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https://www.readbyqxmd.com/read/27913472/novel-agents-in-chronic-lymphocytic-leukemia
#1
Nicole Lamanna, Susan O'Brien
The advent of novel small-molecule inhibitors has transformed the treatment approaches for patients with chronic lymphocytic leukemia (CLL). These therapies are becoming increasingly used in patients with relapsed disease, patients with 17p deletion, and, as of recently, also in the frontline setting for previously untreated patients with CLL. Moreover, many of these are oral therapies that are significantly less myelosuppressive than chemoimmunotherapy. However, these agents have their own set of unique toxicities with which providers must gain familiarity...
December 2, 2016: Hematology—the Education Program of the American Society of Hematology
https://www.readbyqxmd.com/read/27913471/sequencing-of-chronic-lymphocytic-leukemia-therapies
#2
Jacqueline C Barrientos
It is an unprecedented time for the treatment of patients with chronic lymphocytic leukemia (CLL) with the recent approval of several targeted agents for use in frontline, relapsed, refractory, and high-risk disease. Traditionally, frontline management of CLL has been a combination of chemotherapy (fludarabine, cyclophosphamide, bendamustine, or chlorambucil) with an anti-CD20 monoclonal antibody (rituximab, ofatumumab, obinutuzumab). The current landscape is rapidly evolving with the advent of therapies that demonstrate selective inhibition of important pathways necessary for CLL proliferation and survival...
December 2, 2016: Hematology—the Education Program of the American Society of Hematology
https://www.readbyqxmd.com/read/27881039/fludarabine-cyclophosphamide-and-lenalidomide-in-patients-with-relapsed-refractory-chronic-lymphocytic-leukemia-a-multicenter-phase-i-ii-gimema-trial
#3
Francesca R Mauro, Angelo M Carella, Stefano Molica, Francesca Paoloni, Anna M Liberati, Francesco Zaja, Valeria Belsito, Agostino Cortellezzi, Rita Rizzi, Patrizia Tosi, Mauro Spriano, Antonietta Ferretti, Mauro Nanni, Marilisa Marinelli, Maria S De Propris, Sonia M Orlando, Marco Vignetti, Antonio Cuneo, Anna R Guarini, Robin Foà
The activity and safety of a regimen combining lenalidomide with fludarabine and cyclophosphamide (FC) was investigated in patients with relapsed/refractory (R/R) chronic lymphocytic leukemia (CLL). Treatment consisted of six monthly courses of the FC regimen combined with 14 days of lenalidomide given at the starting dose of 2.5 mg during course 1. The maximum tolerated dose of lenalidomide was 5 mg. Forty patients were assessed for response, 66% were IGHV unmutated, 45% showed deletion 11q or 17p. The overall response and complete remission rates were 62...
November 23, 2016: Leukemia & Lymphoma
https://www.readbyqxmd.com/read/27858991/management-of-central-nervous-system-involvement-in-chronic-lymphocytic-leukaemia-a-retrospective-cohort-of-30-patients
#4
Anne Wanquet, Rudy Birsen, Charlotte Bonnet, Marouane Boubaya, Sylvain Choquet, Jehan Dupuis, Stephane Lepretre, Daniel Re, Jonathan Fahri, Anne-Sophie Michallet, Loïc Ysebaert, Richard Lemal, Thierry Lamy, Richard Delarue, Xavier Troussard, Florence Cymbalista, Vincent Levy, Pierre-Yves Dietrich, Veronique Leblond, Therese Aurran-Schleinitz
Central nervous system involvement (CNSi) is a rare and poorly reported complication of chronic lymphocytic leukaemia (CLL). Establishing cause and effect between the CLL and the neurological symptoms remains challenging. We have analysed a retrospective cohort of 30 CLL patients with CNSi, documented by lymphocytic infiltration either by flow cytometry of the cerebrospinal fluid (CSF; n = 29) or CNS biopsy (n = 1). Neurological symptoms were heterogeneous. At the time of CNSi, less than half of the patients had a progressive CLL and 20 had never been treated for CLL...
November 11, 2016: British Journal of Haematology
https://www.readbyqxmd.com/read/27821812/karyotypic-complexity-rather-than-chromosome-8-abnormalities-aggravates-the-outcome-of-chronic-lymphocytic-leukemia-patients-with-tp53-aberrations
#5
Gonzalo Blanco, Anna Puiggros, Panagiotis Baliakas, Anastasia Athanasiadou, MªDolores García-Malo, Rosa Collado, Aliki Xochelli, María Rodríguez-Rivera, Margarita Ortega, Mª José Calasanz, Elisa Luño, MªTeresa Vargas, Javier Grau, Carolina Martínez-Laperche, Alberto Valiente, José Cervera, Achilles Anagnostopoulos, Eva Gimeno, Eugènia Abella, Evangelia Stalika, Jesús Mª Hernández-Rivas, Francisco José Ortuño, Diego Robles, Ana Ferrer, David Ivars, Marcos González, Francesc Bosch, Pau Abrisqueta, Kostas Stamatopoulos, Blanca Espinet
Patients with chronic lymphocytic leukemia (CLL) harboring TP53 aberrations (TP53abs; chromosome 17p deletion and/or TP53 mutation) exhibit an unfavorable clinical outcome. Chromosome 8 abnormalities, namely losses of 8p (8p-) and gains of 8q (8q+) have been suggested to aggravate the outcome of patients with TP53abs. However, the reported series were small, thus hindering definitive conclusions. To gain insight into this issue, we assessed a series of 101 CLL patients harboring TP53 disruption. The frequency of 8p- and 8q+ was 14...
November 4, 2016: Oncotarget
https://www.readbyqxmd.com/read/27803007/management-of-chronic-lymphocytic-leukemia-cll-in-the-elderly-a-position-paper-from-an-international-society-of-geriatric-oncology-siog-task-force
#6
REVIEW
R Stauder, B Eichhorst, M Hamaker, K Kaplanov, V Morrison, A Österborg, I Poddubnaya, J A Woyach, T Shanafelt, L Smolej, L Ysebaert, V Goede
Chronic lymphocytic leukemia (CLL) mainly affects older people: the median age at diagnosis is above seventy years. Elderly patients with CLL are heterogeneous with regard both to the biology of their disease and aging. Following the diagnosis of CLL in an elderly individual, careful risk assessment is essential when treatment options are evaluated. This includes not only clinical staging and evaluation of disease-specific prognostic biomarkers such as 17p deletion and TP53 mutation, but also of comorbidities, physical capacity, nutritional status, cognitive capacity, ability to perform activities of daily living, and social support...
November 1, 2016: Annals of Oncology: Official Journal of the European Society for Medical Oncology
https://www.readbyqxmd.com/read/27797975/long-term-follow-up-of-treatment-with-ibrutinib-and-rituximab-ir-in-patients-with-high-risk-chronic-lymphocytic-leukemia-cll
#7
Preetesh Jain, Michael J Keating, William Wierda, Mariela Sivina, Philip A Thompson, Alessandra Ferrajoli, Zeev Estrov, Hagop Kantarjian, Susan O'Brien, Jan Burger
BACKGROUND: Ibrutinib is an active therapy with acceptable safety profile for patients with CLL, including high-risk patients with del17p or with TP53 mutations. Ibrutinib is broadly indicated for the treatment of patients with chronic lymphocytic leukemia and specifically including those with 17p deletion. The optimal use of ibrutinib in combination with other agents, remains controversial. METHODS: We report the long term outcome [median follow up of 47 months (range 36-51 months)] of 40 patients with high risk CLL, treated on the first ibrutinib combination trial with rituximab (IR)...
October 19, 2016: Clinical Cancer Research: An Official Journal of the American Association for Cancer Research
https://www.readbyqxmd.com/read/27756834/ibrutinib-for-relapsed-refractory-chronic-lymphocytic-leukemia-a-uk-and-ireland-analysis-of-outcomes-in-315-patients
#8
(no author information available yet)
In 2014, ibrutinib was made available for relapsed/refractory chronic lymphocytic leukemia patients. The UK Chronic Lymphocytic Leukaemia Forum collected data from UK/Ireland patients with a minimum of 1 year follow-up with pre-planned primary endpoints; the number of patients still on therapy at 1 year "discontinuation-free survival" and 1 year overall survival. With a median of 16 months follow up, data on 315 patients demonstrated a 1 year discontinuation-free survival of 73.7% and a 1 year overall survival of 83...
December 2016: Haematologica
https://www.readbyqxmd.com/read/27742075/tp53-dysfunction-in-cll-implications-for-prognosis-and-treatment
#9
Gera D Te Raa, Arnon P Kater
Despite the availability of novel targeted agents, TP53 defects remain the most important adverse prognostic factor in chronic lymphocytic leukemia (CLL). Detection of deletion of TP53 locus (17p deletion) by fluorescent in situ hybridization (FISH) has become standard and performed prior to every line of treatment as the incidence dramatically increases as relapses occur. As monoallelic mutations of TP53 equally affect outcome, novel methods are being developed to improve detection of TP53 defects and include next-generation sequencing (NGS) and functional assays...
March 2016: Best Practice & Research. Clinical Haematology
https://www.readbyqxmd.com/read/27742074/biomarkers-in-chronic-lymphocytic-leukemia-clinical-applications-and-prognostic-markers
#10
Carlos I Amaya-Chanaga, Laura Z Rassenti
Chronic lymphocytic leukemia (CLL) is a heterogeneous disease with a variable clinical course. The Rai and Binet staging systems are often used to predict survival. However, they do not take into account other biological characteristics of CLL cells that may influence the disease course and response to treatment. Prognostic factors such as chromosome abnormalities (trisomy 12, 11q deletions and 17p deletions), β2 microglobulin, thymidine kinase, CD38 and ZAP-70 expression, IGHV mutation status, and mutations in genes such as NOTCH1, MYD88, SF3B1, and ATM are also predictors of prognosis...
March 2016: Best Practice & Research. Clinical Haematology
https://www.readbyqxmd.com/read/27719720/-ighv-mutational-statue-in-patients-with-splenic-marginal-zone-lymphoma
#11
W J Yang, Z Yu, R Lyu, Z J Li, H Li, W J Xiong, S H Yi, W Liu, L G Qiu
Objective: To investigate the IGHV mutational status and its differences from Caucasian in splenic marginal zone lymphoma (SMZL). Methods: A retrospective study on 40 SMZL cases were performed to detect the V-D-J sequence of IGHV by plasmid cloning sequencing, comparing the data with the most homologous germ line V sequence in database, identifying the stereotype of patients through cluster analysis and alignment. The clinical and laboratory characteristics were compared between the patients with IGHV mutation and without mutations...
September 14, 2016: Zhonghua Xue Ye Xue za Zhi, Zhonghua Xueyexue Zazhi
https://www.readbyqxmd.com/read/27698805/genetic-landscape-of-a-case-of-extraovarian-peritoneal-serous-papillary-carcinoma
#12
Zhongping Cheng, Weihong Yang, Jing Guo, Ning Luo, Li Chen, Yan Xie, Xiaoyan Qu, Liping Hu, Hong Dai, Xiaoming Zuo
The present report aimed to study genetic alterations underlying extraovarian peritoneal serous papillary carcinoma (EPSPC), which have not previously been systematically investigated. A case of EPSPC was identified, and its genetic alterations were assessed by combining comparative genomic hybridization and whole-exome sequencing technologies to investigate the genomic landscape, including copy number variations and mutations in EPSPC. It was found that a large number of germline mutations were present, which may have predisposed the patient to the occurrence of this disease...
October 2016: Oncology Letters
https://www.readbyqxmd.com/read/27697588/metachronous-anaplastic-sarcoma-of-the-kidney-and-thyroid-follicular-carcinoma-as-manifestations-of-dicer1-abnormalities
#13
Misa Yoshida, Satoshi Hamanoue, Masafumi Seki, Mio Tanaka, Kenichi Yoshida, Hiroaki Goto, Seishi Ogawa, Junko Takita, Yukichi Tanaka
Anaplastic sarcoma of the kidney (ASK) is a tumor found in the pediatric age group and shows many histopathological similarities to pleuropulmonary blastoma (PPB). We present a 12-year-old girl diagnosed with ASK and, three years later, with thyroid follicular carcinoma (TFC) with DICER1 abnormalities. Germline insertion/deletion (p.G1809_S1814delinsA) and independent somatic mutations (p.E1705K in ASK, p.E1813D in TFC) were identified. All of these abnormalities are in the catalytic domain of RNase IIIb. Single-nucleotide polymorphism genotyping microarray revealed independent copy number alterations (trisomy 8, monosomy 10, loss of 17p and partial gain of 17q in ASK; trisomy 5 and partial loss of Xq in TFC)...
September 30, 2016: Human Pathology
https://www.readbyqxmd.com/read/27686109/pharmacokinetic-and-pharmacodynamic-evaluation-of-ibrutinib-for-the-treatment-of-chronic-lymphocytic-leukemia-rationale-for-lower-doses
#14
Prithviraj Bose, Varsha V Gandhi, Michael J Keating
Ibrutinib, a first-in-class covalent inhibitor of Bruton's tyrosine kinase (BTK), is approved in many countries for the treatment of relapsed/refractory chronic lymphocytic leukemia (CLL) and for previously untreated disease with a 17p deletion and, most recently, as a frontline therapy for CLL. In controlled trials in CLL, ibrutinib produced high response rates and improved survival in both the frontline and relapsed settings. While ibrutinib controls CLL with impressive efficacy, it only infrequently induces complete remissions, particularly of relapsed CLL, and does not eradicate minimal residual disease...
October 11, 2016: Expert Opinion on Drug Metabolism & Toxicology
https://www.readbyqxmd.com/read/27683974/cross-resistance-and-synergy-with-bendamustine-in-chronic-lymphocytic-leukemia
#15
Sara E F Kost, Eric D J Bouchard, Élise LaBossière, Xibiao Ye, Michelle L Queau, William S Liang, Versha Banerji, Spencer B Gibson, Sachin Katyal, James B Johnston
Bendamustine (BEN) has structural similarities to an alkylating agent and a nucleoside analog, and effective against tumor cells that are resistant to standard therapy. In this study we compared the activities of BEN against that of the alkylating agent, chlorambucil (CLB), and the nucleoside analogs, fludarabine (FLU) and deoxyadenosine/pentostatin (dADO/PEN), in primary chronic lymphocytic leukemia (CLL) cells in vitro. Cross-resistance was observed between BEN, CLB and FLU, with previously treated patients or those with a deletion 17p being most resistant...
September 20, 2016: Leukemia Research
https://www.readbyqxmd.com/read/27650502/alterations-of-mitochondrial-biogenesis-in-chronic-lymphocytic-leukemia-cells-with-loss-of-p53
#16
Marcia A Ogasawara, Jinyun Liu, Helene Pelicano, Naima Hammoudi, Carlo M Croce, Michael J Keating, Peng Huang
Deletion of chromosome 17p with a loss of p53 is an unfavorable cytogenetic change in chronic lymphocytic leukemia (CLL) with poor clinical outcome. Since p53 affects mitochondrial function and integrity, we examined possible mitochondrial changes in CLL mice with TCL1-Tg/p53(-/-) and TCL1-Tg/p53(+/+) genotypes and in primary leukemia cells from CLL patients with or without 17p-deletion. Although the expression of mitochondrial COX1, ND2, and ND6 decreased in p53(-/-)CLL cells, there was an increase in mitochondrial biogenesis as evidenced by higher mitochondrial mass and mtDNA copy number associated with an elevated expression of TFAM and PGC-1α...
November 2016: Mitochondrion
https://www.readbyqxmd.com/read/27638334/impact-of-venetoclax-exposure-on-clinical-efficacy-and-safety-in-patients-with-relapsed-or-refractory-chronic-lymphocytic-leukemia
#17
Kevin J Freise, Aksana K Jones, Doerthe Eckert, Sven Mensing, Shekman L Wong, Rod A Humerickhouse, Walid M Awni, Ahmed Hamed Salem
BACKGROUND: Venetoclax is a selective, potent, first-in-class B-cell lymphoma-2 inhibitor that restores apoptosis in cancer cells and has demonstrated efficacy in a variety of hematological malignancies. OBJECTIVE: The objective of this research was to characterize the relationship between venetoclax exposures and efficacy and safety in patients with relapsed or refractory (R/R) chronic lymphocytic leukemia (CLL)/small lymphocytic lymphoma (SLL). METHODS: A total of 272 and 338 patients from four clinical studies were pooled for the exposure-efficacy and exposure-safety analyses, respectively...
September 15, 2016: Clinical Pharmacokinetics
https://www.readbyqxmd.com/read/27637986/ibrutinib-holds-promise-for-patients-with-17p-deletion-cll
#18
Paolo Ghia
No abstract text is available yet for this article.
October 2016: Lancet Oncology
https://www.readbyqxmd.com/read/27637985/ibrutinib-for-patients-with-relapsed-or-refractory-chronic-lymphocytic-leukaemia-with-17p-deletion-resonate-17-a-phase-2-open-label-multicentre-study
#19
Susan O'Brien, Jeffrey A Jones, Steven E Coutre, Anthony R Mato, Peter Hillmen, Constantine Tam, Anders Österborg, Tanya Siddiqi, Michael J Thirman, Richard R Furman, Osman Ilhan, Michael J Keating, Timothy G Call, Jennifer R Brown, Michelle Stevens-Brogan, Yunfeng Li, Fong Clow, Danelle F James, Alvina D Chu, Michael Hallek, Stephan Stilgenbauer
BACKGROUND: The TP53 gene, encoding tumour suppressor protein p53, is located on the short arm of chromosome 17 (17p). Patients with 17p deletion (del17p) chronic lymphocytic leukaemia have poor responses and survival after chemoimmunotherapy. We assessed the activity and safety of ibrutinib, an oral covalent inhibitor of Bruton's tyrosine kinase, in relapsed or refractory patients with del17p chronic lymphocytic leukaemia or small lymphocytic lymphoma. METHODS: We did a multicentre, international, open-label, single-arm study at 40 sites in the USA, Canada, Europe, Australia, and New Zealand...
October 2016: Lancet Oncology
https://www.readbyqxmd.com/read/27611921/lncrna-profiling-in-early-stage-chronic-lymphocytic-leukemia-identifies-transcriptional-fingerprints-with-relevance-in-clinical-outcome
#20
D Ronchetti, M Manzoni, L Agnelli, C Vinci, S Fabris, G Cutrona, S Matis, M Colombo, S Galletti, E Taiana, A G Recchia, S Bossio, M Gentile, C Musolino, F Di Raimondo, A Grilli, S Bicciato, A Cortelezzi, P Tassone, F Morabito, M Ferrarini, A Neri
Long non-coding RNAs (lncRNAs) represent a novel class of functional RNA molecules with an important emerging role in cancer. To elucidate their potential pathogenetic role in chronic lymphocytic leukemia (CLL), a biologically and clinically heterogeneous neoplasia, we investigated lncRNAs expression in a prospective series of 217 early-stage Binet A CLL patients and 26 different subpopulations of normal B-cells, through a custom annotation pipeline of microarray data. Our study identified a 24-lncRNA-signature specifically deregulated in CLL compared with the normal B-cell counterpart...
September 9, 2016: Blood Cancer Journal
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