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  1. Article ; Online: Rewriting the rules for care of MDS and AML patients in the time of COVID-19

    Azra Raza / Amer Assal / Abdullah M. Ali / Joseph G. Jurcic

    Leukemia Research Reports, Vol 13, Iss , Pp 100201- (2020)

    2020  

    Abstract: The care of patients with myelodysplastic syndromes (MDS) and acute myeloid leukemia (AML) has been radically altered by COVID-19, especially in New York City, the epicenter of the pandemic. Here we summarize how telemedicine, virtual visits, delayed ... ...

    Abstract The care of patients with myelodysplastic syndromes (MDS) and acute myeloid leukemia (AML) has been radically altered by COVID-19, especially in New York City, the epicenter of the pandemic. Here we summarize how telemedicine, virtual visits, delayed transfusions, and chemotherapy, preferably selecting self-administered medications and visits by home healthcare workers, are employed to minimize exposure of our high-risk population of patients to the virus. The unique challenges of transplants during the pandemic and the consequences of an abrupt halt in all non-essential research activities are described. Not all the changes forced by COVID-19 are detrimental.
    Keywords Myelodysplatic Syndromes ; Acute myeloid leukemia ; telemedicine ; COVID-19 ; stem cell transplantation ; Neoplasms. Tumors. Oncology. Including cancer and carcinogens ; RC254-282 ; covid19
    Language English
    Publishing date 2020-01-01T00:00:00Z
    Publisher Elsevier
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  2. Article ; Online: Gene expression in notochord and nuclei pulposi

    Rahul Raghavan / Ugo Coppola / Yushi Wu / Chibuike Ihewulezi / Lenny J. Negrón-Piñeiro / Julie E. Maguire / Justin Hong / Matthew Cunningham / Han Jo Kim / Todd J. Albert / Abdullah M. Ali / Jean-Pierre Saint-Jeannet / Filomena Ristoratore / Chitra L. Dahia / Anna Di Gregorio

    BMC Ecology and Evolution, Vol 23, Iss 1, Pp 1-

    a study of gene families across the chordate phylum

    2023  Volume 22

    Abstract: Abstract The transition from notochord to vertebral column is a crucial milestone in chordate evolution and in prenatal development of all vertebrates. As ossification of the vertebral bodies proceeds, involutions of residual notochord cells into the ... ...

    Abstract Abstract The transition from notochord to vertebral column is a crucial milestone in chordate evolution and in prenatal development of all vertebrates. As ossification of the vertebral bodies proceeds, involutions of residual notochord cells into the intervertebral discs form the nuclei pulposi, shock-absorbing structures that confer flexibility to the spine. Numerous studies have outlined the developmental and evolutionary relationship between notochord and nuclei pulposi. However, the knowledge of the similarities and differences in the genetic repertoires of these two structures remains limited, also because comparative studies of notochord and nuclei pulposi across chordates are complicated by the gene/genome duplication events that led to extant vertebrates. Here we show the results of a pilot study aimed at bridging the information on these two structures. We have followed in different vertebrates the evolutionary trajectory of notochord genes identified in the invertebrate chordate Ciona, and we have evaluated the extent of conservation of their expression in notochord cells. Our results have uncovered evolutionarily conserved markers of both notochord development and aging/degeneration of the nuclei pulposi.
    Keywords Ciona ; Coronin ; Human ; Mouse ; Notochord ; Nucleus pulposus ; Ecology ; QH540-549.5 ; Evolution ; QH359-425
    Language English
    Publishing date 2023-10-01T00:00:00Z
    Publisher BMC
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  3. Article ; Online: Survey and evaluation of mutations in the human KLF1 transcription unit

    Merlin Nithya Gnanapragasam / John D. Crispino / Abdullah M. Ali / Rona Weinberg / Ronald Hoffman / Azra Raza / James J. Bieker

    Scientific Reports, Vol 8, Iss 1, Pp 1-

    2018  Volume 8

    Abstract: Abstract Erythroid Krüppel-like Factor (EKLF/KLF1) is an erythroid-enriched transcription factor that plays a global role in all aspects of erythropoiesis, including cell cycle control and differentiation. We queried whether its mutation might play a ... ...

    Abstract Abstract Erythroid Krüppel-like Factor (EKLF/KLF1) is an erythroid-enriched transcription factor that plays a global role in all aspects of erythropoiesis, including cell cycle control and differentiation. We queried whether its mutation might play a role in red cell malignancies by genomic sequencing of the KLF1 transcription unit in cell lines, erythroid neoplasms, dysplastic disorders, and leukemia. In addition, we queried published databases from a number of varied sources. In all cases we only found changes in commonly notated SNPs. Our results suggest that if there are mutations in KLF1 associated with erythroid malignancies, they are exceedingly rare.
    Keywords Medicine ; R ; Science ; Q
    Language English
    Publishing date 2018-04-01T00:00:00Z
    Publisher Nature Publishing Group
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  4. Article ; Online: Loss of Grem1-lineage chondrogenic progenitor cells causes osteoarthritis

    Jia Q. Ng / Toghrul H. Jafarov / Christopher B. Little / Tongtong Wang / Abdullah M. Ali / Yan Ma / Georgette A. Radford / Laura Vrbanac / Mari Ichinose / Samuel Whittle / David J. Hunter / Tamsin R. M. Lannagan / Nobumi Suzuki / Jarrad M. Goyne / Hiroki Kobayashi / Timothy C. Wang / David R. Haynes / Danijela Menicanin / Stan Gronthos /
    Daniel L. Worthley / Susan L. Woods / Siddhartha Mukherjee

    Nature Communications, Vol 14, Iss 1, Pp 1-

    2023  Volume 14

    Abstract: Abstract Osteoarthritis (OA) is characterised by an irreversible degeneration of articular cartilage. Here we show that the BMP-antagonist Gremlin 1 (Grem1) marks a bipotent chondrogenic and osteogenic progenitor cell population within the articular ... ...

    Abstract Abstract Osteoarthritis (OA) is characterised by an irreversible degeneration of articular cartilage. Here we show that the BMP-antagonist Gremlin 1 (Grem1) marks a bipotent chondrogenic and osteogenic progenitor cell population within the articular surface. Notably, these progenitors are depleted by injury-induced OA and increasing age. OA is also caused by ablation of Grem1 cells in mice. Transcriptomic and functional analysis in mice found that articular surface Grem1-lineage cells are dependent on Foxo1 and ablation of Foxo1 in Grem1-lineage cells caused OA. FGFR3 signalling was confirmed as a promising therapeutic pathway by administration of pathway activator, FGF18, resulting in Grem1-lineage chondrocyte progenitor cell proliferation, increased cartilage thickness and reduced OA. These findings suggest that OA, in part, is caused by mechanical, developmental or age-related attrition of Grem1 expressing articular cartilage progenitor cells. These cells, and the FGFR3 signalling pathway that sustains them, may be effective future targets for biological management of OA.
    Keywords Science ; Q
    Language English
    Publishing date 2023-10-01T00:00:00Z
    Publisher Nature Portfolio
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  5. Article: U2AF35(S34F) Promotes Transformation by Directing Aberrant ATG7 Pre-mRNA 3′ End Formation

    Park, Sung Mi / Abdullah M. Ali / Azra Raza / Ching-Man Virbasius / Huan Yang / Jianhong Ou / Lihua Julie Zhu / Lynn Chamberlain / Michael R. Green / Siddhartha Mukherjee / Tessa M. Simone

    Molecular cell. 2016 May 19, v. 62, no. 4

    2016  

    Abstract: Recurrent mutations in the splicing factor U2AF35 are found in several cancers and myelodysplastic syndrome (MDS). How oncogenic U2AF35 mutants promote transformation remains to be determined. Here we derive cell lines transformed by the oncogenic U2AF35( ...

    Abstract Recurrent mutations in the splicing factor U2AF35 are found in several cancers and myelodysplastic syndrome (MDS). How oncogenic U2AF35 mutants promote transformation remains to be determined. Here we derive cell lines transformed by the oncogenic U2AF35(S34F) mutant and identify aberrantly processed pre-mRNAs by deep sequencing. We find that in U2AF35(S34F)-transformed cells the autophagy-related factor 7 (Atg7) pre-mRNA is abnormally processed, which unexpectedly is not due to altered splicing but rather selection of a distal cleavage and polyadenylation (CP) site. This longer Atg7 mRNA is translated inefficiently, leading to decreased ATG7 levels and an autophagy defect that predisposes cells to secondary mutations, resulting in transformation. MDS and acute myeloid leukemia patient samples harboring U2AF35(S34F) have a similar increased use of the ATG7 distal CP site, and previous studies have shown that mice with hematopoietic cells lacking Atg7 develop an MDS-like syndrome. Collectively, our results reveal a basis for U2AF35(S34F) oncogenic activity.
    Keywords autophagy ; hematopoietic stem cells ; high-throughput nucleotide sequencing ; messenger RNA ; mice ; mutants ; mutation ; myeloid leukemia ; patients ; translation (genetics)
    Language English
    Dates of publication 2016-0519
    Size p. 479-490.
    Publishing place Elsevier Inc.
    Document type Article
    ZDB-ID 1415236-8
    ISSN 1097-4164 ; 1097-2765
    ISSN (online) 1097-4164
    ISSN 1097-2765
    DOI 10.1016/j.molcel.2016.04.011
    Database NAL-Catalogue (AGRICOLA)

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