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https://www.readbyqxmd.com/read/29052136/human-t-cell-leukemia-virus-type-1-infection-and-adult-t-cell-leukemia
#1
Chi-Ping Chan, Kin-Hang Kok, Dong-Yan Jin
Human T-cell leukemia virus type 1 (HTLV-1) is the first retrovirus discovered to cause adult T-cell leukemia (ATL), a highly aggressive blood cancer. HTLV-1 research in the past 35 years has been most revealing in the mechanisms of viral oncogenesis. HTLV-1 establishes a lifelong persistent infection in CD4(+) T lymphocytes. The infection outcome is governed by host immunity. ATL develops in 2-5% of infected individuals 30-50 years after initial exposure. HTLV-1 encodes two oncoproteins Tax and HBZ, which are required for initiation of cellular transformation and maintenance of cell proliferation, respectively...
2017: Advances in Experimental Medicine and Biology
https://www.readbyqxmd.com/read/29050696/pharmacogenomics-in-acute-lymphoblastic-leukemia
#2
REVIEW
Shawn H R Lee, Jun J Yang
Pharmacogenomics is a fast-growing field of personalized medicine using a patient's genomic profile to determine drug disposition or response to drug therapy, in order to develop safer and more effective pharmacotherapy. Childhood acute lymphoblastic leukemia (ALL), being the most common malignancy in childhood, which is treated with uniform and standardized clinical trials, is remarkably poised for pharmacogenomic studies. In the last decade, unbiased genome-wide association studies have identified multiple germline risk factors that strongly modify host response to drug therapy...
September 2017: Best Practice & Research. Clinical Haematology
https://www.readbyqxmd.com/read/29050694/the-biology-of-philadelphia-chromosome-like-all
#3
REVIEW
Kathryn G Roberts
Philadelphia chromosome-like acute lymphoblastic leukemia (Ph-like ALL) is a recently described subtype of B-cell precursor ALL with a gene expression profile similar to Ph-positive ALL and a high frequency of IKZF1 alterations. The prevalence of Ph-like ALL increases with age, ranging from 10-15% of children to over 25% of young adults with ALL. It occurs more frequently in males and is associated with adverse clinical features including elevated minimal residual disease levels and poor survival in both children and adults...
September 2017: Best Practice & Research. Clinical Haematology
https://www.readbyqxmd.com/read/29050363/role-of-plzf-as-a-tumor-suppressor-in-prostate-cancer
#4
REVIEW
Yang Jin, Hatice Zeynep Nenseth, Fahri Saatcioglu
The promyelocytic leukemia zinc finger (PLZF), also known as ZBTB16 (Zinc Finger And BTB Domain Containing 16), is a transcription factor involved in the regulation of diverse biological processes, including cell proliferation, differentiation, organ development, stem cell maintenance and innate immune cell development. A number of recent studies have now implicated PLZF in cancer progression as a tumor suppressor. However, in certain cancer types, PLZF may function as an oncoprotein. Here, we summarize our current knowledge on the role of PLZF in various cancer types, in particular prostate cancer, including its deregulation, genomic alterations and potential functions in prostate cancer progression...
September 19, 2017: Oncotarget
https://www.readbyqxmd.com/read/29050359/next-generation-sequencing-in-chronic-lymphocytic-leukemia-recent-findings-and-new-horizons
#5
REVIEW
Ana E Rodríguez-Vicente, Vasilis Bikos, María Hernández-Sánchez, Jitka Malcikova, Jesús-María Hernández-Rivas, Sarka Pospisilova
The rapid progress in next-generation sequencing technologies has significantly contributed to our knowledge of the genetic events associated with the development, progression and treatment resistance of chronic lymphocytic leukemia patients. Together with the discovery of new driver mutations, next-generation sequencing has revealed an immense degree of both intra- and inter-tumor heterogeneity and enabled us to describe marked clonal evolution. Advances in immunogenetics may be implemented to detect minimal residual disease more sensitively and to track clonal B cell populations, their dynamics and molecular characteristics...
September 19, 2017: Oncotarget
https://www.readbyqxmd.com/read/29048660/canonical-and-non-canonical-wnt-signaling-in-cancer-stem-cells-and-their-niches-cellular-heterogeneity-omics-reprogramming-targeted-therapy-and-tumor-plasticity-review
#6
Masaru Katoh
Cancer stem cells (CSCs), which have the potential for self-renewal, differentiation and de-differentiation, undergo epigenetic, epithelial-mesenchymal, immunological and metabolic reprogramming to adapt to the tumor microenvironment and survive host defense or therapeutic insults. Intra-tumor heterogeneity and cancer-cell plasticity give rise to therapeutic resistance and recurrence through clonal replacement and reactivation of dormant CSCs, respectively. WNT signaling cascades cross-talk with the FGF, Notch, Hedgehog and TGFβ/BMP signaling cascades and regulate expression of functional CSC markers, such as CD44, CD133 (PROM1), EPCAM and LGR5 (GPR49)...
September 19, 2017: International Journal of Oncology
https://www.readbyqxmd.com/read/29045844/a-b-cell-regulome-links-notch-to-downstream-oncogenic-pathways-in-small-b-cell-lymphomas
#7
Russell J H Ryan, Jelena Petrovic, Dylan M Rausch, Yeqiao Zhou, Caleb A Lareau, Michael J Kluk, Amanda L Christie, Winston Y Lee, Daniel R Tarjan, Bingqian Guo, Laura K H Donohue, Shawn M Gillespie, Valentina Nardi, Ephraim P Hochberg, Stephen C Blacklow, David M Weinstock, Robert B Faryabi, Bradley E Bernstein, Jon C Aster, Warren S Pear
Gain-of-function Notch mutations are recurrent in mature small B cell lymphomas such as mantle cell lymphoma (MCL) and chronic lymphocytic leukemia (CLL), but the Notch target genes that contribute to B cell oncogenesis are largely unknown. We performed integrative analysis of Notch-regulated transcripts, genomic binding of Notch transcription complexes, and genome conformation data to identify direct Notch target genes in MCL cell lines. This B cell Notch regulome is largely controlled through Notch-bound distal enhancers and includes genes involved in B cell receptor and cytokine signaling and the oncogene MYC, which sustains proliferation of Notch-dependent MCL cell lines via a Notch-regulated lineage-restricted enhancer complex...
October 17, 2017: Cell Reports
https://www.readbyqxmd.com/read/29043205/an-extremely-rare-case-of-concurrent-braf-v600e-mutation-driven-hairy-cell-leukemia-and-melanoma-case-report-and-review-of-literature
#8
Amir Ghorbani-Aghbolaghi, Mirna Lechpammer, Saba F Ali, Nam K Ku, Denis M Dwyre, Hooman H Rashidi
BRAF protein is a serine/threonine kinase with 766 amino acids. Approximately 15% of human cancers harbor BRAF mutations as well as other BRAF anomalies (amplifications, fusions). Somatic mutations mainly occur in the catalytic kinase domain (CR3), and the predominant mutation is p.V600E which is the substitution of glutamic acid (E) for valine (V) as result of a mutation at codon 600 of the kinase domain. To our knowledge, the vast majority of the cancers have non-germline BRAF mutations. Here we describe a case of a 60-year-old female with a history of hairy cell leukemia (HCL) who presented with aphasia and forgetfulness...
July 2017: Autopsy & case reports
https://www.readbyqxmd.com/read/29039115/genome-editing-technologies-in-adoptive-t-cell-immunotherapy-for-cancer
#9
REVIEW
Nathan Singh, Junwei Shi, Carl H June, Marco Ruella
PURPOSE OF REVIEW: In this review, we discuss the most recent developments in gene-editing technology and discuss their application to adoptive T cell immunotherapy. RECENT FINDINGS: Engineered T cell therapies targeting cancer antigens have demonstrated significant efficacy in specific patient populations. Most impressively, CD19-directed chimeric antigen receptor T cells (CART19) have led to impressive responses in patients with B-cell leukemia and lymphoma. CTL019, or KYMRIAH™ (tisagenlecleucel), a CD19 CAR T cell product developed by Novartis and the University of Pennsylvania, was recently approved for clinical use by the Food and Drug Administration, representing a landmark in the application of adoptive T cell therapies...
October 16, 2017: Current Hematologic Malignancy Reports
https://www.readbyqxmd.com/read/29035575/hetfhmm-a-novel-approach-to-infer-tumor-heterogeneity-using-factorial-hidden-markov-models
#10
Mohammad S Rahman, Ann E Nicholson, Gholamreza Haffari
Cancer arises from successive rounds of mutations, resulting in tumor cells with different somatic mutations known as clones. Drug responsiveness and therapeutics of cancer depend on the accurate detection of clones in a tumor sample. Recent research has considered inferring clonal composition of a tumor sample using computational models based on short read data of the sample generated using next-generation sequencing (NGS) technology. Short reads (segmented DNA parts of different tumor cells) are noisy; therefore, inferring the clones and their mutations from the data is a difficult and complex problem...
October 16, 2017: Journal of Computational Biology: a Journal of Computational Molecular Cell Biology
https://www.readbyqxmd.com/read/29033451/dasatinib-and-azacitidine-followed-by-haploidentical-stem-cell-transplant-for-chronic-myeloid-leukemia-with-evolving-myelodysplasia-a-case-report-and-review-of-treatment-options
#11
Fabian Lang, Lydia Wunderle, Heike Pfeifer, Susanne Schnittger, Gesine Bug, Oliver G Ottmann
BACKGROUND CML presenting with a variant Philadelphia translocation, atypical BCR-ABL transcript, additional chromosomal aberrations, and evolving MDS is uncommon and therapeutically challenging. The prognostic significance of these genetic findings is uncertain, even as singular aberrations, with nearly no data on management and outcome when they coexist. MDS evolving during the course of CML may be either treatment-associated or an independently coexisting disease, and is generally considered to have an inferior prognosis...
October 16, 2017: American Journal of Case Reports
https://www.readbyqxmd.com/read/29030909/global-gene-expression-profiles-of-hematopoietic-stem-and-progenitor-cells-from-patients-with-chronic-myeloid-leukemia-the-effect-of-in-vitro-culture-with-or-without-imatinib
#12
Sócrates Avilés-Vázquez, Antonieta Chávez-González, Alfredo Hidalgo-Miranda, Dafne Moreno-Lorenzana, Lourdes Arriaga-Pizano, Miguel Á Sandoval-Esquivel, Manuel Ayala-Sánchez, Rafael Aguilar, Luis Alfaro-Ruiz, Hector Mayani
In this study, we determined the gene expression profiles of bone marrow-derived cell fractions, obtained from normal subjects and Chronic Myeloid Leukemia (CML) patients, that were highly enriched for hematopoietic stem (HSCs) and progenitor (HPCs) cells. Our results indicate that the profiles of CML HSCs and HPCs were closer to that of normal progenitors, whereas normal HSCs showed the most different expression profile of all. We found that the expression profiles of HSCs and HPCs from CML marrow were closer to each other than those of HSCs and HPCs from normal marrow...
October 13, 2017: Cancer Medicine
https://www.readbyqxmd.com/read/29029550/b-lymphoblastic-leukemia-lymphoma-new-insights-into-genetics-molecular-aberrations-subclassification-and-targeted-therapy
#13
REVIEW
Xiaohui Zhang, Prerna Rastogi, Bijal Shah, Ling Zhang
B lymphoblastic leukemia/lymphoma (B-ALL) is a clonal hematopoietic stem cell neoplasm derived from B-cell progenitors, which mostly occurs in children and adolescents and is regarded as one of top leading causes of death related to malignancies in this population. Despite the majority of patients with B-ALL have fairly good response to conventional chemotherapeutic interventions followed by hematopoietic stem cell transplant for the last decades, a subpopulation of patients show chemo-resistance and a high relapse rate...
September 12, 2017: Oncotarget
https://www.readbyqxmd.com/read/29027959/radiation-induced-changes-of-microrna-expression-profiles-in-radiosensitive-and-radioresistant-leukemia-cell-lines-with-different-levels-of-chromosome-abnormalities
#14
Daria Liamina, Wladimir Sibirnyj, Anna Khokhlova, Viacheslav Saenko, Eugenia Rastorgueva, Aleksandr Fomin, Yury Saenko
In our study, we estimate an effect from chromosome aberrations and genome mutations on changes in microRNA expression profiles in cancer cell lines demonstrating different radiosensitivity. Here, cell viability and microRNA spectrum have been estimated 1, 4, and 24 h after irradiation. MiSeq high-throughput sequencing system (Illumina, San Diego, CA, USA) is employed to perform microRNA spectrum estimation. In the K562 cell line, the number of expressed microRNAs in chromosomes demonstrates a more pronounced variation...
October 13, 2017: Cancers
https://www.readbyqxmd.com/read/29025907/depletion-of-sirt6-enzymatic-activity-increases-acute-myeloid-leukemia-cells-vulnerability-to-dna-damaging-agents
#15
Antonia Cagnetta, Debora Soncini, Stefania Orecchioni, Giovanna Talarico, Paola Minetto, Fabio Guolo, Veronica Retali, Nicoletta Colombo, Enrico Carminati, Marino Clavio, Maurizio Miglino, Micaela Bergamaschi, Aimable Nahimana, Michael Duchosal, Katia Todoerti, Antonino Neri, Mario Passalacqua, Santina Bruzzone, Alessio Nencioni, Francesco Bertolini, Marco Gobbi, Roberto M Lemoli, Michele Cea
Genomic instability plays a pathological role in various malignancies, including acute myeloid leukemia, and thus represents potential therapeutic target. Recent studies demonstrate that SIRT6, a NAD+-dependent nuclear deacetylase, functions as genome-guardian by preserving DNA integrity in different tumor cells. Here, we demonstrate that also CD34+ blasts from Acute Myeloid Leukemia patients show ongoing DNA damage and SIRT6 overexpression. Indeed, we identified a poor-prognostic subset of patients, with widespread instability, which relies on SIRT6 to compensate for DNA-replication stress...
October 12, 2017: Haematologica
https://www.readbyqxmd.com/read/29023469/the-common-oncogenomic-program-of-notch1-and-notch3-signaling-in-t-cell-acute-lymphoblastic-leukemia
#16
Sung Hee Choi, Eric Severson, Warren S Pear, Xiaole S Liu, Jon C Aster, Stephen C Blacklow
Notch is a major oncogenic driver in T cell acute lymphoblastic leukemia (T-ALL), in part because it binds to an enhancer that increases expression of MYC. Here, we exploit the capacity of activated NOTCH1 and NOTCH3 to induce T-ALL, despite substantial divergence in their intracellular regions, as a means to elucidate a broad, common Notch-dependent oncogenomic program through systematic comparison of the transcriptomes and Notch-bound genomic regulatory elements of NOTCH1- and NOTCH3-dependent T-ALL cells...
2017: PloS One
https://www.readbyqxmd.com/read/29022901/bcr-abl1-induced-downregulation-of-wasp-in-chronic-myeloid-leukemia-involves-epigenetic-modification-and-contributes-to-malignancy
#17
Welbert O Pereira, Daniel D De Carvalho, Maria Emilia Zenteno, Beatriz F Ribeiro, Jacqueline F Jacysyn, Luiz R Sardinha, Maria A Zanichelli, Nelson Hamerschlak, Gareth E Jones, Katia B Pagnano, Fabiola A Castro, Yolanda Calle, Gustavo P Amarante-Mendes
Chronic myeloid leukemia (CML) is a myeloproliferative disease caused by the BCR-ABL1 tyrosine kinase (TK). The development of TK inhibitors (TKIs) revolutionized the treatment of CML patients. However, TKIs are not effective to those at advanced phases when amplified BCR-ABL1 levels and increased genomic instability lead to secondary oncogenic modifications. Wiskott-Aldrich syndrome protein (WASP) is an important regulator of signaling transduction in hematopoietic cells and was shown to be an endogenous inhibitor of the c-ABL TK...
October 12, 2017: Cell Death & Disease
https://www.readbyqxmd.com/read/29018079/setd2-alterations-impair-dna-damage-recognition-and-lead-to-resistance-to-chemotherapy-in-leukemia
#18
Brenton G Mar, S Haihua Chu, Josephine D Kahn, Andrei V Krivstov, Richard Koche, Cecilia A Castellano, Jacob L Kotlier, Rebecca L Zon, Marie E McConkey, Jonathan Chabon, Ryan Chappell, Peter V Grauman, James J Hsieh, Scott A Armstrong, Benjamin L Ebert
Mutations in SETD2, encoding the histone 3 lysine 36 trimethyltransferase, are enriched in relapsed acute lymphoblastic leukemia and MLL rearranged acute leukemia. We investigated the impact of SETD2 mutations on chemotherapy sensitivity in isogenic leukemia cell lines and in murine leukemia generated from a conditional knockout of Setd2SETD2 mutations led to resistance to DNA-damaging agents, cytarabine, 6-thioguanine, doxorubicin, and etoposide, but not to a non-DNA damaging agent, L-asparaginase. H3K36me3 localizes components of the DNA damage response pathway and SETD2 mutation impaired the DNA damage response (DDR), blunting apoptosis induced by cytotoxic chemotherapy...
October 10, 2017: Blood
https://www.readbyqxmd.com/read/28993637/htlv-1-bzip-factor-suppresses-tdp1-expression-through-inhibition-of-nrf-1-in-adult-t-cell-leukemia
#19
Yoko Takiuchi, Masayuki Kobayashi, Kohei Tada, Fumie Iwai, Maki Sakurada, Shigeki Hirabayashi, Kayoko Nagata, Kotaro Shirakawa, Keisuke Shindo, Jun-Ichirou Yasunaga, Yasuhiro Murakawa, Vinodh Rajapakse, Yves Pommier, Masao Matsuoka, Akifumi Takaori-Kondo
Adult T-cell leukemia (ATL) is an aggressive T-cell malignancy caused by human T-cell leukemia virus type 1 (HTLV-1). We recently reported that abacavir, an anti-HIV-1 drug, potently and selectively kills ATL cells. This effect was attributed to the reduced expression of tyrosyl-DNA-phosphodiesterase 1 (TDP1), a DNA repair enzyme, in ATL cells. However, the molecular mechanism underlying the downregulation of TDP1 in ATL cells remains elusive. Here we identified the core promoter of the TDP1 gene, which contains a conserved nuclear respiratory factor 1 (NRF-1) binding site...
October 9, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28992762/mutations-in-tet2-and-dnmt3a-genes-are-associated-with-changes-in-global-and-gene-specific-methylation-in-acute-myeloid-leukemia
#20
Alberto Ponciano-Gómez, Adolfo Martínez-Tovar, Jorge Vela-Ojeda, Irma Olarte-Carrillo, Federico Centeno-Cruz, Efraín Garrido
Acute myeloid leukemia is characterized by its high biological and clinical heterogeneity, which represents an important barrier for a precise disease classification and accurate therapy. While epigenetic aberrations play a pivotal role in acute myeloid leukemia pathophysiology, molecular signatures such as change in the DNA methylation patterns and genetic mutations in enzymes needed to the methylation process can also be helpful for classifying acute myeloid leukemia. Our study aims to unveil the relevance of DNMT3A and TET2 genes in global and specific methylation patterns in acute myeloid leukemia...
October 2017: Tumour Biology: the Journal of the International Society for Oncodevelopmental Biology and Medicine
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