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https://www.readbyqxmd.com/read/29216285/myocardial-adaption-to-hi-r-t-in-previously-untrained-men-with-a-randomized-longitudinal-cardiac-mr-imaging-study-physical-adaptions-in-untrained-on-strength-and-heart-trial-push-trial
#1
Michael Scharf, Derya Oezdemir, Axel Schmid, Wolfgang Kemmler, Simon von Stengel, Matthias S May, Michael Uder, Michael M Lell
OBJECTIVE: Although musculoskeletal effects in resistance training are well described, little is known about structural and functional cardiac adaption in formerly untrained subjects. We prospectively evaluated whether short term high intensity (resistance) training (HI(R)T) induces detectable morphologic cardiac changes in previously untrained men in a randomized controlled magnetic resonance imaging (MRI) study. MATERIALS AND METHODS: 80 untrained middle-aged men were randomly assigned to a HI(R)T-group (n = 40; 43...
2017: PloS One
https://www.readbyqxmd.com/read/29204341/case-report-exome-sequencing-identifies-t-all-with-myeloid-features-as-a-ikzf1-struck-early-precursor-t-cell-malignancy
#2
Marcus C Hansen, Line Nederby, Eigil Kjeldsen, Marianne A Petersen, Hans B Ommen, Peter Hokland
No abstract text is available yet for this article.
2018: Leukemia Research Reports
https://www.readbyqxmd.com/read/29202016/inhibition-of-ngly1-inactivates-the-transcription-factor-nrf1-and-potentiates-proteasome-inhibitor-cytotoxicity
#3
Frederick M Tomlin, Ulla I M Gerling-Driessen, Yi-Chang Liu, Ryan A Flynn, Janakiram R Vangala, Christian S Lentz, Sandra Clauder-Muenster, Petra Jakob, William F Mueller, Diana Ordoñez-Rueda, Malte Paulsen, Naoko Matsui, Deirdre Foley, Agnes Rafalko, Tadashi Suzuki, Matthew Bogyo, Lars M Steinmetz, Senthil K Radhakrishnan, Carolyn R Bertozzi
Proteasome inhibitors are used to treat blood cancers such as multiple myeloma (MM) and mantle cell lymphoma. The efficacy of these drugs is frequently undermined by acquired resistance. One mechanism of proteasome inhibitor resistance may involve the transcription factor Nuclear Factor, Erythroid 2 Like 1 (NFE2L1, also referred to as Nrf1), which responds to proteasome insufficiency or pharmacological inhibition by upregulating proteasome subunit gene expression. This "bounce-back" response is achieved through a unique mechanism...
November 22, 2017: ACS Central Science
https://www.readbyqxmd.com/read/29200162/study-of-notch1-and-fbxw7-mutations-and-its-prognostic-significance-in-south-indian-t-cell-acute-lymphoblastic-leukemia
#4
Natarajan Valliyammai, Nirmala K Nancy, Tenali G Sagar, Thangarajan Rajkumar
NOTCH1/FBXW7 mutations trigger oncogenic NOTCH1 signaling and its downstream target genes play crucial roles in the molecular pathogenesis of T-cell acute lymphoblastic leukemia (T-ALL). In the present study, NOTCH1 and FBXW7 mutations were studied in 25 primary T-ALL samples. All 34 exons of NOTCH1 and hotspot exons (exon 9 and exon 10) of FBXW7 were polymerase chain reaction amplified and sequenced for mutations. Our results showed that 13/25 (52%) were NOTCH1-mutated, of which 11 patients (44%) showed mutation in the hotspot exons...
December 1, 2017: Journal of Pediatric Hematology/oncology
https://www.readbyqxmd.com/read/29189509/successful-treatment-of-a-very-late-isolated-relapse-in-an-adolescent-with-a-picalm-mllt10-positive-t-lineage-acute-lymphoblastic-leukemia
#5
Emanuela Cannata, Piera Samperi, Carla Cimino, Silvia Marino, Federica Sullo, Elena Mirabile, Andrea Di Cataldo, Giovanna Russo, Luca Lo Nigro
T-lineage ALL is an aggressive disease that needs to be treated with intensive treatment schedules. A late relapse rarely occurs and a clear choice for second-line treatment is on debate. We report on a young adult with a very late isolated extramedullary relapse of PICALM-MLLT10 positive T-ALL, successfully treated with a chemotherapy-based and radiotherapy-based pediatric protocol. We demonstrate that relapse can occur in T-ALL although a SR-MRD behavior treated with a high-risk protocol; specific molecular diagnostic aberrations, as PICALM-MLLT10, are still conserved at very late relapse; a second-line treatment based on pediatric protocol can be effective...
November 17, 2017: Journal of Pediatric Hematology/oncology
https://www.readbyqxmd.com/read/29187889/t-cell-acute-lymphoblastic-leukemia-cells-display-activation-of-different-survival-pathways
#6
Sausan A Moharram, Kinjal Shah, Julhash U Kazi
T-cell acute lymphoblastic leukemia (T-ALL) is a disease of the blood affecting T-lymphocytes. Although notable improvements have been achieved in T-ALL treatment, half of the adult T-ALL patients still experience treatment failure. In order to develop a targeted therapy, we need a better understanding of T-ALL pathogenesis. In this study, we used patient-derived cell lines which display resistance to glucocorticoids. We observed that different cell lines are dependent on different survival signaling pathways...
2017: Journal of Cancer
https://www.readbyqxmd.com/read/29187379/mutant-jak3-signaling-is-increased-by-loss-of-wild-type-jak3-or-by-acquiring-secondary-jak3-mutations-in-t-all
#7
Sandrine Degryse, Simon Bornschein, Charles E de Bock, Emilie Leroy, Marlies Vanden Bempt, Sofie Demeyer, Kris Jacobs, Ellen Geerdens, Olga Gielen, Jean Soulier, Christine J Harrison, Stefan N Constantinescu, Jan Cools
The JAK3 tyrosine kinase is mutated in 10 to 16% of T-cell acute lymphoblastic leukemia (T-ALL) cases. JAK3 mutants induce constitutive JAK/STAT signaling and cause leukemia when expressed in the bone marrow cells of mice. Surprisingly, we observed that one third of the JAK3 mutant T-ALL cases harbor two JAK3 mutations, some of which are mono-allelic and others that are bi-allelic. Our data suggest that wild type JAK3 competes with mutant JAK3(M511I) for binding to the common gamma chain and thereby suppresses its oncogenic potential...
November 29, 2017: Blood
https://www.readbyqxmd.com/read/29184402/cooperation-of-irak1-4-inhibitor-and-abt-737-in-nanoparticles-for-synergistic-therapy-of-t-cell-acute-lymphoblastic-leukemia
#8
Xiaoyan Wu, Lin Wang, Yining Qiu, Bingyu Zhang, Zhenhua Hu, Runming Jin
T cell acute lymphoblastic leukemia (T-ALL) is caused by clonal expansion of variant T cell progenitors and is considered as a high risk leukemia. Contemporary single chemotherapy has a limited effect due to dynamic and versatile properties of T-ALL. Here IRAK1/4 inhibitor and ABT-737 were co-encapsulated into polyethylene glycol modified poly (lactic-co-glycolic acid) nanoparticles (IRAK/ABT-NP) to enhance synergistic therapy of T-ALL. The formulation was optimized to achieve high drug loading using Box-Behnken design and response surface methodology...
2017: International Journal of Nanomedicine
https://www.readbyqxmd.com/read/29175378/increased-activity-of-both-cdk1-and-cdk2-is-necessary-for-the-combinatorial-activity-of-wee1-inhibition-and-cytarabine
#9
Tamara B Garcia, Susan P Fosmire, Christopher C Porter
Inhibition of WEE1 is emerging as a promising chemosensitization strategy in many cancers including acute leukemia. Our lab and others have demonstrated that a small-molecule inhibitor of WEE1, AZD1775, sensitizes acute leukemia cells to cytarabine; however, a mechanism of combinatorial activity has remained elusive. Thus, we sought to determine the relative contribution of WEE1 targets CDK1 and CDK2 to the combinatorial activity of AZD1775 and cytarabine. To accomplish this, we expressed "WEE1 resistant" CDK1 (CDK1-AF) and CDK2 (CDK2-AF) constructs in a T-ALL cell line...
November 11, 2017: Leukemia Research
https://www.readbyqxmd.com/read/29158376/leukemia-specific-delivery-of-mutant-notch1-targeted-therapy
#10
Giovanni Roti, Jun Qi, Samuel Kitara, Marta Sanchez-Martin, Amy Saur Conway, Anthony C Varca, Angela Su, Lei Wu, Andrew L Kung, Adolfo A Ferrando, James E Bradner, Kimberly Stegmaier
On-target drug delivery remains a challenge in cancer precision medicine; it is difficult to deliver a targeted therapy to cancer cells without incurring toxicity to normal tissues. The SERCA (sarco-endoplasmic reticulum Ca2+ ATPase) inhibitor thapsigargin inhibits mutant NOTCH1 receptors compared with wild type in T cell acute lymphoblastic leukemia (T-ALL), but its administration is predicted to be toxic in humans. Leveraging the addiction of ALL to folic acid, we conjugated folate to an alcohol derivative of thapsigargin via a cleavable ester linkage...
November 20, 2017: Journal of Experimental Medicine
https://www.readbyqxmd.com/read/29156664/molecular-regulation-of-t-all-cell-infiltration-into-the-cns
#11
EDITORIAL
Judy L Cannon, Sreenivasa Rao Oruganti, Devan W Vidrine
No abstract text is available yet for this article.
October 17, 2017: Oncotarget
https://www.readbyqxmd.com/read/29151585/defining-the-molecular-basis-of-oncogenic-cooperation-between-tal1-expression-and-pten-deletion-in-t-all-using-a-novel-pro-t-cell-model-system
#12
S Bornschein, S Demeyer, R Stirparo, O Gielen, C Vicente, E Geerdens, B Ghesquière, S Aerts, J Cools, C E de Bock
T-cell acute lymphoblastic leukemia (T-ALL) is caused by the accumulation of multiple mutations combined with the ectopic expression of transcription factors in developing T cells. However, the molecular basis underlying cooperation between transcription factor expression and additional oncogenic mutations in driving T-ALL has been difficult to assess due to limited robust T cell model systems. Here we utilize a new ex vivo pro-T cell model to study oncogenic cooperation. Using a systems biological approach we first dissect the pro-T cell signaling network driven by interleukin-7 (Il7), stem cell factor (Scf) and Notch1 and identify key downstream Akt, Stat, E2f and Myc genetic signaling networks...
November 20, 2017: Leukemia: Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K
https://www.readbyqxmd.com/read/29147589/%C3%AE-%C3%AE-t-cell-acute-lymphoblastic-leukemia-lymphoma-discussion-of-two-pediatric-cases-and-its-distinction-from-other-mature-%C3%AE-%C3%AE-t-cell-malignancies
#13
Eric X Wei, Vasiliki Leventaki, John K Choi, Susana C Raimondi, Elizabeth M Azzato, Sheila A Shurtleff, Menchu G Ong, Diana M Veillon, James D Cotelingam, Rodney E Shackelford
Gamma delta (γδ) T-cell antigen receptor (TCR) expression and its related T-cell differentiation are not commonly reported in T-cell acute lymphoblastic leukemia/lymphoma (T-ALL). Here we report two pediatric T-ALL cases and present their clinical features, histology, immunophenotypes, cytogenetics, and molecular diagnostic findings. The first patient is a two-year-old girl with leukocytosis, circulating lymphoblasts, and a cryptic insertion of a short-arm segment at 10p12 into the long-arm segment of 11q23 resulting in an MLL and AF10 fusion transcript, which may be the first reported in γδ T-ALL...
2017: Case Reports in Hematology
https://www.readbyqxmd.com/read/29138297/mafb-enhances-oncogenic-notch-signaling-in-t-cell-acute-lymphoblastic-leukemia
#14
Kostandin V Pajcini, Lanwei Xu, Lijian Shao, Jelena Petrovic, Karol Palasiewicz, Yumi Ohtani, Will Bailis, Curtis Lee, Gerald B Wertheim, Rajeswaran Mani, Natarajan Musuthamy, Yunlei Li, Jules P P Meijerink, Stephen C Blacklow, Robert B Faryabi, Sara Cherry, Warren S Pear
Activating mutations in the gene encoding the cell-cell contact signaling protein Notch1 are common in human T cell acute lymphoblastic leukemias (T-ALLs). However, expressing Notch1 mutant alleles in mice fails to efficiently induce the development of leukemia. We performed a gain-of-function screen to identify proteins that enhanced signaling by leukemia-associated Notch1 mutants. The transcription factors MAFB and ETS2 emerged as candidates that individually enhanced Notch1 signaling, and when coexpressed, they synergistically increased signaling to an extent similar to that induced by core components of the Notch transcriptional complex...
November 14, 2017: Science Signaling
https://www.readbyqxmd.com/read/29136506/a-paradoxical-tumor-suppressor-role-for-the-rac1-exchange-factor-vav1-in-t-cell-acute-lymphoblastic-leukemia
#15
Javier Robles-Valero, L Francisco Lorenzo-Martín, Mauricio Menacho-Márquez, Isabel Fernández-Pisonero, Antonio Abad, Mireia Camós, María L Toribio, Lluis Espinosa, Anna Bigas, Xosé R Bustelo
Rho guanine exchange factors (GEFs), the enzymes that stimulate Rho GTPases, are deemed as potential therapeutic targets owing to their protumorigenic functions. However, the understanding of the spectrum of their pathobiological roles in tumors is still very limited. We report here that the GEF Vav1 unexpectedly possesses tumor-suppressor functions in immature T cells. This function entails the noncatalytic nucleation of complexes between the ubiquitin ligase Cbl-b and the intracellular domain of Notch1 (ICN1) that favors ICN1 ubiquitinylation and degradation...
November 13, 2017: Cancer Cell
https://www.readbyqxmd.com/read/29116180/the-ephb6-receptor-is-overexpressed-in-pediatric-t-cell-acute-lymphoblastic-leukemia-and-increases-its-sensitivity-to-doxorubicin-treatment
#16
Amr El Zawily, Emily McEwen, Behzad Toosi, Frederick S Vizeacoumar, Tanya Freywald, Franco J Vizeacoumar, Andrew Freywald
While impressive improvements have been achieved in T-ALL therapy, current treatment approaches fail in approximately 25% of patients and these patients have limited treatment options. Another significant group of patients is being overtreated, which causes long-lasting side effects. Identification of molecules controlling drug resistance in T-ALL is crucial for treatment optimisation in both scenarios. We report here the EphB6 receptor is frequently overexpressed in T-ALL. Remarkably, our observations indicate that EphB6 acts in T-ALL cells to enhance sensitivity to a DNA-damaging drug, doxorubicin, as interruption of EphB6 activity interferes with the efficiency of doxorubicin-induced eradication of T-ALL cells in cell culture and in xenograft animals...
November 7, 2017: Scientific Reports
https://www.readbyqxmd.com/read/29115896/drugging-dna-repair-to-target-t-all-cells
#17
Yashodhara Dasgupta, Konstantin Golovine, Margaret Nieborowska-Skorska, Li Luo, Ksenia Matlawska-Wasowska, Charles G Mullighan, Tomasz Skorski
No abstract text is available yet for this article.
November 8, 2017: Leukemia & Lymphoma
https://www.readbyqxmd.com/read/29113211/aberrant-expression-of-cd133-and-cd82-in-patients-with-pediatric-acute-lymphoblastic-leukemia-and-the-clinical-significance
#18
Hongyan Ji, Li Chen, Yunpeng Dai, Xiaojun Sun, Xiuli Li, Qi Wang, Daoxin Ma, Dongdong Du, Ping Zhao, Yulin Wang
Cluster of differentiation (CD)133 is considered to be a marker of leukemia stem cells (LSCs), which are one of the primary causes of occurrence, drug resistance and relapse of acute lymphoblastic leukemia (ALL). CD82, an adhesion molecule, performs an important role in the interaction between LSCs and their niche. The purpose of the present study was to assess CD133 and CD82 expression in patients with pediatric ALL, and to evaluate the association with the clinical data. Using flow cytometric assessment and reverse transcription-polymerase chain reaction, CD133 and CD82 expression levels were measured in the bone marrow (BM) of 37 patients with newly diagnosed (ND) pediatric ALL [ALL-ND; 30 B-cell-ALL (B-ALL) and 7 T-cell-ALL (T-ALL)], in 22 patients with complete remission pediatric ALL (ALL-CR) and in 16 age-matched children without BM disease...
November 2017: Oncology Letters
https://www.readbyqxmd.com/read/29104587/notch-and-its-oncogenic-activity-in-human-malignancies
#19
REVIEW
Marlena Brzozowa-Zasada, Adam Piecuch, Marek Michalski, Oliwia Segiet, Józef Kurek, Marzena Harabin-Słowińska, Romuald Wojnicz
Background: Increasing evidence has demonstrated that Notch signaling is deregulated in human hematological malignancies and solid tumors. This signaling has a protumorigenic effect but may also act as a tumor suppressor. How induction of a single pathway gives rise to the opposite effects in different cell types is still unknown. Methods: This review article includes available data from peer-reviewed publications associated with the role of Notch signaling during cancer pathogenesis...
2017: European Surgery: ACA: Acta Chirurgica Austriaca
https://www.readbyqxmd.com/read/29101238/glucocorticoid-resistance-is-reverted-by-lck-inhibition-in-pediatric-t-cell-acute-lymphoblastic-leukemia
#20
Valentina Serafin, Giorgia Capuzzo, Gloria Milani, Sonia Anna Minuzzo, Marica Pinazza, Roberta Bortolozzi, Silvia Bresolin, Elena Porcù, Chiara Frasson, Stefano Indraccolo, Giuseppe Basso, Benedetta Accordi
Pediatric T-acute lymphoblastic leukemia (T-ALL) patients often display resistance to glucocorticoid (GC) treatment. These patients, classified as Prednisone Poor Responders (PPR), have poorer outcome compared to the other pediatric T-ALL patients receiving a high-risk adapted therapy. Since glucocorticoids are administered to ALL patients during all the different phases of therapy, GC resistance represents an important challenge to be addressed in order to improve the outcome for these patients. Mechanisms underlying resistance are not yet fully unraveled, thus our research focused on the identification of deregulated signaling pathways to point out new targeted approaches...
November 3, 2017: Blood
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