Issue Archive

The biologic, clinical, and molecular heterogeneity of myeloproliferative neoplasms (MPNs), as well as the unique treatment goals of individuals, often lead to a melding of data-driven algorithms with personalized care approaches informed by shared decision-making between patients and their physicians. Associate Editor Jason Gotlib introduces this How I Treat series commissioned to bring readers up to date with leading-edge practice related to several MPNs. In each, experts illustrate their points through consideration of several real-world cases. McMullin and Harrison tackle low-risk polycythemia vera, while 2 articles focus on myelofibrosis: Masarova and Chifotides discuss how to individualize selection of Janus kinase inhibitor therapy, and Jain and Gerds address the common problem of anemia in this disease. Deepti H. Radia discusses how to approach the challenges of systemic mastocytosis with an associated hematologic neoplasm in the modern KIT inhibitor era. Some MPNs are very rare, such as the collection of myeloid/lymphoid neoplasms driven by tyrosine kinase gene fusions, and Reiter and colleagues discuss the variable prognoses of these diseases and best available treatment options. Across all MPNs, thrombosis is a major problem, so the final article by Guy et al discusses their preferred cytoreductive, antiplatelet, and antithrombotic strategies for preventing arterial and venous thrombosis occurrence and recurrence.

The biologic, clinical, and molecular heterogeneity of myeloproliferative neoplasms (MPNs), as well as the unique treatment goals of individuals, often lead to a melding of data-driven algorithms with personalized care approaches informed by shared decision-making between patients and their physicians. Associate Editor Jason Gotlib introduces this How I Treat series commissioned to bring readers up to date with leading-edge practice related to several MPNs. In each, experts illustrate their points through consideration of several real-world cases. McMullin and Harrison tackle low-risk polycythemia vera, while 2 articles focus on myelofibrosis: Masarova and Chifotides discuss how to individualize selection of Janus kinase inhibitor therapy, and Jain and Gerds address the common problem of anemia in this disease. Deepti H. Radia discusses how to approach the challenges of systemic mastocytosis with an associated hematologic neoplasm in the modern KIT inhibitor era. Some MPNs are very rare, such as the collection of myeloid/lymphoid neoplasms driven by tyrosine kinase gene fusions, and Reiter and colleagues discuss the variable prognoses of these diseases and best available treatment options. Across all MPNs, thrombosis is a major problem, so the final article by Guy et al discusses their preferred cytoreductive, antiplatelet, and antithrombotic strategies for preventing arterial and venous thrombosis occurrence and recurrence.

The biologic, clinical, and molecular heterogeneity of myeloproliferative neoplasms (MPNs), as well as the unique treatment goals of individuals, often lead to a melding of data-driven algorithms with personalized care approaches informed by shared decision-making between patients and their physicians. Associate Editor Jason Gotlib introduces this How I Treat series commissioned to bring readers up to date with leading-edge practice related to several MPNs. In each, experts illustrate their points through consideration of several real-world cases. McMullin and Harrison tackle low-risk polycythemia vera, while 2 articles focus on myelofibrosis: Masarova and Chifotides discuss how to individualize selection of Janus kinase inhibitor therapy, and Jain and Gerds address the common problem of anemia in this disease. Deepti H. Radia discusses how to approach the challenges of systemic mastocytosis with an associated hematologic neoplasm in the modern KIT inhibitor era. Some MPNs are very rare, such as the collection of myeloid/lymphoid neoplasms driven by tyrosine kinase gene fusions, and Reiter and colleagues discuss the variable prognoses of these diseases and best available treatment options. Across all MPNs, thrombosis is a major problem, so the final article by Guy et al discusses their preferred cytoreductive, antiplatelet, and antithrombotic strategies for preventing arterial and venous thrombosis occurrence and recurrence.

The biologic, clinical, and molecular heterogeneity of myeloproliferative neoplasms (MPNs), as well as the unique treatment goals of individuals, often lead to a melding of data-driven algorithms with personalized care approaches informed by shared decision-making between patients and their physicians. Associate Editor Jason Gotlib introduces this How I Treat series commissioned to bring readers up to date with leading-edge practice related to several MPNs. In each, experts illustrate their points through consideration of several real-world cases. McMullin and Harrison tackle low-risk polycythemia vera, while 2 articles focus on myelofibrosis: Masarova and Chifotides discuss how to individualize selection of Janus kinase inhibitor therapy, and Jain and Gerds address the common problem of anemia in this disease. Deepti H. Radia discusses how to approach the challenges of systemic mastocytosis with an associated hematologic neoplasm in the modern KIT inhibitor era. Some MPNs are very rare, such as the collection of myeloid/lymphoid neoplasms driven by tyrosine kinase gene fusions, and Reiter and colleagues discuss the variable prognoses of these diseases and best available treatment options. Across all MPNs, thrombosis is a major problem, so the final article by Guy et al discusses their preferred cytoreductive, antiplatelet, and antithrombotic strategies for preventing arterial and venous thrombosis occurrence and recurrence.

The biologic, clinical, and molecular heterogeneity of myeloproliferative neoplasms (MPNs), as well as the unique treatment goals of individuals, often lead to a melding of data-driven algorithms with personalized care approaches informed by shared decision-making between patients and their physicians. Associate Editor Jason Gotlib introduces this How I Treat series commissioned to bring readers up to date with leading-edge practice related to several MPNs. In each, experts illustrate their points through consideration of several real-world cases. McMullin and Harrison tackle low-risk polycythemia vera, while 2 articles focus on myelofibrosis: Masarova and Chifotides discuss how to individualize selection of Janus kinase inhibitor therapy, and Jain and Gerds address the common problem of anemia in this disease. Deepti H. Radia discusses how to approach the challenges of systemic mastocytosis with an associated hematologic neoplasm in the modern KIT inhibitor era. Some MPNs are very rare, such as the collection of myeloid/lymphoid neoplasms driven by tyrosine kinase gene fusions, and Reiter and colleagues discuss the variable prognoses of these diseases and best available treatment options. Across all MPNs, thrombosis is a major problem, so the final article by Guy et al discusses their preferred cytoreductive, antiplatelet, and antithrombotic strategies for preventing arterial and venous thrombosis occurrence and recurrence.

The biologic, clinical, and molecular heterogeneity of myeloproliferative neoplasms (MPNs), as well as the unique treatment goals of individuals, often lead to a melding of data-driven algorithms with personalized care approaches informed by shared decision-making between patients and their physicians. Associate Editor Jason Gotlib introduces this How I Treat series commissioned to bring readers up to date with leading-edge practice related to several MPNs. In each, experts illustrate their points through consideration of several real-world cases. McMullin and Harrison tackle low-risk polycythemia vera, while 2 articles focus on myelofibrosis: Masarova and Chifotides discuss how to individualize selection of Janus kinase inhibitor therapy, and Jain and Gerds address the common problem of anemia in this disease. Deepti H. Radia discusses how to approach the challenges of systemic mastocytosis with an associated hematologic neoplasm in the modern KIT inhibitor era. Some MPNs are very rare, such as the collection of myeloid/lymphoid neoplasms driven by tyrosine kinase gene fusions, and Reiter and colleagues discuss the variable prognoses of these diseases and best available treatment options. Across all MPNs, thrombosis is a major problem, so the final article by Guy et al discusses their preferred cytoreductive, antiplatelet, and antithrombotic strategies for preventing arterial and venous thrombosis occurrence and recurrence.

The biologic, clinical, and molecular heterogeneity of myeloproliferative neoplasms (MPNs), as well as the unique treatment goals of individuals, often lead to a melding of data-driven algorithms with personalized care approaches informed by shared decision-making between patients and their physicians. Associate Editor Jason Gotlib introduces this How I Treat series commissioned to bring readers up to date with leading-edge practice related to several MPNs. In each, experts illustrate their points through consideration of several real-world cases. McMullin and Harrison tackle low-risk polycythemia vera, while 2 articles focus on myelofibrosis: Masarova and Chifotides discuss how to individualize selection of Janus kinase inhibitor therapy, and Jain and Gerds address the common problem of anemia in this disease. Deepti H. Radia discusses how to approach the challenges of systemic mastocytosis with an associated hematologic neoplasm in the modern KIT inhibitor era. Some MPNs are very rare, such as the collection of myeloid/lymphoid neoplasms driven by tyrosine kinase gene fusions, and Reiter and colleagues discuss the variable prognoses of these diseases and best available treatment options. Across all MPNs, thrombosis is a major problem, so the final article by Guy et al discusses their preferred cytoreductive, antiplatelet, and antithrombotic strategies for preventing arterial and venous thrombosis occurrence and recurrence.

As new therapies become available, old practices come into question, such as autologous transplantation as a salvage therapy for relapsed multiple myeloma (MM) in patients who have had an autograft as part of first-line therapy. Randomized trials offer the best answers. After extended follow-up of the ReLApsE trial, Baertsch et al report no significant progression-free or overall survival benefit from salvage autograft compared with lenalidomide/dexamethasone salvage in the intention-to-treat population, confirming that salvage autografts can be largely retired from the standard armamentarium for MM.

CD30 is a suitable target for immunotherapy for Hodgkin lymphoma and some T-cell lymphomas with limited expression in normal tissues, but what is the best way to build an effective CD30 chimeric antigen receptor (CAR) T-cell product? Caballero and colleagues report design and phase 1 clinical trial testing of HSP-CAR30, manufactured with the goal of promoting less-differentiated memory T cells. Preliminary efficacy data indicate high rates of durable responses, with expansion and long-term persistence of memory CD30-directed CAR T cells in patients, encouraging ongoing trials of this approach.

Germinal center B cells depend on the epigenetic enzymes disruptor of telomeric silencing 1-like (DOT1L) and enhancer of zeste homolog 2 (EZH2) for development and immune responses. Using cell lines and in vivo murine models, Göbel et al showed that germinal center–type diffuse large B-cell lymphoma (DLBCL) depends on EZH2, whose gain-of-function mutations occur in DLBCL, and DOT1L to enable sustained proliferation. Treatment with the combination of DOT1L and EZH2 inhibitors demonstrates synergistic antilymphoma activity and may offer opportunities for future clinical studies.

Desmopressin (1-desamino-8-d-arginine vasopressin [DDAVP]) is widely used to prevent or stop bleeding in many clinical circumstances, but the evidence underlining its use varies. In this month’s CME article, Laan and colleagues report the first major meta-analysis of response rate and determinants of response to DDAVP, including data from 1772 patients. While determinants of response are identified for specific bleeding disorders, the absence of a standardized response definition is a clear gap that needs attention in future studies.