Hematology
9.2K views | +3 today
Follow
Hematology
Diagnosis, Therapy, Follow-up
Your new post is loading...
Your new post is loading...
Scooped by Gilbert C FAURE
Scoop.it!

Hematology, or Haematology

... was a major interest for our lab, during many years in the context of the GEIL still thriving, then EGIL, then European Leukemia Net.

 

Gilbert C FAURE's insight:

Hospital choices did not allow to pursue the efforts locally...

but to stay informed and allow others to surf the information wave....

 

Much information is available in the cloud, focusing on immunophenotyping of leukemias, and also on other haematology topics.


Blood cells being also immunocompetent cells, other topics curated should be of interest

http://www.scoop.it/t/immunology

http://www.scoop.it/t/from-flow-cytometry-to-cytomics

http://www.scoop.it/t/immunology-and-biotherapies

 

 

 

more...
No comment yet.
Scooped by Gilbert C FAURE
Scoop.it!

Emerging epigenetic-modulating therapies in lymphoma

Emerging epigenetic-modulating therapies in lymphoma | Hematology | Scoop.it
Patients with lymphoma typically receive chemotherapy as the first-line treatment. However, patients who fail to respond or develop relapsed disease often have poor outcomes. In this Review, the authors summarize the available data on therapeutics designed to modulate epigenetic changes, including DNA methylation and histone acetylation, in patients with lymphoma and describe the most promising directions of future research.
more...
No comment yet.
Scooped by Gilbert C FAURE
Scoop.it!

Hematopathology Case Study: A 39 Year Old Woman Presenting with Persistent Cough and Pericardial Effusion –

Hematopathology Case Study: A 39 Year Old Woman Presenting with Persistent Cough and Pericardial Effusion – | Hematology | Scoop.it
Case history The patient is a 39 year old woman presenting with a persistent cough. Upon work up, a pericardial effusion is noted. Pericardiocentesis is performed and a smear made from the pericardial fluid reveals atypical lymphoid cells. Cytology of the Pericardial Fluid Image 1. Pericardial fluid cytology showing reactive mesothelial cells surrounded by benign…
more...
No comment yet.
Suggested by LIGHTING
Scoop.it!

PeerView - Building Innovative Treatment Options for Patients With B-Cell Malignancies: Practical Insights on Clinical Evidence and Integration Strategies

PeerView - Building Innovative Treatment Options for Patients With B-Cell Malignancies: Practical Insights on Clinical Evidence and Integration Strategies | Hematology | Scoop.it
I participated in “Building Innovative Treatment Options for Patients With B-Cell Malignancies,” a CME/CNE activity from @PeerView
more...
No comment yet.
Rescooped by Gilbert C FAURE from Immunology and Biotherapies
Scoop.it!

Haploidentical versus unrelated allogeneic stem cell transplantation for relapsed/refractory acute myeloid leukemia: a report on 1578 patients from the Acute Leukemia Working Party of the EBMT

Haploidentical versus unrelated allogeneic stem cell transplantation for relapsed/refractory acute myeloid leukemia: a report on 1578 patients from the Acute Leukemia Working Party of the EBMT | Hematology | Scoop.it
Primary refractory or relapsed acute myeloid leukemia is associated with a dismal prognosis. Allogeneic stem cell transplantation is the only therapeutic option that offers prolonged survival and cure in this setting.

Via Krishan Maggon
more...
No comment yet.
Scooped by Gilbert C FAURE
Scoop.it!

Bob Löwenberg's perspective on CAR-T and immunotherapy for AML

Bob Löwenberg, MD, PhD, of Erasmus University Medical Centre, Rotterdam, Netherlands, discusses his thoughts on CAR T-cell therapy and other immuno-oncology ...
more...
No comment yet.
Scooped by Gilbert C FAURE
Scoop.it!

The HLA ligandome landscape of chronic myeloid leukemia delineates novel T-cell epitopes for immunotherapy

The HLA ligandome landscape of chronic myeloid leukemia delineates novel T-cell epitopes for immunotherapy | Hematology | Scoop.it
Antileukemia immunity plays an important role in disease control and maintenance of tyrosine kinase inhibitor (TKI)-free remission in chronic myeloid leukemia (CML). Thus, antigen-specific immunotherapy holds promise for strengthening immune control in CML but requires the identification of CML-
more...
No comment yet.
Scooped by Gilbert C FAURE
Scoop.it!

Hydroxyurea for Children With Sickle Cell Anemia in Sub-Saharan Africa: The Child That Comes and Goes Away Can Come to Stay With Hydroxyurea

Hydroxyurea for Children With Sickle Cell Anemia in Sub-Saharan Africa: The Child That Comes and Goes Away Can Come to Stay With Hydroxyurea | Hematology | Scoop.it
Dr. Osunkwo discusses the REACH Trial, which demonstrates the safety and efficacy of hydroxyurea use among children in four sub-Saharan African countries, and its implications for treating sickle cell disease.
more...
No comment yet.
Scooped by Gilbert C FAURE
Scoop.it!

Synergy Satellite Event: Biosimilars in haemato-oncology - new blood, old questions (sponsored by an educational grant from Sandoz) | European Association of Hospital Pharmacists

Linked to EAHP Statements Section 1 - Introductory Statements and Governance: Statements 1.1, 1.6 Section 4 - Clinical Pharmacy Services: Statement 4.1 ACPE UAN: 0475-0000-19-007-L01-P. A knowledge based activity. Abstract For many years, biological drugs have not been subject to competition by generics. There are good reasons for this, as complex biological molecules cannot be shown to be bioequivalent based solely on analytical data and pharmacokinetic studies. Drug regulatory authorities acknowledged this, and the European Union (EU) pioneered the concept of biosimilars with detailed guidance to show bioequivalence of biological drugs. This concept has been applied for several medicinal products, such as growth hormone, epoietin or granulocyte colony stimulating factors, and more recently, monoclonal antibodies (infliximab) and a fusion protein (etanercept). In all cases, there are no reports of efficacy or safety concerns, and biosimilar use is now widespread in many countries. This is now also an issue in the treatment of hematologic cancers, especially Non-Hodgkin Lymphoma. Since the beginning of this century, rituximab changes the disease. Patients live longer with a better quality of life, and with better survival rates, but the cost has been very high. A Biosimilar of rituximab is coming to market. The opportunity for savings is huge. On the other hand, this drug is so important that this may lead to some concerns, especially regarding extrapolation of data from small-scale biosimilar clinical trials. To complicate matters further, major innovation companies are coming to the market with new drugs to replace rituximab, and this may prove to be an expensive and not always useful option. To make the best of this new frontier, hospital pharmacists must understand the concepts and facts, to be able to provide a scientific unbiased approach to this issue, with a focus on patient care in a world of limited resources. Learning objectives After this Synergy session, participants should be able to: • acquire new understanding of the key facts which support biosimilar approval in the EU as applied to onco-haematology therapy; • recognise biased trends of change in first line therapy; • advise as how to implement biosimilar of monoclonal antibodies used in Non-Hodgkin Lymphoma and other hematologic diseases. Educational need addressed The recent availability of rituximab biosimilars drives a need for specific knowledge on the quality and clinical background of the approval process, and also of the role of biosimilars in budget management in haemato-oncology setting, considering all the new therapeutic options available for these diseases. This is mostly relevant for all pharmacists involved in oncology, as they will likely be questioned by other healthcare professionals, management or even by patients. Keywords: lymphoma, biosimilars, future therapeutic options, monoclonal antibodies.
more...
No comment yet.
Scooped by Gilbert C FAURE
Scoop.it!

Doctor payments drove scripts for cancer drugs from Pfizer, Novartis and more: study | FiercePharma

Doctor payments drove scripts for cancer drugs from Pfizer, Novartis and more: study | FiercePharma | Hematology | Scoop.it
Are physicians who receive money from drug companies more likely to prescribe the treatments tied to that cash? A new study suggests that consistent payments—not mere payments themselves—are more likely to sway prescribing.
more...
No comment yet.
Scooped by Gilbert C FAURE
Scoop.it!

Targeting MEK in vemurafenib-resistant hairy cell leukemia - Europe PMC Article - Europe PMC

Targeting MEK in vemurafenib-resistant hairy cell leukemia - Europe PMC Article - Europe PMC | Hematology | Scoop.it
Hairy cell leukemia (HCL) is a chronic, incurable B cell malignancy that presents with splenomegaly, bone marrow infiltration, and cytopenias [1]. Long remissions are typically achieved with purine analogs such as cladribine, but most cases will relapse and require further therapy. The discovery of the BRAF V600E mutation in almost all cases of HCL [2] has led to the widespread adoption of the BRAF inhibitor vemurafenib for treatment of patients relapsing after cladribine [3–5]. Impressive responses are reported; however, relapse is inevitable [5, 6] and hematologists are now faced with a growing number of patients with vemurafenib-resistant HCL. The optimal management of these patients remains unclear. The molecular basis of vemurafenib resistance has been extensively investigated in recent years in patients with BRAF mutant solid organ malignancies such as melanoma and colorectal cancer [7]. Resistance to vemurafenib in melanoma frequently results from reactivation of ERK pathway signaling by a variety of genetic mechanisms that include activating mutations of NRAS or KRAS, amplification of mutant BRAF, aberrant splicing of BRAF, and activating mutation of MAP2K1, which encodes the MEK1 protein [7, 8]. ERK-independent mechanisms are less frequent and include activation of PI3K signaling [7]. The predominance of genetic mechanisms converging on ERK reactivation has led to the successful use of dual MEK/BRAF inhibition in melanoma [9]. In colorectal cancer however, different mechanisms apply; here primary resistance usually results from reduced feedback inhibition upon upstream receptor tyrosine kinase activity leading to restoration of ERK activity [10]. In this scenario, combined BRAF and MEK inhibition has not proved effective [11]. In contrast to our comprehensive understanding in solid organ cancer, very little is known about the mechanistic basis of vemurafenib resistance in HCL. Given the diversity of resistance mechanisms established in other cancers, it is unclear which, if any, of these might predominate in HCL. Two acquired subclonal, activating KRAS mutations were previously reported in a single patient with vemurafenib resistance [5]. Deletions of NF1 and NF2 have been proposed as an alternative mechanism in another case of primary resistance [12]. The use of MEK inhibition has been suggested as a logical therapeutic strategy in patients who have reactivated ERK signaling. However, the use of MEK inhibition has never previously been reported in a patient with HCL and at present there is no consensus on the optimal management of patients relapsing on vemurafenib. A 74-year-old patient with HCL had been treated at our institution with splenectomy, cladribine, and pentostatin. We previously reported his initial response to vemurafenib at a dose of 240mg twice daily [4]. This dose was lower than used in the initial phase II trial [5], but has since been shown in several reports to be an effective dosing strategy for HCL [3, 13, 14]. Vemurafenib was initially stopped after 58 days; however, this was associated with rapid return of marrow infiltration and thrombocytopenia. Vemurafenib was restarted at the same dose and cytopenias rapidly resolved. Continuous low-dose vemurafenib continued to sustain his remission for over 3 years, attesting to the efficacy of this dosing schedule. However, 38 months after restarting vemurafenib, his blood indices deteriorated, and he required platelet transfusion (Fig. 1a). Bone marrow trephine biopsy confirmed relapse of HCL. A trial of rituximab with continued vemurafenib led to transient recovery of hematological indices. However, bone marrow infiltration did not improve over the next 4 months, and the patient became anemic, thrombocytopenic, and required further platelet transfusion. A second trial of two doses of rituximab produced a minimal improvement of platelet count to 30×109/l. The patient became systemically unwell with B symptoms. Bone marrow trephine biopsy confirmed 99% infiltration with HCL. To elucidate the mechanism of his resistance we performed whole-genome and deep-targeted sequencing of 292 genes (Supplementary Table 1) of DNA from purified tumor cells collected prior to starting vemurafenib and again at relapse. Samples were used with informed written patient consent in accordance with the Declaration of Helsinki and appropriate institutional ethical approvals. Sequencing studies revealed the presence of the known BRAF V600E mutation and chromosome 7q deletion. Remarkably, we also identified seven distinct activating mutations in KRAS and two mutations in MAP2K1 (encoding MEK1) (Fig. 1b and Supplementary Table 2). These were detectable at relapse but were not detectable prior to vemurafenib exposure. Allele frequencies were consistent with the parallel, convergent evolution of multiple clones. Deep-targeted amplicon sequencing at multiple time points showed how KRAS mutations developed early, initially with codon 146 mutations, followed by emergence of the more classical activating mutations of codons 12 and 61 [15]. MAP2K1 mutations appeared later with MAP2K1 p.K57T expanding to become the dominant clone (Fig. 2c and Supplementary Table 2). The convergent nature of these mutations strongly implicated reactivation of MEK-ERK signaling as the likely mechanism of resistance. Indeed, immunohistochemistry confirmed strong pERK activity in all tumor cells (Fig. 2a). We looked for other mechanisms of resistance reported in melanoma. Specifically, we found no genetic or protein evidence of either increased pAKT activity or altered BRAF splicing (Supplementary Figure 1A & B). We concluded that reactivation of MEK/ERK activity was the most likely driver of relapse and hypothesized that MEK inhibition might be a successful therapeutic strategy. Expression of the KRAS and MAP2K1 mutants in a lymphoid cell line showed that while each mutation was able to activate ERK in the presence of vemurafenib, all mutations remained sensitive to MEK inhibition (Fig. 1d). Exposure of the patient’s purified tumor cells to vemurafenib ex vivo failed to completely suppress ERK activity and did not induce apoptosis. In contrast, ERK activity was completely suppressed and apoptosis induced by exposure to a MEK inhibitor (Supplementary Figure 1C and Fig. 1c). Based on our in vitro experiments, we treated the patient with the MEK inhibitor cobimetinib, initially at 20mg daily combined with vemurafenib 240mg twice daily. Remarkably, B symptoms resolved within 1 week, followed by rapid platelet count recovery. A bone marrow biopsy at 4 months showed complete suppression of ERK activity (Fig. 2a). However, HCL marrow infiltration persisted, and therefore cobimetinib dose was increased to 60mg daily (taken 21 out of 28 days). The dose was well tolerated and was associated with further resolution of cytopenias, a substantial reduction in bone marrow cellularity and HCL infiltration, ongoing suppression of ERK activity and restoration of normal hematopoiesis (Fig. 2a, b). Ongoing treatment was also associated with suppression of mutant allele frequencies for BRAF, KRAS, and MAP2K1 mutations (Fig. 2c). At 12 months, the patient remains well and asymptomatic with continued combination therapy. The finding of nine activating mutations, all converging upon the activation of RAS/RAF/MEK/ERK signaling, underscores the centrality of this pathway in HCL and its reactivation as a potent mechanism of resistance to vemurafenib in this disease. This report provides a detailed analysis of the molecular basis for acquired vemurafenib resistance in HCL. It is the first reported use of a MEK inhibitor to treat vemurafenib-resistant HCL. It proposes a new therapeutic option for such patients and provides impetus for testing in a formal trial setting.
more...
No comment yet.
Suggested by Société Francaise d'Immunologie
Scoop.it!

Complex karyotype in de novo acute myeloid leukemia: typical and atypical subtypes differ molecularly and clinically

Complex karyotype in de novo acute myeloid leukemia: typical and atypical subtypes differ molecularly and clinically | Hematology | Scoop.it
Article...
more...
No comment yet.
Suggested by Société Francaise d'Immunologie
Scoop.it!

Clinical feasibility of immunotherapy for acute leukemia – a review - WCRJ

Clinical feasibility of immunotherapy for acute leukemia – a review - WCRJ | Hematology | Scoop.it
Abstract Leukemia is a malignant cancerous condition of hematopoietic stem cells associated with increased number of white blood cells within the blood circulation and bone marrow. We aimed to assess the clinical feasibility of immunotherapy for treating acute leukemia. The innate immune response provides the first line of defense for the body; whereas, adaptive immune response is recognized as a separate aberration, associated with the cancer cells. The process of immunotherapy is divided into seven different types of therapies including; monoclonal antibody therapy, vaccination, chimeric antigen receptors, radio-immunotherapy, cytokine therapy, donor lymphocyte infusion, and stem cell transplantation. However, the general treatment of leukemia involves allogeneic bone marrow transplantation, post-induction therapy, and autologous bone marrow transplantation. The study has concluded that immunotherapy depicts promising outcomes in treating acute leukemia. Free PDF Download To cite this article Helmi N., Asiri B., Al-jehani W., Al-hashmi R., Al-Gamdi S., Abdulsabour R. Clinical feasibility of immunotherapy for acute leukemia – a review WCRJ 2018; 5 (4): e1176 Publication History Submission date: 11 Aug 2018 Revised on: 03 Sep 2018 Accepted on: 20 Sep 2018 Published online: 04 Dec 2018
more...
No comment yet.
Scooped by Gilbert C FAURE
Scoop.it!

Reshaping the Treatment Landscape in Refractory Multiple Myeloma - The ASCO Post

Reshaping the Treatment Landscape in Refractory Multiple Myeloma - The ASCO Post | Hematology | Scoop.it
Reshaping the Treatment Landscape in Refractory Multiple Myeloma By Shaji K. Kumar, MD March 10, 2019 Shaji K. Kumar, MD THE TREATMENT approaches for multiple myeloma, both newly diagnosed and relapsed disease, continue to undergo major transformation as new agents and combinations are being introduced.1 This change has been driven by the introduction of novel drug classes such as monoclonal antibodies, as well as newer agents from the existing classes of drugs such as proteasome inhibitors and immunomodulatory drugs. The monoclonal antibodies elotuzumab and daratumumab in particular have reshaped the treatment landscape of multiple myeloma during the past few years, given their efficacy in patients with multiple myeloma that has become refractory to the available drug classes.2-5 Challenge of Sequencing Therapies Over Time GIVEN THE chronic nature of multiple myeloma today, patients continue to require repeated lines of therapy to maintain adequate disease control over long periods. As a result, the sequence of use of the different available therapies has taken on more significance. The uniform adoption of proteasome inhibitors and immunomodulatory drugs in the setting of newly diagnosed disease and the increasing use of continuous therapy in the initial treatment setting have a major impact on the therapeutic choices at the time of relapse.6 In particular, lenalidomide along with a proteasome inhibitor forms the backbone of initial treatment in older, frailer patients and is used for maintenance after autologous stem cell transplant in transplant-eligible patients, as well as the rest of patients after triplet induction. As a result, increasingly, patients are refractory to lenalidomide at the time of initial relapse. Use of proteasome inhibitors in the first relapse, often in combination, also increases proteasome inhibitor–refractory disease in the later lines of therapy. Although several of the newer drugs, including the monoclonal antibodies have been studied in combination with lenalidomide in phase III studies, the clinical relevance of those studies remains limited given the pattern of upfront use of lenalidomide.2,3,7,8 Pomalidomide is a next-generation immunomodulatory drug that has demonstrated efficacy in patients who are refractory to lenalidomide. Hence, this drug has been studied in combination with proteasome inhibitors and monoclonal antibodies in the relapsed setting.9-11 More recent randomized and single-arm trials have examined the combination of pomalidomide with proteasome inhibitors (bortezomib, carfilzomib, and ixazomib) as well as the monoclonal antibody daratumumab (Table 1).11-15 Key Findings From ELOQUENT-3 THE RANDOMIZED phase II ELOQUENT-3 trial, reported by Dimopoulos and colleagues and reviewed in this issue of The ASCO Post, has examined the efficacy of elotuzumab in combination with pomalidomide in patients with relapsed disease who are refractory to bortezomib and lenalidomide, a population that increasingly makes up the majority of patients with relapsed myeloma.14 The trial compared the three-drug combination of elotuzumab plus pomalidomide/dexamethasone (EPd) with pomalidomide/dexamethasone, demonstrating a higher response rate, deeper response, and improved progression-free survival, without a significant increase in toxicity. The overall response rate was 53% for EPd compared with 26% for pomalidomide/dexamethasone, including 20% vs 9% with a very good partial response or better. With 9.1 months of median follow-up, the median progression-free survival was significantly better with EPd at 10.3 months vs 4.7 months with pomalidomide/dexamethasone. The benefit was seen across the entire patient group regardless of age, prior lines of therapy, and disease risk status. Although overall survival was numerically better with EPd, the follow-up remains rather short. The combination was well tolerated, with no significant increase in hematologic or nonhematologic toxicity with the addition of the antibody. The most common grade 3 or 4 adverse events were neutropenia, anemia, and hyperglycemia. Of note, the dosing strategy of elotuzumab differed in the current study compared with the lenalidomide combination, with use of a higher dose (20 mg/kg) every cycle after 2 cycles instead of 10 mg/kg every 2 weeks. Comparing Trial Results With Caution THE RESULTS of the current study need to be interpreted in the context of other pomalidomide combinations, especially with daratumumab or carfilzomib, when making the treatment choice in the clinic. Although the data with pomalidomide in combination with bortezomib from the OPTIMISSM trial appear promising, many patients at the time of relapse may be refractory or unable to tolerate bortezomib due to toxicities such as peripheral neuropathy. The results from the current trial and the trial with the daratumumab combination appear to be quite comparable, even though there are critical differences.12,14 The daratumumab study was a single-arm trial but had more heavily pretreated patients, with a median of 4 prior lines of therapy including one-third who had been exposed to carfilzomib. Although the response rate with daratumumab plus pomalidomide/dexamethasone was higher and deeper responses were seen, the overall progression-free survival was similar to that with EPd. In terms of tolerability, infusion reactions were seen less often with EPd, and hematologic toxicity appeared to be of a lesser magnitude as well. The once-every- 4-week dosing of elotuzumab also makes the administration logistics of the two regimens similar. “Given the chronic nature of multiple myeloma today, patients continue to require repeated lines of therapy to maintain adequate disease control over long periods.” — Shaji K. Kumar, MD Tweet this quote Questions for the Future WHAT THE TRIALS do not clearly convey is the activity of either of the monoclonal antibodies in combination with pomalidomide in a patient population that would have seen the other antibody in combination with lenalidomide. This will clearly be a question for the future, as daratumumab in combination with lenalidomide moves to the upfront setting in the treatment of newly diagnosed myeloma based on the recent data from the MAIA study. Depending on the results of the phase III ELOQUENT-1 study (which should be completed later this year), the converse may also be a relevant question for the future, if elotuzumab plus lenalidomide/dexamethasone becomes part of the initial therapy. For now, the promising results from the current trial clearly demonstrates an important role for the EPd combination in patients with myeloma that is refractory to bortezomib and lenalidomide. ■ Dr. Kumar is Professor of Medicine, Mayo Clinic, Rochester, Minnesota. DISCLOSURE: Dr. Kumar has received research funding (with no personal payments) from Celgene, Takeda, Janssen, Bistol-Myers Squibb, Sanoffi, KITE, Merck, AbbVie, MedImmune, Novartis, Roche-Genentech, and Amgen; and is a consultant (with no personal payments) for Celgene, Takeda, Janssen, KITE, Merck, AbbVie, MedImmune, Genentech, and Amgen; and has received honoraria from Ono Pharmaceuticals, Reddys Laboratory, and Adaptive Technologies. REFERENCES 1. Kumar SK, Rajkumar SV: The multiple myelomas: Current concepts in cytogenetic classification and therapy. Nat Rev Clin Oncol 15:409-421, 2018. 2. Lonial S, Dimopoulos M, Palumbo A, et al: Elotuzumab therapy for relapsed or refractory multiple myeloma. N Engl J Med 373:621-631, 2015. 3. Dimopoulos MA, Oriol A, Nahi H, et al: Daratumumab, lenalidomide, and dexamethasone for multiple myeloma. N Engl J Med 375:1319-1331, 2016. 4. Lonial S, Weiss BM, Usmani SZ, et al: Daratumumab monotherapy in patients with treatment-refractory multiple myeloma (SIRIUS): An open-label, randomised, phase 2 trial. Lancet 387:1551-1560, 2016. 5. Palumbo A, Chanan-Khan A, Weisel K, et al: Daratumumab, bortezomib, and dexamethasone for multiple myeloma. N Engl J Med 375:754-766, 2016. 6. Durie BG, Hoering A, Abidi MH, et al: Bortezomib with lenalidomide and dexamethasone versus lenalidomide and dexamethasone alone in patients with newly diagnosed myeloma without intent for immediate autologous stem-cell transplant (SWOG S0777): A randomised, open-label, phase 3 trial. Lancet 389:519-527, 2017. 7. Stewart AK, Rajkumar SV, Dimopoulos MA, et al: Carfilzomib, lenalidomide, and dexamethasone for relapsed multiple myeloma. N Engl J Med 372:142-152, 2015. 8. Moreau P, Masszi T, Grzasko N, et al: Oral ixazomib, lenalidomide, and dexamethasone for multiple myeloma. N Engl J Med 374:1621-1634, 2016. 9. Lacy MQ, Hayman SR, Gertz MA, et al: Pomalidomide (CC4047) plus low dose dexamethasone (Pom/dex) is active and well tolerated in lenalidomide refractory multiple myeloma. Leukemia 24:1934-1939, 2010. 10. Richardson PG, Siegel DS, Vij R, et al: Pomalidomide alone or in combination with low-dose dexamethasone in relapsed and refractory multiple myeloma: A randomized phase 2 study. Blood 123:1826-1832, 2014. 11. Dimopoulos MA, Palumbo A, Corradini P, et al: Safety and efficacy of pomalidomide plus low-dose dexamethasone in STRATUS (MM-010): A phase 3b study in refractory multiple myeloma. Blood 128:497-503, 2016. 12. Chari A, Suvannasankha A, Fay JW, et al: Daratumumab plus pomalidomide and dexamethasone in relapsed and/or refractory multiple myeloma. Blood 130:974-981, 2017. 13. Shah JJ, Stadtmauer EA, Abonour R, et al: Carfilzomib, pomalidomide, and dexamethasone for relapsed or refractory myeloma. Blood 126:2284- 2290, 2015. 14. Dimopoulos MA, Dytfeld D, Grosicki S, et al: Elotuzumab plus pomalidomide and dexamethasone for multiple myeloma. N Engl J Med 379:1811- 1822, 2018. 15. Sonneveld P, Zweegman S, Cavo M, et al: Carfilzomib, pomalidomide and dexamethasone in patients with multiple myeloma refractory to bortezomib and lenalidomide: The EMN011 trial. Blood 132:801, 2018. Related Articles Addition of Elotuzumab to Pomalidomide and Dexamethasone in Previously Treated Patients With Multiple Myeloma Meletios A. Dimopoulos, MD AS REPORTED in The New England Journal of Medicine by Meletios A. Dimopoulos, MD, of the National and Kapodistrian University of Athens, and colleagues, the phase II ELOQUENT-3 trial has shown that the addition of elotuzumab to pomalidomide and dexamethasone...
more...
No comment yet.
Scooped by Gilbert C FAURE
Scoop.it!

About

About | Hematology | Scoop.it
Le réseau CRYOSTEM a été créé avec la participation de 21 unités de greffe adultes et pédiatriques associées à 15 Centres de Ressources Biologiques.
more...
No comment yet.
Scooped by Gilbert C FAURE
Scoop.it!

A fully human anti-IL-7Rα antibody promotes antitumor activity against T-cell acute lymphoblastic leukemia.

A fully human anti-IL-7Rα antibody promotes antitumor activity against T-cell acute lymphoblastic leukemia. | Hematology | Scoop.it
T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive hematological cancer for which treatment options often result in incomplete therapeutic efficacy an...
more...
No comment yet.
Scooped by Gilbert C FAURE
Scoop.it!

CD4+CD25highCD127low/-FoxP3+ Regulatory T-Cell Population in Acute Leukemias: A Review of the Literature

CD4+CD25highCD127low/-FoxP3+ Regulatory T-Cell Population in Acute Leukemias: A Review of the Literature | Hematology | Scoop.it
Journal of Immunology Research is a peer-reviewed, Open Access journal that provides a platform for scientists and clinicians working in different areas of immunology and therapy. The journal publishes research articles, review articles, as well as clinical studies related to classical immunology,...
more...
No comment yet.
Scooped by Gilbert C FAURE
Scoop.it!

On Waldenström’s macroglobulinemia and IgM related disorders

On Waldenström’s macroglobulinemia and IgM related disorders | Hematology | Scoop.it
Author J.M.I. Vos Title On Waldenström’s macroglobulinemia and IgM related disorders Supervisors M.J. Kersten S.T. Pals Co-supervisors S.P. Treon M.C. Minnema Award date 8 February 2019 Number of pages 153 ISBN 9789463612111 Document type PhD thesis Faculty Faculty of Medicine (AMC-UvA)Abstract Waldenström’s Macroglobulinemia (WM) and IgM-related disorders are rare B-cell malignancies that have unique clinical features, pathophysiology and reactions to therapeutic agents. The research described in this thesis was conducted to gain insight into various disease manifestations of WM and IgM-related disorders, aiming to help improve diagnosis, therapy, and patient outcomes. Chapter 2 describes the efficacy of rituximab-fludarabin in the treatment of central nervous system involvement of WM (Bing Neel Syndrome). Chapter 3 contains a study on the clinicopathological aspects and outcomes of renal disease related to WM. This study revealed a large variance in renal pathology including the first description of Thrombotic Microangiopathy in this setting, and demonstrated a shorter overall survival for patients with WM related renal disease. Chapter 4 contains an international consensus guideline on the diagnosis and management of IgM related neuropathies. Chapter 5 comprises a study that identified the presence of the MYD88 L265P mutation in the majority of patients with IgM paraprotein related anti-MAG peripheral neuropathy, suggesting a biological link to WM. Finally, chapter 6 contains a study on the effect of a novel oral BTK inhibitor (ibrutinib), on serum chemokines, cytokines, hepcidin and iron metabolism, identifying the pretreatment level of the chemokine CXCL13 as a predictor for the response to ibrutinib. Permalink http://hdl.handle.net/11245.1/eb0dff45-d009-44b6-a8cd-d2670bbbff98 Downloads Thesis (complete) (Embargo up to and including 8 February 2021) Front matter Chapter 1: General introduction and outline of the thesis Chapter 2: Effective treatment of Bing‐Neel Syndrome with oral fludarabine: a case series of four consecutive patients Chapter 3: Renal disease related to Waldenström macroglobulinaemia: incidence, pathology and clinical outcomes Chapter 4: Investigation and management of IgM and Waldenström-associated peripheral neuropathies: recommendations from the IWWM-8 consensus panel Chapter 5: High prevalence of the MYD88 L265P mutation in IgM anti-MAG paraprotein-associated peripheral neuropathy (Embargo up to and including 8 February 2021) Chapter 6: CXCL13 levels are elevated in patients with Waldenström macroglobulinemia, and are predictive of major response to ibrutinib Chapter 7: Summary, discussion and future perspectives Chapter 8: Nederlandse samenvatting List of contributing authors and affiliations; List of publications; PhD portfolio; Curriculum vitae; Dankwoord (Acknowledgements) Stellingen Disclaimer/Complaints regulations If you believe that digital publication of certain material infringes any of your rights or (privacy) interests, please let the Library know, stating your reasons. In case of a legitimate complaint, the Library will make the material inaccessible and/or remove it from the website. Please Ask the Library, or send a letter to: Library of the University of Amsterdam, Secretariat, Singel 425, 1012 WP Amsterdam, The Netherlands. You will be contacted as soon as possible.
more...
No comment yet.
Scooped by Gilbert C FAURE
Scoop.it!

MRD monitoring by NGS in AML over time: revealing predictors of relapse

Peter Valk, PhD, of Erasmus University Medical Center, Rotterdam, Netherlands, discusses the relevance of MRD monitoring by next-generation sequencing in acu...
more...
No comment yet.
Scooped by Gilbert C FAURE
Scoop.it!

The developmental stage of the hematopoietic niche regulates lineage in MLL-rearranged leukemia

The developmental stage of the hematopoietic niche regulates lineage in MLL-rearranged leukemia | Hematology | Scoop.it
Leukemia phenotypes vary with age of onset. Delineating mechanisms of age specificity in leukemia could improve disease models and uncover new therapeutic approaches. Here, we used heterochronic transplantation of leukemia driven by MLL / KMT2A translocations to investigate the contribution of the age of the hematopoietic microenvironment to age-specific leukemia phenotypes. When driven by MLL-AF9 , leukemia cells in the adult microenvironment sustained a myeloid phenotype, whereas the neonatal microenvironment supported genesis of mixed early B cell/myeloid leukemia. In MLL-ENL leukemia, the neonatal microenvironment potentiated B-lymphoid differentiation compared with the adult. Ccl5 elaborated from adult marrow stroma inhibited B-lymphoid differentiation of leukemia cells, illuminating a mechanism of age-specific lineage commitment. Our study illustrates the contribution of the developmental stage of the hematopoietic microenvironment in defining the age specificity of leukemia.
more...
No comment yet.
Suggested by Société Francaise d'Immunologie
Scoop.it!

Aberrant Wnt signaling in multiple myeloma: molecular mechanisms and targeting options

Aberrant Wnt signaling in multiple myeloma: molecular mechanisms and targeting options | Hematology | Scoop.it
Review Article...
more...
No comment yet.
Scooped by Gilbert C FAURE
Scoop.it!

Follicular Lymphoma Quiz: Testing Your Knowledge

Follicular Lymphoma Quiz: Testing Your Knowledge | Hematology | Scoop.it
How well do you know the current treatment options?
more...
No comment yet.
Scooped by Gilbert C FAURE
Scoop.it!

Genome-wide association study of monoclonal gammopathy of unknown significance (MGUS): comparison with multiple myeloma

Letter...
more...
No comment yet.
Scooped by Gilbert C FAURE
Scoop.it!

Blinatumomab versus Chemotherapy for Advanced Acute Lymphoblastic Leukemia | NEJM

Original Article from The New England Journal of Medicine — Blinatumomab versus Chemotherapy for Advanced Acute Lymphoblastic Leukemia...
more...
No comment yet.
Rescooped by Gilbert C FAURE from PARP Inhibitors Cancer Review
Scoop.it!

The reference epigenome and regulatory chromatin landscape of chronic lymphocytic leukemia - Europe PMC Article - Europe PMC

The reference epigenome and regulatory chromatin landscape of chronic lymphocytic leukemia - Europe PMC Article - Europe PMC | Hematology | Scoop.it
Chronic lymphocytic leukemia (CLL) is a frequent hematological neoplasm in which underlying epigenetic alterations are only partially understood. Here we analyze the reference epigenome of seven primary CLLs and the regulatory chromatin landscape of 107 ...

Via Krishan Maggon
more...
No comment yet.
Suggested by Société Francaise d'Immunologie
Scoop.it!

T Cell Acute Lymphoblastic Leukemia as a Consequence of Thymus Autonomy

T Cell Acute Lymphoblastic Leukemia as a Consequence of Thymus Autonomy | Hematology | Scoop.it
Thymus autonomy is the capacity of the thymus to maintain T lymphocyte development and export independently of bone marrow contribution. Prolonging thymus autonomy was shown to be permissive to the development of T cell acute lymphoblastic leukemia (T-ALL), similar to the human disease.
more...
No comment yet.