot scratch the surface of possible sequence combinations, and thus there is a need for perturbation-based approaches to better understand how DNA encodes gene regulatory functions...
February 2017: Current opinion in systems biology
https://www.readbyqxmd.com/read/28947971/dynamic-circulating-tumor-dna-quantificaton-for-the-individualization-of-non-small-cell-lung-cancer-patients-treatment
#4
Mariano Provencio, María Torrente, Virgina Calvo, Lourdes Gutiérrez, David Pérez-Callejo, Clara Pérez-Barrios, Miguel Barquín, Ana Royuela, Begoña Rodriguez-Alfonso, Miguel Sotelo, Juan Luis Cruz-Bermúdez, Miriam Mendez, Alberto Cruz-Bermúdez, Atocha Romero
BACKGROUND: Liquid biopsy has evolved from being a promising line to becoming a validated approach for biomarker testing. However, its utility for individualization of therapy has been scarcely reported. In this study, we show how monitoring levels of EGFR mutation in plasma can be useful for the individualization of treatment. RESULTS: Longitudinal EGFR mutation levels in plasma always correlated with tumor response ascertained by RECIST criteria. Moreover, decreasing EGFR mutation levels were detected in all patients benefiting from locoregional radiotherapy, whereas the opposite occurred when a patient progressed soon after radiotherapy treatment...
September 1, 2017: Oncotarget
https://www.readbyqxmd.com/read/28927527/dna-mismatch-repair-and-its-many-roles-in-eukaryotic-cells
#5
REVIEW
Dekang Liu, Guido Keijzers, Lene Juel Rasmussen
DNA mismatch repair (MMR) is an important DNA repair pathway that plays critical roles in DNA replication fidelity, mutation avoidance and genome stability, all of which contribute significantly to the viability of cells and organisms. MMR is widely-used as a diagnostic biomarker for human cancers in the clinic, and as a biomarker of cancer susceptibility in animal model systems. Prokaryotic MMR is well-characterized at the molecular and mechanistic level; however, MMR is considerably more complex in eukaryotic cells than in prokaryotic cells, and in recent years, it has become evident that MMR plays novel roles in eukaryotic cells, several of which are not yet well-defined or understood...
July 2017: Mutation Research
https://www.readbyqxmd.com/read/28798901/translational-dysregulation-in-cancer-molecular-insights-and-potential-clinical-applications-in-biomarker-development
#6
REVIEW
Christos Vaklavas, Scott W Blume, William E Grizzle
Although transcript levels have been traditionally used as a surrogate measure of gene expression, it is increasingly recognized that the latter is extensively and dynamically modulated at the level of translation (messenger RNA to protein). Over the recent years, significant progress has been made in dissecting the complex posttranscriptional mechanisms that regulate gene expression. This advancement in knowledge came hand in hand with the progress made in the methodologies to study translation both at gene-specific as well as global genomic level...
2017: Frontiers in Oncology
https://www.readbyqxmd.com/read/28757314/using-ion-torrent-sequencing-to-study-genetic-mutation-profiles-of-fatal-thyroid-cancers
#7
Jin-Ying Lu, Wern-Cherng Cheng, Kuen-Yuan Chen, Chia-Chi Lin, Ching-Chung Chang, Kuan-Ting Kuo, Pei-Lung Chen
BACKGROUND/PURPOSE: Surgery followed by radioiodine is a mainstay of treatment for thyroid cancers of follicular origins. However, about 5% of the thyroid cancers are non-operable and/or radioiodine-refractory diseases, which are either locally advanced or metastatic and result in a survival of less than 5 years. How to treat this population of thyroid cancer patients becomes a critical issue requiring further understanding of the tumor's genetic information. METHODS: We used formalin-fixed paraffin-embedded specimens of 22 fatal thyroid cancers and their corresponding non-tumor parts, if available, to yield genomic DNA, and applied the Ion Torrent™ Personal Genome Machine (IT-PGM) System (Life Technologies), a next generation sequencing technology, to interrogate 740 mutational hotspots in 46 oncogenes...
July 27, 2017: Journal of the Formosan Medical Association, Taiwan Yi Zhi
https://www.readbyqxmd.com/read/28738540/regulatory-players-of-dna-damage-repair-mechanisms-role-in-cancer-chemoresistance
#8
REVIEW
Kunnathur Murugesan Sakthivel, Sreedharan Hariharan
DNA damaging agents are most common in chemotherapeutic molecules that act against cancer. However, cancer cells possess inherent biological features to overcome DNA damages by activating various distinct repair mechanisms and pathways. Importantly, various oncogenes, cancer stem cells (CSCs), hypoxic environment, transcription factors and bystander signaling that are activated in the cancer cells influence DNA repair, thereby effectively repairing the DNA damage. Repaired cancer cells often become more resistance to further therapy and results in disease recurrence...
September 2017: Biomedicine & Pharmacotherapy, Biomédecine & Pharmacothérapie
https://www.readbyqxmd.com/read/28738408/cgas-surveillance-of-micronuclei-links-genome-instability-to-innate-immunity
#9
Karen J Mackenzie, Paula Carroll, Carol-Anne Martin, Olga Murina, Adeline Fluteau, Daniel J Simpson, Nelly Olova, Hannah Sutcliffe, Jacqueline K Rainger, Andrea Leitch, Ruby T Osborn, Ann P Wheeler, Marcin Nowotny, Nick Gilbert, Tamir Chandra, Martin A M Reijns, Andrew P Jackson
DNA is strictly compartmentalized within the nucleus to prevent autoimmunity; despite this, cyclic GMP-AMP synthase (cGAS), a cytosolic sensor of double-stranded DNA, is activated in autoinflammatory disorders and by DNA damage. Precisely how cellular DNA gains access to the cytoplasm remains to be determined. Here, we report that cGAS localizes to micronuclei arising from genome instability in a mouse model of monogenic autoinflammation, after exogenous DNA damage and spontaneously in human cancer cells. Such micronuclei occur after mis-segregation of DNA during cell division and consist of chromatin surrounded by its own nuclear membrane...
August 24, 2017: Nature
https://www.readbyqxmd.com/read/28723516/the-molecular-evolution-of-castration-resistant-prostate-cancer
#10
REVIEW
Yvonne Ceder, Anders Bjartell, Zoran Culig, Mark A Rubin, Scott Tomlins, Tapio Visakorpi
CONTEXT: Androgen deprivation therapy (ADT) is the backbone of treatment for advanced prostate cancer. However, castration-resistant prostate cancer (CRPC) nearly invariably develops through a range of different molecular mechanisms accompanied by progression to a more aggressive phenotype. OBJECTIVE: To understand the key molecular mechanisms leading to CRPC and the functional implications of this progression. Understanding molecular evolutionary mechanisms in CRPC is essential for the development of novel curative therapeutic approaches...
December 2016: European Urology Focus
https://www.readbyqxmd.com/read/28521333/drugging-the-cancers-addicted-to-dna-repair
#11
REVIEW
Jac A Nickoloff, Dennie Jones, Suk-Hee Lee, Elizabeth A Williamson, Robert Hromas
Defects in DNA repair can result in oncogenic genomic instability. Cancers occurring from DNA repair defects were once thought to be limited to rare inherited mutations (such as BRCA1 or 2). It now appears that a clinically significant fraction of cancers have acquired DNA repair defects. DNA repair pathways operate in related networks, and cancers arising from loss of one DNA repair component typically become addicted to other repair pathways to survive and proliferate. Drug inhibition of the rescue repair pathway prevents the repair-deficient cancer cell from replicating, causing apoptosis (termed synthetic lethality)...
November 1, 2017: Journal of the National Cancer Institute
https://www.readbyqxmd.com/read/28500256/tzap-ing-telomeres-down-to-size
#12
Laura Garcia-Exposito, Roderick J O'Sullivan
The phenomenon of gradual telomere shortening has become a paradigm for how we understand the biology of aging and cancer. Cell proliferation is accompanied by cumulative telomere loss, and the aged cell either senesces, dies or transforms toward cancer. This transformation requires the activation of telomere elongation mechanisms in order to restore telomere length such that cell death or senescence programs are not induced. Most of the time, this occurs through telomerase reactivation. In other rare cases, the Alternative lengthening of telomeres (ALT) pathway hijacks DNA recombination-associated mechanisms to hyperextend telomeres, often to more than 50 kb...
June 2017: EMBO Reports
https://www.readbyqxmd.com/read/28415565/rad52-deficiency-decreases-development-of-lung-squamous-cell-carcinomas-by-enhancing-immuno-surveillance
#13
Rachel Lieberman, Jing Pan, Qi Zhang, Ming You
RAD52 is involved in homologous recombination and DNA repair. This study focuses on lung cancer progression and how the DNA repair gene, Rad52, enables tumor cells to have sufficient genome integrity, i.e., the ability to repair lethal DNA damage, to avoid cell death. In this report, we analyze the phenotypic differences between wild type and Rad52-/- in inhibition of tumor phenotypes including cell growth, viability, cytolysis, and immune profiling. We demonstrated that loss of Rad52 not only increases the death of cells undergoing carcinogen-induced transformation in vivo, but that Rad52 loss also augments in vivo antitumor activity through an enhanced capacity for direct killing of LLC tumor cells by stimulated Rad52-/- NK and CD8+ T cells...
May 23, 2017: Oncotarget
https://www.readbyqxmd.com/read/28378010/epigenetic-therapy-for-the-treatment-of-epithelial-ovarian-cancer-a-clinical-review
#14
REVIEW
Haller J Smith, J Michael Straughn, Donald J Buchsbaum, Rebecca C Arend
Despite a good initial response to chemotherapy, the majority of patients with epithelial ovarian cancer will eventually recur and die of their disease. The introduction of targeted therapies to traditional chemotherapy regimens has done little to improve overall survival in women with ovarian cancer. It has become increasingly apparent that the cancer epigenome contributes significantly to the pathogenesis of ovarian cancer and may play an important role in cell proliferation, metastasis, chemoresistance, and immune tolerance...
May 2017: Gynecologic Oncology Reports
https://www.readbyqxmd.com/read/28374555/understanding-cell-cycle-and-cell-death-regulation-provides-novel-weapons-against-human-diseases
#15
REVIEW
K G Wiman, B Zhivotovsky
Cell division, cell differentiation and cell death are the three principal physiological processes that regulate tissue homoeostasis in multicellular organisms. The growth and survival of cells as well as the integrity of the genome are regulated by a complex network of pathways, in which cell cycle checkpoints, DNA repair and programmed cell death have critical roles. Disruption of genomic integrity and impaired regulation of cell death may both lead to uncontrolled cell growth. Compromised cell death can also favour genomic instability...
May 2017: Journal of Internal Medicine
https://www.readbyqxmd.com/read/28344745/can-molecular-biomarkers-replace-a-clinical-risk-score-for-resectable-colorectal-liver-metastasis
#16
EDITORIAL
Torhild Veen, Kjetil Søreide
In resectable colorectal liver metastasis (CRLM) the role and use of molecular biomarkers is still controversial. Several biomarkers have been linked to clinical outcomes in CRLM, but none have so far become routine for clinical decision making. For several reasons, the clinical risk score appears to no longer hold the same predictive value. Some of the reasons include the ever expanding indications for liver resection, which now increasingly tend to involve extrahepatic disease, such as lung metastases (both resectable and non-resectable) and the shift in indication from "what is taken out" (e...
March 15, 2017: World Journal of Gastrointestinal Oncology
https://www.readbyqxmd.com/read/28323334/the-emerging-role-of-homologous-recombination-repair-and-parp-inhibitors-in-genitourinary-malignancies
#17
REVIEW
Kalen J Rimar, Phuoc T Tran, Richard S Matulewicz, Maha Hussain, Joshua J Meeks
As cells age and are exposed to genotoxic stress, preservation of the genomic code requires multiple DNA repair pathways to remove single-strand or double-strand breaks. Loss of function somatic genomic aberrations or germline deficiency in genes involved in DNA repair can result in acute cell death or, after a latency period, cellular transformation. Therapeutic exploitation of DNA repair by inhibition of poly (adenosine diphosphate [ADP]) ribose polymerases (PARP), a family of enzymes involved in the repair of single-strand and in some cases double-strand breaks, has become a novel cancer treatment...
June 1, 2017: Cancer
https://www.readbyqxmd.com/read/28291774/brca2-secondary-mutation-mediated-resistance-to-platinum-and-parp-inhibitor-based-therapy-in-pancreatic-cancer
#18
Michael J Pishvaian, Andrew V Biankin, Peter Bailey, David K Chang, Daniel Laheru, Christopher L Wolfgang, Jonathan R Brody
BACKGROUND: Pancreatic cancer has become the third leading cause of cancer death with minimal improvements in outcome for over 40 years. Recent trials of therapies that target-defective DNA maintenance using poly (ADP-ribose) polymerase (PARP) inhibitors are showing promising results, yet invariably patients recur and succumb to disease. Mechanisms of resistance to platinum-based and PARP inhibitor therapy in other cancer types include secondary mutations, which restore the integrity of DNA repair through an increasing number of different mechanisms...
April 11, 2017: British Journal of Cancer
https://www.readbyqxmd.com/read/28257429/early-mutation-bursts-in-colorectal-tumors
#19
Junsong Zhao, Matthew P Salomon, Darryl Shibata, Christina Curtis, Kimberly Siegmund, Paul Marjoram
Tumor growth is an evolutionary process involving accumulation of mutations, copy number alterations, and cancer stem cell (CSC) division and differentiation. As direct observation of this process is impossible, inference regarding when mutations occur and how stem cells divide is difficult. However, this ancestral information is encoded within the tumor itself, in the form of intratumoral heterogeneity of the tumor cell genomes. Here we present a framework that allows simulation of these processes and estimation of mutation rates at the various stages of tumor development and CSC division patterns for single-gland sequencing data from colorectal tumors...
2017: PloS One
https://www.readbyqxmd.com/read/27977688/regulation-of-the-human-telomerase-gene-tert-by-telomere-position-effect-over-long-distances-tpe-old-implications-for-aging-and-cancer
#20
Wanil Kim, Andrew T Ludlow, Jaewon Min, Jerome D Robin, Guido Stadler, Ilgen Mender, Tsung-Po Lai, Ning Zhang, Woodring E Wright, Jerry W Shay
Telomerase is expressed in early human development and then becomes silenced in most normal tissues. Because ~90% of primary human tumors express telomerase and generally maintain very short telomeres, telomerase is carefully regulated, particularly in large, long-lived mammals. In the current report, we provide substantial evidence for a new regulatory control mechanism of the rate limiting catalytic protein component of telomerase (hTERT) that is determined by the length of telomeres. We document that normal, young human cells with long telomeres have a repressed hTERT epigenetic status (chromatin and DNA methylation), but the epigenetic status is altered when telomeres become short...
December 2016: PLoS Biology
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