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Leukemia chemoresistance

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https://www.readbyqxmd.com/read/29449434/msh6-haploinsufficiency-at-relapse-contributes-to-the-development-of-thiopurine-resistance-in-pediatric-b-lymphoblastic-leukemia
#1
Nikki A Evensen, P Pallavi Madhusoodhan, Julia Meyer, Jason Saliba, Ashfiyah Chowdhury, David J Araten, Jacob Nersting, Teena Bhatla, Tiffaney L Vincent, David Teachey, Stephen P Hunger, Jun Yang, Kjeld Schmiegelow, William L Carroll
Survival of children with relapsed acute lymphoblastic leukemia is poor and understanding mechanisms underlying resistance is essential in developing new therapy. Relapse-specific heterozygous deletions in MSH6, a crucial part of DNA Mismatch Repair, are frequently detected. Our aim was to determine whether MSH6 deletion results in a hypermutator phenotype associated with generation of secondary mutations involved in drug resistance or leads to a failure to initiate apoptosis directly in response to chemotherapeutic agents...
February 15, 2018: Haematologica
https://www.readbyqxmd.com/read/29445159/microfluidic-cell-sorting-by-stiffness-to-examine-heterogenic-responses-of-cancer-cells-to-chemotherapy
#2
Muhymin Islam, Roman Mezencev, Brynn McFarland, Hannah Brink, Betsy Campbell, Bushra Tasadduq, Edmund K Waller, Wilbur Lam, Alexander Alexeev, Todd Sulchek
Cancers consist of a heterogeneous populations of cells that may respond differently to treatment through drug-resistant sub-populations. The scarcity of these resistant sub-populations makes it challenging to understand how to counter their resistance. We report a label-free microfluidic approach to separate cancer cells treated with chemotherapy into sub-populations enriched in chemoresistant and chemosensitive cells based on the differences in cellular stiffness. The sorting approach enabled analysis of the molecular distinctions between resistant and sensitive cells...
February 14, 2018: Cell Death & Disease
https://www.readbyqxmd.com/read/29435192/microrna-expression-and-activity-in-t-cell-acute-lymphoblastic-leukemia
#3
REVIEW
Fang Ye
T-cell acute lymphoblastic leukemia (T-ALL) is a lymphoid malignancy caused by the oncogenic transformation of immature T-cell progenitors. Many biologically relevant genetic and epigenetic alterations have been identified as driving factors for this transformation. Recently, microRNAs (miRNAs) have been shown to influence various leukemias, including T-ALL. Aberrant expression of miRNAs can function as either oncogenes or tumor suppressors in T-ALL through the regulation of cell migration, invasion, proliferation, apoptosis, and chemoresistance...
January 12, 2018: Oncotarget
https://www.readbyqxmd.com/read/29431698/mef2c-phosphorylation-is-required-for-chemotherapy-resistance-in-acute-myeloid-leukemia
#4
Fiona C Brown, Eric Still, Richard P Koche, Christina Y Yim, Sumiko Takao, Paolo Cifani, Casie Reed, Shehana Gunasekera, Scott B Ficarro, Peter Romanienko, Willie Mark, Craig McCarthy, Elisa de Stanchina, Mithat Gonen, Venkatraman Seshan, Patrick Bhola, Conor O'Donnell, Barbara Spitzer, Crystal Stutzke, Vincent-Philippe Lavallée, Josée Hébert, Andrei V Krivstov, Ari Melnick, Elisabeth M Paietta, Martin S Tallman, Anthony Letai, Guy Sauvageau, Gayle Pouliot, Ross Levine, Jarrod A Marto, Scott A Armstrong, Alex Kentsis
In acute myeloid leukemia, chemotherapy resistance remains prevalent and poorly understood. Using functional proteomics of patient AML specimens, we identified MEF2C S222 phosphorylation as a specific marker of primary chemoresistance. We found that Mef2c S222A/S222A knock-in mutant mice engineered to block MEF2C phosphorylation exhibited normal hematopoiesis, but were resistant to leukemogenesis induced by MLL-AF9. MEF2C phosphorylation was required for leukemia stem cell maintenance, and induced by MARK kinases in cells...
February 5, 2018: Cancer Discovery
https://www.readbyqxmd.com/read/29427526/nup98-bptf-gene-fusion-identified-in-primary-refractory-acute-megakaryoblastic-leukemia-of-infancy
#5
Mathieu Roussy, Mélanie Bilodeau, Loubna Jouan, Pauline Tibout, Louise Laramée, Emmanuelle Lemyre, Sophie Cardin, Camille Sauvageau, Françoise Couture, Aurélien Choblet, Natalie Patey, Patrick Gendron, Michel Duval, Pierre Teira, Josée Hébert, Brian T Wilhelm, John K Choi, Tanja A Gruber, Henrique Bittencourt, Sonia Cellot
The advent of large scale genomic sequencing technologies significantly improved the molecular classification of acute megakaryoblastic leukaemia (AMKL). AMKL represents a subset (∼10%) of high fatality pediatric acute myeloid leukemia (AML). Recurrent and mutually exclusive chimeric gene fusions associated with pediatric AMKL are found in 60-70% of cases and include RBM15-MKL1, CBFA2T3-GLIS2, NUP98-KDM5A and MLL rearrangements. In addition, another 4% of AMKL harbor NUP98 rearrangements (NUP98r), with yet undetermined fusion partners...
February 10, 2018: Genes, Chromosomes & Cancer
https://www.readbyqxmd.com/read/29399180/characteristics-of-doxorubicin-selected-multidrug-resistant-human-leukemia-hl-60-cells-with-tolerance-to-arsenic-trioxide-and-contribution-of-leukemia-stem-cells
#6
Jing Chen, Hulai Wei, Jie Cheng, Bei Xie, Bei Wang, Juan Yi, Baoying Tian, Zhuan Liu, Feifei Wang, Zhewen Zhang
The present study selected and characterized a multidrug-resistant HL-60 human acute promyelocytic leukemia cell line, HL-60/RS, by exposure to stepwise incremental doses of doxorubicin. The drug-resistant HL-60/RS cells exhibited 85.68-fold resistance to doxorubicin and were cross-resistant to other chemotherapeutics, including cisplatin, daunorubicin, cytarabine, vincristine and etoposide. The cells over-expressed the transporters P-glycoprotein, multidrug-resistance-related protein 1 and breast-cancer-resistance protein, encoded by the adenosine triphosphate-binding cassette (ABC)B1, ABCC1 and ABCG2 genes, respectively...
January 2018: Oncology Letters
https://www.readbyqxmd.com/read/29382485/proteomic-changes-in-a-childhood-acute-lymphoblastic-leukemia-cell-line-during-the-adaptation-to-vincristine
#7
Ana Laura Guzmán-Ortiz, Gerardo Aparicio-Ozores, Ricardo Valle-Rios, Oscar Medina-Contreras, Genaro Patiño-López, Héctor Quezada
INTRODUCTION: Relapse occurs in approximately 20% of Mexican patients with childhood acute lymphoblastic leukemia (ALL). In this group, chemoresistance may be one of the biggest challenges. An overview of complex cellular processes like drug tolerance can be achieved with proteomic studies. METHODS: The B-lineage pediatric ALL cell line CCRF-SB was gradually exposed to the chemotherapeutic vincristine until proliferation was observed at 6nM, control cells were cultured in the absence of vincristine...
May 2017: Boletín Médico del Hospital Infantil de México
https://www.readbyqxmd.com/read/29367945/cd19-car-t-cells-expressing-il-12-eradicate-lymphoma-in-fully-lymphoreplete-mice-through-induction-of-host-immunity
#8
Gray Kueberuwa, Milena Kalaitsidou, Eleanor Cheadle, Robert Edward Hawkins, David Edward Gilham
Chimeric antigen receptor (CAR) T cell therapy represents a significant advancement in cancer therapy. Larger studies have shown ∼90% complete remission rates against chemoresistant and/or refractory CD19+ leukemia or lymphoma. Effective CAR T cell therapy is highly dependent on lymphodepleting preconditioning, which is achieved through chemotherapy or radiotherapy that carries with it significant toxicities. These can exclude patients of low performance status. In order to overcome the need for preconditioning, we constructed fully mouse first and second generation anti-murine CD19 CARs with or without interleukin-12 (IL-12) secretion...
March 30, 2018: Molecular Therapy Oncolytics
https://www.readbyqxmd.com/read/29357914/cell-adhesion-mediated-mitochondria-transfer-contributes-to-mesenchymal-stem-cell-induced-chemoresistance-on-t-cell-acute-lymphoblastic-leukemia-cells
#9
Jiancheng Wang, Xin Liu, Yuan Qiu, Yue Shi, Jianye Cai, Boyan Wang, Xiaoyue Wei, Qiong Ke, Xin Sui, Yi Wang, Yinong Huang, Hongyu Li, Tao Wang, Ren Lin, Qifa Liu, Andy Peng Xiang
BACKGROUND: Despite the high cure rate of T cell acute lymphoblastic leukemia (T-ALL), drug resistance to chemotherapy remains a significant clinical problem. Bone marrow mesenchymal stem cells (MSCs) protect leukemic cells from chemotherapy, but the underlying mechanisms are poorly understood. In this study, we aimed to uncover the mechanism of MSC-induced chemoresistance in T-ALL cells, thus providing a promising clinical therapy target. METHODS: Cell viability was determined using the viability assay kit CCK-8...
January 22, 2018: Journal of Hematology & Oncology
https://www.readbyqxmd.com/read/29351753/mesenchymal-stem-cells-show-functional-defect-and-decreased-anti-cancer-effect-after-exposure-to-chemotherapeutic-drugs
#10
Chinnapaka Somaiah, Atul Kumar, Renu Sharma, Amit Sharma, Trishna Anand, Jina Bhattacharyya, Damodar Das, Sewali Deka Talukdar, Bithiah Grace Jaganathan
BACKGROUND: Mesenchymal stem cells (MSC) are used for several therapeutic applications to improve the functions of bone, cardiac, nervous tissue as well as to facilitate the repopulation of hematopoietic stem cells. MSC give rise to the non-hematopoietic stromal cells of the bone marrow and are important for the maintenance of normal hematopoiesis. Chemotherapeutic drugs used for treatment of leukemia extensively damage the stromal cells and alter their gene expression profiles. METHODS: We determined the changes in adipogenic, osteogenic differentiation, phenotypic and gene expression in MSC during treatment with chemotherapeutic drugs cytarabine, daunorubicin and vincristine...
January 19, 2018: Journal of Biomedical Science
https://www.readbyqxmd.com/read/29344203/mucin-1-promotes-radioresistance-in-hepatocellular-carcinoma-cells-through-activation-of-jak2-stat3-signaling
#11
Feng-Tao Yi, Qi-Ping Lu
Mucin 1 (MUC1) is aberrantly overexpressed in numerous human cancer types, including hepatocellular carcinoma (HCC) and contributes to chemoresistance of tumor cells. The aim of the present study was to evaluate the possible implication of MUC1 in radioresistance of HCC cells and the underlying mechanisms. It was demonstrated that MUC1 was significantly upregulated in HCC cells following irradiation exposure, which was coupled with increased phosphorylation of signal transducer and activator of transcription 3 (STAT3)...
December 2017: Oncology Letters
https://www.readbyqxmd.com/read/29342970/the-possible-importance-of-%C3%AE-3-integrins-for-leukemogenesis-and-chemoresistance-in-acute-myeloid-leukemia
#12
REVIEW
Silje Johansen, Annette K Brenner, Sushma Bartaula-Brevik, Håkon Reikvam, Øystein Bruserud
Acute myeloid leukemia (AML) is an aggressive bone marrow malignancy where the immature leukemia cells communicate with neighboring cells through constitutive cytokine release and through their cell surface adhesion molecules. The primary AML cells express various integrins. These heterodimeric molecules containing an α and a β chain are cell surface molecules that bind extracellular matrix molecules, cell surface molecules and soluble mediators. The β3 integrin (ITGB3) chain can form heterodimers only with the two α chains αIIb and αV...
January 15, 2018: International Journal of Molecular Sciences
https://www.readbyqxmd.com/read/29296822/bone-marrow-sites-differently-imprint-dormancy-and-chemoresistance-to-t-cell-acute-lymphoblastic-leukemia
#13
Xavier Cahu, Julien Calvo, Sandrine Poglio, Nais Prade, Benoit Colsch, Marie-Laure Arcangeli, Thierry Leblanc, Arnaud Petit, Frederic Baleydier, Andre Baruchel, Judith Landman-Parker, Christophe Junot, Jerome Larghero, Paola Ballerini, Eric Delabesse, Benjamin Uzan, Francoise Pflumio
T-cell acute lymphoblastic leukemia (T-ALL) expands in various bone marrow (BM) sites of the body. We investigated whether different BM sites could differently modulate T-ALL propagation using in vivo animal models. We observed that mouse and human T-ALL develop slowly in the BM of tail vertebrae compared with the BM from thorax vertebrae. T-ALL recovered from tail BM displays lower cell-surface marker expression and decreased metabolism and cell-cycle progression, demonstrating a dormancy phenotype. Functionally, tail-derived T-ALL exhibit a deficient short-term ex vivo growth and a delayed in vivo propagation...
September 12, 2017: Blood Advances
https://www.readbyqxmd.com/read/29296751/a-novel-cxcr4-antagonist-igg1-antibody-pf-06747143-for-the-treatment-of-hematologic-malignancies
#14
Shu-Hui Liu, Yin Gu, Bernadette Pascual, Zhengming Yan, Max Hallin, Cathy Zhang, Conglin Fan, Wenlian Wang, Justine Lam, Mary E Spilker, Rolla Yafawi, Eileen Blasi, Brett Simmons, Nanni Huser, Wei-Hsien Ho, Kevin Lindquist, Thomas-Toan Tran, Jyothirmayee Kudaravalli, Jing-Tyan Ma, Gretchen Jimenez, Ishita Barman, Colleen Brown, Sherman Michael Chin, Maria J Costa, David Shelton, Tod Smeal, Valeria R Fantin, Flavia Pernasetti
The chemokine receptor CXCR4 is highly expressed and associated with poor prognosis in multiple malignancies. Upon engagement by its ligand, CXCL12, CXCR4 triggers intracellular signaling pathways that control trafficking of cells to tissues where the ligand is expressed, such as the bone marrow (BM). In hematologic cancers, CXCR4-driven homing of malignant cells to the BM protective niche is a key mechanism driving disease and therapy resistance. We developed a humanized CXCR4 immunoglobulin G1 (IgG1) antibody (Ab), PF-06747143, which binds to CXCR4 and inhibits CXCL12-mediated signaling pathways, as well as cell migration...
June 27, 2017: Blood Advances
https://www.readbyqxmd.com/read/29222236/how-and-when-to-decide-between-epigenetic-therapy-and-chemotherapy-in-patients-with-aml
#15
REVIEW
Hervé Dombret, Raphael Itzykson
Remission induction with chemotherapy has long been the frontline treatment of acute myeloid leukemia (AML). However, intensive therapy is limited in frail patients by its associated toxicity and higher rates of failure or relapse in patients with chemoresistant disease, such as secondary AML or poor-risk cytogenetics. Frailty and chemoresistance are more frequent in older adults with AML. In recent years, epigenetic therapies with the hypomethylating agents decitabine and azacitidine have been thoroughly explored in AML...
December 8, 2017: Hematology—the Education Program of the American Society of Hematology
https://www.readbyqxmd.com/read/29208667/etk-interaction-with-pfkfb4-modulates-chemoresistance-of-small-cell-lung-cancer-by-regulating-autophagy
#16
Qiongyao Wang, Fanrui Zeng, Yanqin Sun, Qianqian Qiu, Jian Zhang, Weimei Huang, Jie Huang, Xiaomin Huang, Linlang Guo
PURPOSE: Epithelial and endothelial tyrosine kinase (Etk), also known as bone marrow X kinase (Bmx), was found to be critical in modulating the chemoresistance of small cell lung cancer (SCLC) in our preliminary study. However, the molecular mechanisms of Etk in SCLC chemoresistance remain poorly understood. The present study investigated the downstream factor and pathway involved. EXPERIMENTAL DESIGN: We demonstrated first that knockdown of Etk by siRNAs suppressed autophagy in chemoresistant SCLC cells, and that direct inhibition of autophagy sensitized cells to chemotherapy...
December 5, 2017: Clinical Cancer Research: An Official Journal of the American Association for Cancer Research
https://www.readbyqxmd.com/read/29192326/eps8-regulates-proliferation-apoptosis-and-chemosensitivity-in-bcr-abl-positive-cells-via-the-bcr-abl-pi3k-akt-mtor-pathway
#17
Rui Huang, Huimin Liu, Yiran Chen, Yanjie He, Qian Kang, Sanfang Tu, Yingzhi He, Xuan Zhou, Lei Wang, Jilong Yang, Anqin Wu, Yuhua Li
Although the introduction of tyrosine kinase inhibitors greatly improved the survival of patients with chronic myeloid leukemia (CML), drug resistance remains a problem. Thus, mechanism-based novel therapeutic targets warrant exploration. Recently, epidermal growth factor receptor kinase substrate 8 (EPS8), which has been identified as an oncogene and plays an important role in a broad spectrum of solid tumours, was reported to be related to poor prognosis or chemoresistance in acute leukemia patients. However, its role in CML remains unclear...
January 2018: Oncology Reports
https://www.readbyqxmd.com/read/29172076/gemtuzumab-ozogamicin-go-inclusion-to-induction-chemotherapy-eliminates-leukemic-initiating-cells-and-significantly-improves-survival-in-mouse-models-of-acute-myeloid-leukemia
#18
Cathy C Zhang, Zhengming Yan, Bernadette Pascual, Amy Jackson-Fisher, Donghui Stephen Huang, Qing Zong, Mark Elliott, Conglin Fan, Nanni Huser, Joseph Lee, Matthew Sung, Puja Sapra
Gemtuzumab ozogamicin (GO) is an anti-CD33 antibody-drug conjugate for the treatment of acute myeloid leukemia (AML). Although GO shows a narrow therapeutic window in early clinical studies, recent reports detailing a modified dosing regimen of GO can be safely combined with induction chemotherapy, and the combination provides significant survival benefits in AML patients. Here we tested whether the survival benefits seen with the combination arise from the enhanced reduction of chemoresidual disease and leukemic initiating cells (LICs)...
November 21, 2017: Neoplasia: An International Journal for Oncology Research
https://www.readbyqxmd.com/read/29168399/vacuolar-atpase-as-a-possible-therapeutic-target-in-human-acute-myeloid-leukemia
#19
Elise Aasebø, Sushma Bartaula-Brevik, Maria Hernandez-Valladares, Øystein Bruserud
V-ATPase is a proton pump expressed both in the membrane of intracellular organelles (e.g. endosomes, lysosomes, Golgi structures) and the plasma membrane. It is an important regulator of organellar functions, intracellular molecular trafficking, intercellular communication and intracellular signaling. It is therefore considered as a possible therapeutic target in the treatment of human malignancies. Areas covered: Relevant publications were identified through literature searches in the PubMed database. We searched for original articles and reviews describing the possible importance of V-ATPase for leukemogenesis and chemosensitivity in human myeloid cells, especially acute myeloid leukemia (AML) cells...
November 23, 2017: Expert Review of Hematology
https://www.readbyqxmd.com/read/29164055/micrornas-and-acute-myeloid-leukemia-chemoresistance-a-mechanistic-overview
#20
REVIEW
Martino Marco Gabra, Leonardo Salmena
Up until the early 2000s, a functional role for microRNAs (miRNAs) was yet to be elucidated. With the advent of increasingly high-throughput and precise RNA-sequencing techniques within the last two decades, it has become well established that miRNAs can regulate almost all cellular processes through their ability to post-transcriptionally regulate a majority of protein-coding genes and countless other non-coding genes. In cancer, miRNAs have been demonstrated to play critical roles by modifying or controlling all major hallmarks including cell division, self-renewal, invasion, and DNA damage among others...
2017: Frontiers in Oncology
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