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https://www.readbyqxmd.com/read/28440315/tet2-loss-leads-to-hypermutagenicity-in-haematopoietic-stem-progenitor-cells
#1
Feng Pan, Thomas S Wingo, Zhigang Zhao, Rui Gao, Hideki Makishima, Guangbo Qu, Li Lin, Miao Yu, Janice R Ortega, Jiapeng Wang, Aziz Nazha, Li Chen, Bing Yao, Can Liu, Shi Chen, Ophelia Weeks, Hongyu Ni, Brittany Lynn Phillips, Suming Huang, Jianlong Wang, Chuan He, Guo-Min Li, Tomas Radivoyevitch, Iannis Aifantis, Jaroslaw P Maciejewski, Feng-Chun Yang, Peng Jin, Mingjiang Xu
TET2 is a dioxygenase that catalyses multiple steps of 5-methylcytosine oxidation. Although TET2 mutations frequently occur in various types of haematological malignancies, the mechanism by which they increase risk for these cancers remains poorly understood. Here we show that Tet2(-/-) mice develop spontaneous myeloid, T- and B-cell malignancies after long latencies. Exome sequencing of Tet2(-/-) tumours reveals accumulation of numerous mutations, including Apc, Nf1, Flt3, Cbl, Notch1 and Mll2, which are recurrently deleted/mutated in human haematological malignancies...
April 25, 2017: Nature Communications
https://www.readbyqxmd.com/read/28436936/the-u2af1s34f-mutation-induces-lineage-specific-splicing-alterations-in-myelodysplastic-syndromes
#2
Bon Ham Yip, Violetta Steeples, Emmanouela Repapi, Richard N Armstrong, Miriam Llorian, Swagata Roy, Jacqueline Shaw, Hamid Dolatshad, Stephen Taylor, Amit Verma, Matthias Bartenstein, Paresh Vyas, Nicholas C P Cross, Luca Malcovati, Mario Cazzola, Eva Hellström-Lindberg, Seishi Ogawa, Christopher W J Smith, Andrea Pellagatti, Jacqueline Boultwood
Mutations of the splicing factor-encoding gene U2AF1 are frequent in the myelodysplastic syndromes (MDS), a myeloid malignancy, and other cancers. Patients with MDS suffer from peripheral blood cytopenias, including anemia, and an increasing percentage of bone marrow myeloblasts. We studied the impact of the common U2AF1S34F mutation on cellular function and mRNA splicing in the main cell lineages affected in MDS. We demonstrated that U2AF1S34F expression in human hematopoietic progenitors impairs erythroid differentiation and skews granulomonocytic differentiation toward granulocytes...
April 24, 2017: Journal of Clinical Investigation
https://www.readbyqxmd.com/read/28435069/age-related-increase-in-wnt-inhibitor-causes-a-senescence-like-phenotype-in-human-cardiac-stem-cells
#3
Tamami Nakamura, Tohru Hosoyamaa, Junichi Murakami, Makoto Samura, Koji Ueno, Hiroshi Kurazumi, Ryo Suzuki, Akihito Mikamo, Kimikazu Hamano
Aging of cardiac stem/progenitor cells (CSCs) impairs heart regeneration and leads to unsatisfactory outcomes of cell-based therapies. As the precise mechanisms underlying CSC aging remain unclear, the use of therapeutic strategies for elderly patients with heart failure is severely delayed. In this study, we used human cardiosphere-derived cells (CDCs), a subtype of CSC found in the postnatal heart, to identify secreted factor(s) associated with CSC aging. Human CDCs were isolated from heart failure patients of various ages (2-83 years old)...
April 20, 2017: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/28427227/high-dose-ascorbate-and-arsenic-trioxide-selectively-kill-acute-myeloid-leukemia-and-acute-promyelocytic-leukemia-blasts-in-vitro
#4
Nélida I Noguera, Elvira Pelosi, Daniela F Angelini, Maria Liliana Piredda, Gisella Guerrera, Eleonora Piras, Luca Battistini, Lauretta Massai, Anna Berardi, Gianfranco Catalano, Laura Cicconi, Germana Castelli, Agnese D'Angiò, Luca Pasquini, Grazia Graziani, Giuseppe Fioritoni, Maria Teresa Voso, Domenico Mastrangelo, Ugo Testa, Francesco Lo-Coco
The use of high-dose ascorbate (ASC) for the treatment of human cancer has been attempted several decades ago and has been recently revived by several in vitro and in vivo studies in solid tumors. We tested the cytotoxic effects of ASC, alone or in combination with arsenic trioxide (ATO) in acute myeloid leukemia (AML) and acute promyelocytic leukemia (APL). Leukemic cell lines and primary blasts from AML and APL patients were treated with graded concentrations of ASC, alone or in association with standard concentration (1 μM) of ATO...
March 6, 2017: Oncotarget
https://www.readbyqxmd.com/read/28424425/ephrin-b3-supports-glioblastoma-growth-by-inhibiting-apoptosis-induced-by-the-dependence-receptor-epha4
#5
Amélie Royet, Laura Broutier, Marie-May Coissieux, Céline Malleval, Nicolas Gadot, Denis Maillet, Lise Gratadou-Hupon, Agnès Bernet, Pascale Nony, Isabelle Treilleux, Jérôme Honnorat, Daniel Liebl, Laurent Pelletier, François Berger, David Meyronet, Marie Castets, Patrick Mehlen
EphA4, an Ephrins tyrosine kinase receptor, behaves as a dependence receptor (DR) by triggering cell apoptosis in the absence of its ligand Ephrin-B3. DRs act as conditional tumor suppressors, engaging cell death based on ligand availability; this mechanism is bypassed by overexpression of DRs ligands in some aggressive cancers. The pair EphA4/Ephrin-B3 favors survival of neuronal progenitors of the brain subventricular zone, an area where glioblastoma multiform (GBM) are thought to originate. Here, we report that Ephrin-B3 is highly expressed in human biopsies and that it inhibits EphA4 pro-apoptotic activity in tumor cells...
March 10, 2017: Oncotarget
https://www.readbyqxmd.com/read/28423606/ephrin-b3-supports-glioblastoma-growth-by-inhibiting-apoptosis-induced-by-the-dependence-receptor-epha4
#6
Amélie Royet, Laura Broutier, Marie-May Coissieux, Céline Malleval, Nicolas Gadot, Denis Maillet, Lise Gratadou-Hupon, Agnès Bernet, Pascale Nony, Isabelle Treilleux, Jérôme Honnorat, Daniel Liebl, Laurent Pelletier, François Berger, David Meyronet, Marie Castets, Patrick Mehlen
EphA4, an Ephrins tyrosine kinase receptor, behaves as a dependence receptor (DR) by triggering cell apoptosis in the absence of its ligand Ephrin-B3. DRs act as conditional tumor suppressors, engaging cell death based on ligand availability; this mechanism is bypassed by overexpression of DRs ligands in some aggressive cancers. The pair EphA4/Ephrin-B3 favors survival of neuronal progenitors of the brain subventricular zone, an area where glioblastoma multiform (GBM) are thought to originate. Here, we report that Ephrin-B3 is highly expressed in human biopsies and that it inhibits EphA4 pro-apoptotic activity in tumor cells...
April 4, 2017: Oncotarget
https://www.readbyqxmd.com/read/28423605/pregnancy-at-early-age-is-associated-with-a-reduction-of-progesterone-responsive-cells-and-epithelial-wnt-signaling-in-human-breast-tissue
#7
Simone Muenst, Robert Mechera, Silvio Däster, Salvatore Piscuoglio, Charlotte K Y Ng, Fabienne Meier-Abt, Walter P Weber, Savas D Soysal
BACKGROUND: Pregnancy at early age is the most significant modifiable factor which consistently decreases lifetime breast cancer risk. However, the underlying mechanisms haven't been conclusively identified. Studies in mice suggest a reduction in progesterone-receptor (PR) sensitive epithelial cells as well as a downregulation of the Wnt signaling pathway as being one of the main mechanisms for the protective effect of early pregnancy. The aim of our study was to validate these findings in humans...
April 4, 2017: Oncotarget
https://www.readbyqxmd.com/read/28423321/hepatocellular-carcinomas-originate-predominantly-from-hepatocytes-and-benign-lesions-from-hepatic-progenitor-cells
#8
Krishna S Tummala, Marta Brandt, Ana Teijeiro, Osvaldo Graña, Robert F Schwabe, Cristian Perna, Nabil Djouder
Hepatocellular carcinoma (HCC) is an aggressive primary liver cancer. However, its origin remains a debated question. Using human data and various hepatocarcinogenesis mouse models, we show that, in early stages, transformed hepatocytes, independent of their proliferation status, activate hepatic progenitor cell (HPC) expansion. Genetic lineage tracing of HPCs and hepatocytes reveals that, in all models, HCC originates from hepatocytes. However, whereas in various models tumors do not emanate from HPCs, tracking of progenitors in a model mimicking human hepatocarcinogenesis indicates that HPCs can generate benign lesions (regenerative nodules and adenomas) and aggressive HCCs...
April 18, 2017: Cell Reports
https://www.readbyqxmd.com/read/28423296/eltrombopag-added-to-standard-immunosuppression-for-aplastic-anemia
#9
Danielle M Townsley, Phillip Scheinberg, Thomas Winkler, Ronan Desmond, Bogdan Dumitriu, Olga Rios, Barbara Weinstein, Janet Valdez, Jennifer Lotter, Xingmin Feng, Marie Desierto, Harshraj Leuva, Margaret Bevans, Colin Wu, Andre Larochelle, Katherine R Calvo, Cynthia E Dunbar, Neal S Young
Background Acquired aplastic anemia results from immune-mediated destruction of bone marrow. Immunosuppressive therapies are effective, but reduced numbers of residual stem cells may limit their efficacy. In patients with aplastic anemia that was refractory to immunosuppression, eltrombopag, a synthetic thrombopoietin-receptor agonist, led to clinically significant increases in blood counts in almost half the patients. We combined standard immunosuppressive therapy with eltrombopag in previously untreated patients with severe aplastic anemia...
April 20, 2017: New England Journal of Medicine
https://www.readbyqxmd.com/read/28418845/preclinical-development-of-g1t38-a-novel-potent-and-selective-inhibitor-of-cyclin-dependent-kinases-4-6-for-use-as-an-oral-antineoplastic-in-patients-with-cdk4-6-sensitive-tumors
#10
John E Bisi, Jessica A Sorrentino, Jamie L Jordan, David D Darr, Patrick J Roberts, Francis X Tavares, Jay C Strum
Inhibition of the p16INK4a/cyclin D/CDK4/6/RB pathway is an effective therapeutic strategy for the treatment of estrogen receptor positive (ER+) breast cancer. Although efficacious, current treatment regimens require a dosing holiday due to severe neutropenia potentially leading to an increased risk of infections, as well as tumor regrowth and emergence of drug resistance. Therefore, a next generation CDK4/6 inhibitor that can inhibit proliferation of CDK4/6-dependent tumors while minimizing neutropenia could reduce both the need for treatment holidays and the risk of inducing drug resistance...
March 15, 2017: Oncotarget
https://www.readbyqxmd.com/read/28416638/eya2-a-target-activated-by-plzf-is-critical-for-plzf-rara-induced-leukemogenesis
#11
Ryoichi Ono, Masahiro Masuya, Satomi Ishii, Naoyuki Katayama, Tetsuya Nosaka
PLZF is a transcription factor that confers aberrant self-renewal in leukemogenesis, and the PLZF-RARA fusion gene causes acute promyelocytic leukemia (APL) through differentiation block. However, the molecular mechanisms of aberrant self-renewal underlying PLZF-mediated leukemogenesis are poorly understood. To investigate these mechanisms, comprehensive expression profiling of mouse hematopoietic stem/progenitor cells transduced with Plzf was performed, which revealed the involvement of a key transcriptional coactivator, Eya2, a target molecule shared by Plzf and PLZF-RARA, in the aberrant self-renewal...
April 17, 2017: Molecular and Cellular Biology
https://www.readbyqxmd.com/read/28415725/stat3-positive-tumor-cells-contribute-to-vessels-neoformation-in-primary-central-nervous-system-lymphoma
#12
Simona Ruggieri, Roberto Tamma, Nicoletta Resta, Francesco Albano, Nicoletta Coccaro, Daria Loconte, Tiziana Annese, Mariella Errede, Giorgina Specchia, Rebecca Senetta, Paola Cassoni, Domenico Ribatti, Beatrice Nico
With the aim of elucidating the relationship between Stat3 expression and tumor vessels abnormalities in the PCNLs, in this study we evaluated Stat3 and pStat3 expression by Real-time PCR and by immunohistochemistry in biopsy sections from PCNSL patients. Correlations of the expression levels with the presence of aberrant vessels were analyzed by confocal laser microscopy analysis, using FVIII as endothelial cell marker, CD133 and nestin as cancer stem cell (CSC) marker, CD20 as tumor cell marker, and Stat3...
March 10, 2017: Oncotarget
https://www.readbyqxmd.com/read/28414317/p16-controls-epithelial-cell-growth-and-suppresses-carcinogenesis-through-mechanisms-that-do-not-require-rb1-function
#13
M Sen, N Akeno, A Reece, A L Miller, D S Simpson, K A Wikenheiser-Brokamp
The p16/RB1 tumor suppressor pathway is inactivated in the vast majority, if not all, human cancers. The current paradigm is that p16 and RB1 function in a linear pathway to suppress tumorigenesis; however p16 is preferentially lost in human cancers suggesting that p16 has critical tumor suppressive functions not mediated through RB1. Carcinomas arise from transformed epithelial cells and account for 80% of adult malignancies highlighting the need to understand p16/RB1 pathway function in organ epithelia. Lung cancer is the leading cause of cancer deaths and is associated with p16/RB1 pathway deregulation...
April 17, 2017: Oncogenesis
https://www.readbyqxmd.com/read/28409344/tissue-specific-functions-of-p53-during-kidney-development
#14
Zubaida Saifudeen
p53 is best identified as a tumor suppressor for its transcriptional control of genes involved in cell cycle progression and apoptosis. Beyond its irrefutable involvement in restraining unchecked cell proliferation, research over the past several years has indicated a requirement for p53 function in sustaining normal development. Here I summarize the role of p53 in embryonic development, with a focus on knowledge gained from p53 loss and overexpression during kidney development. In contrast to its classical role in suppressing proliferative pathways, p53 positively regulates nephron progenitor cell (NPC) renewal...
2017: Results and Problems in Cell Differentiation
https://www.readbyqxmd.com/read/28409314/regulation-of-asymmetric-cell-division-in-mammalian-neural-stem-and-cancer-precursor-cells
#15
Mathieu Daynac, Claudia K Petritsch
Stem and progenitor cells are characterized by their abilities to self-renew and produce differentiated progeny. The balance between self-renewal and differentiation is achieved through control of cell division mode, which can be either asymmetric or symmetric. Failure to properly control cell division mode may result in premature depletion of the stem/progenitor cell pool or abnormal growth and impaired differentiation. In many tissues, including the brain, stem cells and progenitor cells undergo asymmetric cell division through the establishment of cell polarity...
2017: Results and Problems in Cell Differentiation
https://www.readbyqxmd.com/read/28409313/extracellular-regulation-of-the-mitotic-spindle-and-fate-determinants-driving-asymmetric-cell-division
#16
Prestina Smith, Mark Azzam, Lindsay Hinck
Stem cells use mode of cell division, symmetric (SCD) versus asymmetric (ACD), to balance expansion with self-renewal and the generation of daughter cells with different cell fates. Studies in model organisms have identified intrinsic mechanisms that govern this process, which involves partitioning molecular components between daughter cells, frequently through the regulation of the mitotic spindle. Research performed in vertebrate tissues is revealing both conservation of these intrinsic mechanisms and crucial roles for extrinsic cues in regulating the frequency of these divisions...
2017: Results and Problems in Cell Differentiation
https://www.readbyqxmd.com/read/28408396/novel-role-of-immature-myeloid-cells-in-formation-of-new-lymphatic-vessels-associated-with-inflammation-and-tumors
#17
REVIEW
Sophia Ran, Andrew Wilber
Inflammation triggers an immune cell-driven program committed to restoring homeostasis to injured tissue. Central to this process is vasculature restoration, which includes both blood and lymphatic networks. Generation of new vessels or remodeling of existing vessels are also important steps in metastasis-the major cause of death for cancer patients. Although roles of the lymphatic system in regulation of inflammation and cancer metastasis are firmly established, the mechanisms underlying the formation of new lymphatic vessels remain a subject of debate...
April 13, 2017: Journal of Leukocyte Biology
https://www.readbyqxmd.com/read/28408238/novel-roles-for-podocalyxin-in-regulating-stress-myelopoiesis-rap1a-and-neutrophil-migration
#18
Pan Li, Aldona A Karaczyn, Rose McGlauflin, Amanda Favreau, Edward Jachimowicz, Calvin Vary, Kailin Xu, Don M Wojchowski, Pradeep Sathyanarayana
Podocalyxin (Podxl) is a CD34 orthologue and cell surface sialomucin with reported roles in renal podocyte diaphragm slit development, vascular cell integrity, and the progression of blood, breast, and prostate cancers. Roles for Podxl during non-malignant hematopoiesis, however, are largely undefined. Presently we have developed a Vav-Cre Podxl knockout mouse model, and report on novel roles for Podxl in governing stress myelopoiesis. At steady-state, Podxl expression among hematopoietic progenitor cells was low-level but was induced by GCSF (granulocyte colony stimulating factor) in myeloid progenitors, and by TPO (thrombopoietin) in HSCs...
April 10, 2017: Experimental Hematology
https://www.readbyqxmd.com/read/28406476/wisp-1-positively-regulates-angiogenesis-by-controlling-vegf-a-expression-in-human-osteosarcoma
#19
Hsiao-Chi Tsai, Huey-En Tzeng, Chun-Yin Huang, Yuan-Li Huang, Chun-Hao Tsai, Shih-Wei Wang, Po-Chuan Wang, An-Chen Chang, Yi-Chin Fong, Chih-Hsin Tang
In recent years, much research has focused on the role of angiogenesis in osteosarcoma, which occurs predominantly in adolescents and young adults. The vascular endothelial growth factor-A (VEGF-A) pathway is the key regulator of angiogenesis and in osteosarcoma. VEGF-A expression has been recognized as a prognostic marker in angiogenesis. Aberrant WNT1-inducible signaling pathway protein-1 (WISP-1) expression is associated with various cancers. However, the function of WISP-1 in osteosarcoma angiogenesis is poorly understood...
April 13, 2017: Cell Death & Disease
https://www.readbyqxmd.com/read/28406439/protein-coding-genes-retrocopies-and-their-functions
#20
REVIEW
Magdalena Regina Kubiak, Izabela Makałowska
Transposable elements, often considered to be not important for survival, significantly contribute to the evolution of transcriptomes, promoters, and proteomes. Reverse transcriptase, encoded by some transposable elements, can be used in trans to produce a DNA copy of any RNA molecule in the cell. The retrotransposition of protein-coding genes requires the presence of reverse transcriptase, which could be delivered by either non-long terminal repeat (non-LTR) or LTR transposons. The majority of these copies are in a state of "relaxed" selection and remain "dormant" because they are lacking regulatory regions; however, many become functional...
April 13, 2017: Viruses
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