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Translational Oncogenomics

Hariyono Winarto, Marselina Irasonia Tan, Mohamad Sadikin, Septelia Inawati Wanandi
Oxidative stress is considered an important factor in the development of endometriosis, including its malignant transformation. Previous studies have found that AT-rich interactive domain 1A (ARID1A), a tumor suppressor gene, is frequently mutated and inactivated in endometriosis-associated ovarian cancer (EAOC), and such a change in this gene is considered an early event in malignant transformation. We observed oxidative stress status by measuring the activity of the antioxidant enzyme manganese superoxide dismutase (MnSOD), malondialdehyde (MDA), and ARID1A gene expression in tissue samples from patients with endometriosis, EAOC, or non-endometriosis-associated ovarian cancer (non-EAOC)...
2017: Translational Oncogenomics
Yesim Eralp
Recent advances in genomic technology have led to considerable improvement in our understanding of the molecular basis that underpins breast cancer biology. Through the use of comprehensive whole genome genomic profiling by next-generation sequencing, an unprecedented bulk of data on driver mutations, key genomic rearrangements, and mechanisms on tumor evolution has been generated. These developments have marked the beginning of a new era in oncology called "personalized or precision medicine." Elucidation of biologic mechanisms that underpin carcinogenetic potential and metastatic behavior has led to an inevitable explosion in the development of effective targeted agents, many of which have gained approval over the past decade...
2016: Translational Oncogenomics
Debra H Josephs, Debashis Sarker
The phosphatidylinositol 3-kinase (PI3K) signaling pathway is integral to many essential cell processes, including cell growth, differentiation, proliferation, motility, and metabolism. Somatic mutations and genetic amplifications that result in activation of the pathway are frequently detected in cancer. This has led to the development of rationally designed therapeutics targeting key members of the pathway. Critical to the successful development of these drugs are pharmacodynamic biomarkers that aim to define the degree of target and pathway inhibition...
2015: Translational Oncogenomics
Aastha Arora, Saurabh Singh, Anant Narayan Bhatt, Sanjay Pandey, Rajat Sandhir, Bilikere S Dwarakanath
Cancer is a complex disease that arises from the alterations in the composition and regulation of several genes leading to the disturbances in signaling pathways, resulting in the dysregulation of cell proliferation and death as well as the ability of transformed cells to invade the host tissue and metastasize. It is increasingly becoming clear that metabolic reprograming plays a critical role in tumorigenesis and metastasis. Therefore, targeting this phenotype is considered as a promising approach for the development of therapeutics and adjuvants...
2015: Translational Oncogenomics
Ingrid Garajová, Elisa Giovannetti, Guido Biasco, Godefridus J Peters
MET and its ligand HGF are involved in many biological processes, both physiological and pathological, making this signaling pathway an attractive therapeutic target in oncology. Downstream signaling effects are transmitted via mitogen-activated protein kinase (MAPK), PI3K (phosphoinositide 3-kinase protein kinase B)/AKT, signal transducer and activator of transcription proteins (STAT), and nuclear factor-κB. The final output of the terminal effector components of these pathways is activation of cytoplasmic and nuclear processes leading to increases in cell proliferation, survival, mobilization and invasive capacity...
2015: Translational Oncogenomics
Juanita Lopez, Sam Harris, Desam Roda, Timothy A Yap
Precision medicine in oncology promises the matching of genomic, molecular, and clinical data with underlying mechanisms of a range of novel anticancer therapeutics to develop more rational and effective antitumor strategies in a timely manner. However, despite the remarkable progress made in the understanding of novel drivers of different oncogenic processes, success rates for the approval of oncology drugs remain low with substantial fiscal consequences. In this article, we focus on how recent rapid innovations in technology have brought greater clarity to the biological and clinical complexities of different cancers and advanced the development of molecularly targeted agents and immunotherapies in clinical trials...
2015: Translational Oncogenomics
Laura D Hover, Ty W Abel, Philip Owens
Glioblastoma multiforme (GBM) is a grade IV glioma with a median survival of 15 months. Recently, bone morphogenetic protein (BMP) signaling has been shown to promote survival in xenograft murine models. To gain a better understanding of the role of BMP signaling in human GBMs, we examined the genomic alterations of 90 genes associated with BMP signaling in GBM patient samples. We completed this analysis using publically available datasets compiled through Te Cancer Genome Atlas and the Glioma Molecular Diagnostic Initiative...
2015: Translational Oncogenomics
Cody Weston, James Connor
Proteins involved in iron regulation are modifiers of cancer risk and progression. Of these, the HFE protein (high iron gene and its protein product) is of particular interest because of its interaction with both iron handling and immune function and the high rate of genetic polymorphisms resulting in a mutant protein. Clinical studies suggest that HFE polymorphisms increase the risk of certain cancers, but the inconsistent outcomes suggest a more nuanced effect, possibly interacting with other genetic or environmental factors...
2014: Translational Oncogenomics
Daochun Sun, Michael A Tainsky, Ramsi Haddad
Malignant peripheral nerve sheath tumors (MPNST) are a type of soft tissue sarcoma that can be associated with germline mutations in Neurofibromatosis type 1 (NF1) or may occur sporadically. Although the etiology of MPNST is poorly understood, it is clear that a loss of function of the NF1 gene, encoding a Ras-GAP, is an important factor in the tumorigenesis of the inherited form of MPNST. Tumor latency in NF1 patients suggests that additional mutational events are probably required for malignancy. In order to define oncogene mutations associated with 5 MPNST cell lines, we assayed the 238 most frequent mutations in 19 commonly activated oncogenes using mass spectroscopy-based analysis...
2012: Translational Oncogenomics
Haneef Awan, Viggo Jønsson, Tom B Johannesen, Bernt Ly, Geir E Tjønnfjord
Fifty-one parent-offspring pairs with chronic lymphocytic leukemia (CLL) or other lymphoproliferative disorders (nonCLL) such as malignant lymphoma, multiple myeloma, or other types of lymphocytic leukemia than CLL were ascertained independently in 38 families. There were 30 CLL-CLL parent-offspring pairs and 21 pairs with nonCLL in parents and/or in offspring. The median age of onset of disease was 13 years lower in the offspring than in the parents when comparing all 51 pairs (P < 0.001). This difference was mainly caused by a significantly lower age at onset in offspring with parental nonCLL (P < 0...
2010: Translational Oncogenomics
Joseph Z Zaretsky, Daniel H Wreschner
In the review, the nature of protein multifunctionality is analyzed. In the first part of the review the principles of structural/functional organization of protein are discussed. In the second part, the main mechanisms involved in development of multiple functions on a single gene product(s) are analyzed. The last part represents a number of examples showing that multifunctionality is a basic feature of biologically active proteins.
2008: Translational Oncogenomics
Patricia Gangoiti, Maria H Granado, Alicia Alonso, Félix M Goñi, Antonio Gómez-Muñoz
In the last two decades there has been considerable progress in our understanding of the role of sphingolipids in controlling signal transduction processes, particularly in the mechanisms leading to regulation of cell growth and death. Ceramide is a well-characterized sphingolipid metabolite and second messenger that can be produced by cancer cells in response to a variety of stimuli, including therapeutic drugs, leading to cell cycle arrest and apoptosis. Although this is a promising aspect when thinking of treating cancer, it should be borne in mind that ceramide production may not always be a growth inhibitory or pro-apoptotic signal...
2008: Translational Oncogenomics
Shreeram C Nallar, Sudhakar Kalakonda, Peng Sun, Dhan V Kalvakolanu
Gene associated with retinoid-interferon-β-induced mortality (GRIM)-19, was originally identified as a critical regulatory protein necessary for Interferon-β-Retinoic acid-induced cell death. Overexpression of GRIM-19 activates cell death and its suppression or inactivation promotes cell growth. GRIM-19 targets multiple proteins/pathways for exerting growth control and cell death. However, GRIM-19 is also required for normal cellular processes. In addition, viruses 'hijack' GRIM-19 for their survival. Intracellular bacterial infections and bacterial products have been reported to induce the expression of GRIM-19...
2008: Translational Oncogenomics
Yan Dai, Douglas V Faller
Sirtuins are NAD(+)-dependent histone deacetylases (Class III HDACs). Recently, Sirtuins have been shown to play important roles, both direct and indirect, in transcriptional regulation. This transcriptional control, through incorporation of Sirtuins into transcription complexes and deacetylation of histones locally at gene promoters, or direct interaction with specific transcription factors, is central to the participation of Sirtuins in multiple diverse processes, including aging, apoptosis, hormone responses, stress tolerance, differentiation, metabolism and development...
2008: Translational Oncogenomics
Takayuki Masaki, Hironobu Yoshimatsu
A great amount of literature has demonstrated a connection between obesity, visceral fat and the metabolic disorders such as hyperglycemia, hypertension, and hyperlipidemia. Lately, there has been an increased interest in understanding if cancer is related to obesity and visceral fat accumulation. The prevalence of both obesity and cancer are increasing and there has been keen interest in the relationship between visceral adiposity and the biology of cancers. White adipose tissue (WAT) provides a limitless capacity for triglyceride storage vital for survival...
2008: Translational Oncogenomics
Sudeep K Bose, Rebecca S Bullard, Carlton D Donald
Prostate cancer is the second leading cause of cancer death among men in the United States of America. However, the molecular mechanisms underlying the disease remain largely unknown. Therefore, the identification of tumor specific molecules that serve as targets for the development of new cancer drugs is considered to be a major goal in cancer research. The mouse Engrailed-2 (En-2) gene, which is a homeobox-containing transcription factor was recently identified as a candidate oncogene in breast cancer. Here, we demonstrate that En-2 is over-expressed in human prostate cancer cells as compared to normal prostate epithelial cells...
2008: Translational Oncogenomics
Sheng Wang, Douglas V Faller
Tumor formation results from alterations in the normal control of cell proliferation. In the past decade, much attention in cancer research has been focused on the function of proto-oncogenes and tumor suppressors. Prohibitin is a potential tumor suppressor which was originally identified because of its anti-proliferative activities. Subsequent investigations led to the discovery of prohibitin mutations in sporadic breast cancers. Recent studies established that prohibitin directly regulates E2F-mediated transcription and growth suppression Prohibitin further attracted the attention of the translational cancer research community when it was recently connected to the regulation of estrogen receptor and androgen receptor activity...
2008: Translational Oncogenomics
Viggo Jønsson, Geir E Tjønnfjord, Tom B Johannesen, Sven Ove Samuelsen, Bernt Ly
Based on the concept that the tumorogenesis in chronic lymphocytic leukaemia comprises both an initial, inherited mutation and subsequent somatic mutations, the pleiotypic diversity of familial chronic lymphocytic leukaemia and related malignant lymphoproliferative disorders is generally explained by a repertoire of monoallelic polygenes in the initial mutation. Epigenetic genomic imprinting is a likely mechanism behind of the asynchroneous replicating monoallelic polygenes which is discussed in the light of pleiotrophy and birth order effect...
2008: Translational Oncogenomics
Tobias Gremmel, Susanne Wild, Winfried Schuller, Viola Kürten, Klaus Dietz, Jean Krutmann, Mark Berneburg
Xeroderma pigmentosum (XP) is a genetic disorder characterised by hypo-/hyperpigmentation, increased sensitivity to ultraviolet (UV)-radiation and an up to 2000-fold increased skin cancer risk. Cells from XP-patients are defective in nucleotide excision repair (NER) responsible for repair of UV-induced DNA damage. This defect accounts for their mutator phenotype but does not predict their increased skin cancer risk. Therefore, we carried out array analysis to measure the expression of more than 1000 genes after UVB-irradiation in XP cells from three complementation groups with different clinical severity (XP-A, XP-D, XP-F) as well as from patients with normal DNA repair but increased skin cancer risk (≥2 basal or squamous cell carcinoma at age <40yrs)...
2008: Translational Oncogenomics
Merav Bar, Derek Stirewalt, Era Pogosova-Agadjanyan, Vitas Wagner, Ted Gooley, Nissa Abbasi, Ravi Bhatia, H Joachim Deeg, Jerald Radich
The myelodysplastic syndromes (MDS) are clonal stem cell disorders, characterized by ineffective and dysplastic hematopoiesis. The genetic and epigenetic pathways that determine disease stage and progression are largely unknown. In the current study we used gene expression microarray methodology to examine the gene expression differences between normal hematopoietic cells and hematopoietic cells from patients with MDS at different disease stages, using both unselected and CD34+ selected cells. Significant differences between normal and MDS hematopoietic cells were observed for several genes and pathways...
2008: Translational Oncogenomics
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