Clinical Lymphoma and Myeloma最新文献

{"title":"Rituximab plus Short-Duration Chemotherapy Followed by Yttrium-90 Ibritumomab Tiuxetan as First-Line Treatment for Patients with Follicular Non-Hodgkin Lymphoma: A Phase II Trial of the Sarah Cannon Oncology Research Consortium","authors":"John D. Hainsworth ,&nbsp;David R. Spigel ,&nbsp;Tiffanie M. Markus ,&nbsp;Dianna Shipley ,&nbsp;Dana Thompson ,&nbsp;Richard Rotman ,&nbsp;Charles Dannaher ,&nbsp;F. Anthony Greco","doi":"10.3816/CLM.2009.n.044","DOIUrl":"10.3816/CLM.2009.n.044","url":null,"abstract":"<div><h3>Purpose</h3><p>To evaluate the efficacy and safety of treatment with Yttrium-90 (90Y) ibritumomab tiuxetan following completion of short-course rituximab/chemotherapy in patients with previously untreated follicular non-Hodgkin lymphoma.</p></div><div><h3>Patients and Methods</h3><p>Forty-one patients with previously untreated follicular lymphoma received rituximab for 4 consecutive weeks, followed by 3 cycles of rituximab combined with either CHOP (cyclophosphamide/doxorubicin/vincristine/prednisone; 88%) or CVP (cyclophosphamide/ vincristine/prednisone; 12%). To complete treatment, all patients received 90Y ibritumomab tiuxetan 4-6 weeks after the final dose of chemotherapy. The primary efficacy endpoint was the clinical complete response (CR) rate after completion of therapy; all patients were followed for progression-free survival (PFS) and overall survival (OS).</p></div><div><h3>Results</h3><p>After completion of shortcourse rituximab/chemotherapy, 95% had objective responses, with a 30% clinical CR rate. The clinical CR rate increased to 72% following 90Y ibritumomab tiuxetan. After a median follow-up of 67 months, the estimated 5-year PFS and OS rates are 64% and 96%, respectively. Reversible grade 3/4 neutropenia and thrombocytopenia occurred in 39% and 36% of the patients, respectively, following 90Y ibritumomab tiuxetan; nonhematologic toxicity was uncommon.</p></div><div><h3>Conclusion</h3><p>90Y ibritumomab tiuxetan was well tolerated after short-course rituximab/chemotherapy and resulted in a high CR rate and a long PFS. Definitive demonstration of improved efficacy versus rituximab/chemotherapy alone will require a randomized phase III trial.</p></div>","PeriodicalId":100272,"journal":{"name":"Clinical Lymphoma and Myeloma","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2009-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3816/CLM.2009.n.044","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"28242320","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"t(11;14) Plasma Cell Disorder Presents as a True Nonsecretory, Nonproducer Multiple Myeloma","authors":"Wei Chen ,&nbsp;Mark McNamara ,&nbsp;Young Kim ,&nbsp;Qin Huang","doi":"10.3816/CLM.2009.n.048","DOIUrl":"10.3816/CLM.2009.n.048","url":null,"abstract":"<div><p>We describe an extremely rare case of so-called nonsecretory, nonproducer myeloma in an 80-year-old man who presented with weight loss and anemia. The patient's serum protein electrophoresis was negative for M protein spike, and quantitation of his immunoglobulin level was far below the normal range. The bone marrow biopsy showed a sheet-like diffuse plasmacytic infiltrate with essential absence of trilineage hematopoiesis. Flow cytometry analysis and immunohistochemical study demonstrated a strong CD38/CD138/immunoglobulin G heavy chain—positive plasma cell population but failed to detect either cytoplasmic κ or λ light chain expression. Chromosomal analysis and dual fluorescence in situ hybridization studies clearly demonstrated the presence of t(11;14)(q13;q32) translocation in the neoplastic plasma cells.</p></div>","PeriodicalId":100272,"journal":{"name":"Clinical Lymphoma and Myeloma","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2009-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3816/CLM.2009.n.048","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"28242325","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Durable Complete Remissions in HIV-Associated Hodgkin Lymphoma After Treatment with Only One Cycle of Chemotherapy Complicated by Sepsis","authors":"Peter Martin,&nbsp;John P. Leonard,&nbsp;Morton Coleman,&nbsp;Richard R. Furman","doi":"10.3816/CLM.2009.n.049","DOIUrl":"10.3816/CLM.2009.n.049","url":null,"abstract":"<div><p>The infiltration of nonmalignant cells surrounding the Reed-Sternberg cells within the tumors of Hodgkin lymphoma (HL) might be central to the pathophysiology of the disease. Severe sepsis results in a flood of cytokines that activate the immune system and is associated with generalized lymphocyte apoptosis. We report on 2 patients with HIV infection and HL who achieved durable complete remissions following only one cycle of chemotherapy that was complicated by neutropenic sepsis. An understanding of the pathophysiology of sepsis and immunologic activation that appear to have led to these long-term remissions might lead to novel therapeutic approaches for patients with HL.</p></div>","PeriodicalId":100272,"journal":{"name":"Clinical Lymphoma and Myeloma","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2009-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3816/CLM.2009.n.049","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"28242326","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"National Cancer Institute–Sponsored Cooperative Groups: Changing Process to Speed Progress","authors":"Mike Montello PharmD,&nbsp;Margaret Mooney MD,&nbsp;Andrea Denicoff MS,&nbsp;Jeanne Adler MPH,&nbsp;Jacquelyn Goldberg JD,&nbsp;Jeffrey Abrams MD","doi":"10.3816/CLM.2009.n.040","DOIUrl":"10.3816/CLM.2009.n.040","url":null,"abstract":"Recent independent analyses of the National Cancer Institute’s (NCI) clinical trials systems have indicated an urgent need to re-evaluate ingrained processes and to find novel solutions if investigators are to take full advantage of the scientific opportunities available today for clinical research.1-3 The NCI-sponsored Cooperative Groups remain NCI’s primary outlet for phase III definitive trials in cancer prevention, control, and treatment.4 Cooperative Groups have the significant advantage of maintaining a regulatory and operational foundation that is readily available and fully experienced in the conduct and coordination of large, multicenter trials. This infrastructure has undergone a series of changes since 2000 that have positively affected Group operations. Some of the most important ones include the pivotal role of the Cancer Trials Support Unit (CTSU), the NCI’s Central Institutional Review Board (CIRB), and the recently introduced Disease-Specific Steering Committees (DSSC). In order for these projects to achieve their aims, however, increased attention must be devoted to the numerous processes underlying clinical trial development.","PeriodicalId":100272,"journal":{"name":"Clinical Lymphoma and Myeloma","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2009-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3816/CLM.2009.n.040","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"28242962","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Primary Central Nervous System Mucosa-Associated Lymphoid Tissue Lymphoma: Case Report and Literature Review","authors":"Wajeeha Razaq ,&nbsp;Anupama Goel ,&nbsp;Ali Amin ,&nbsp;Michael L. Grossbard","doi":"10.3816/CLM.2009.n.052","DOIUrl":"10.3816/CLM.2009.n.052","url":null,"abstract":"<div><p>Primary presentation of intradural non-Hodgkin lymphoma is rare. Recently, B-cell lymphomas of mucosa-associated lymphoid tissue (MALT) have been recognized as an important pathologic subtype. When MALT lymphomas present in the central nervous system (CNS), they are distinguishable from primary high-grade CNS lymphomas. We present the clinicopathologic features of 5 patients with primary CNS MALT lymphoma treated at our institution from 1999 to 2006. Four out of 5 patients were women, and all patients presented with headaches, focal motor deficits, or cranial nerve palsy. Radiologic studies demonstrated ill-defined dural masses in 3 and well-defined masses in 2 patients. Pathology revealed small to medium-sized cells with a moderate amount of cytoplasm and irregular nuclear borders, expressing pan B-cell markers (CD19, CD20, and CD79a) but lacking CD10, CD23, and cyclin D1, confirming low-grade MALT lymphoma. Plasma cells were encountered in all the biopsies with variable reactive T-cell infiltration. δ chain restriction was seen in 3 patients. Therapy consisted of either surgical resection, whole-brain radiation, or systemic or intrathecal chemotherapy. There was no evidence of recurrence or systemic relapse in 4 patients at 4 years of follow-up. One patient died in 2 months, unrelated to CNS lymphoma. This case series illustrates the rare occurrence of low-grade dural B-cell lymphoma and the need to consider this entity in the differential diagnosis of CNS lesions.</p></div>","PeriodicalId":100272,"journal":{"name":"Clinical Lymphoma and Myeloma","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2009-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3816/CLM.2009.n.052","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"28242961","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hodgkin Lymphoma: An Update on its Biology with New Insights into Classification","authors":"Haresh Mani,&nbsp;Elaine S. Jaffe","doi":"10.3816/CLM.2009.n.042","DOIUrl":"10.3816/CLM.2009.n.042","url":null,"abstract":"<div><p>In the past few years, there has been a greater understanding of the spectrum and biology of Hodgkin lymphoma (HL). In standard texts, HL is classified as 2 distinct entities, namely nodular lymphocyte-predominant HL and classical HL (CHL). However, recent evidence suggests that CHL is not a single disease. Although the mixed cellularity and lymphocyte-depleted subtypes might be part of a biologic continuum, the nodular sclerosis subtype has a distinct epidemiology, clinical presentation, and histology. Nodular sclerosis HL might also be related to primary mediastinal B-cell lymphoma and mediastinal gray-zone lymphomas. We present an update on the pathobiology of HL and discuss these biologic and clinical differences in this review.</p></div>","PeriodicalId":100272,"journal":{"name":"Clinical Lymphoma and Myeloma","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2009-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3816/CLM.2009.n.042","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"28242321","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Response Dynamics in Chronic-Phase Chronic Myeloid Leukemia","authors":"Michael J. Mauro","doi":"10.3816/CLM.2009.n.043","DOIUrl":"10.3816/CLM.2009.n.043","url":null,"abstract":"<div><p>Cytogenetic response (CyR), especially complete CyR (CCyR), has historically and is currently associated with a significant survival advantage in patients with chronic-phase chronic myeloid leukemia (CP-CML). CCyR represents a critical level of disease reduction irrespective of treatment type, and timely achievement demonstrates treatment-sensitive disease. Guidelines from European LeukemiaNet and the National Comprehensive Cancer Network therefore state that alternative therapies should be considered for patients not achieving CCyR by 6 or 12 months. Data from clinical trials indicate that early CCyR affords the best benefit:risk ratio by minimizing the mounting risk of disease progression, and the duration of CCyR when achieved affects disease progression. Treatment options for patients who fail to achieve CCyR on standard-dose imatinib (400 mg/day) include imatinib dose escalation, dasatinib, nilotinib, stem-cell transplantation, or a clinical trial. While molecular testing gauges further risk reduction, disease stability, and often elimination of BCR-ABL transcripts below detection threshold, CCyR remains the most important surrogate for long-term survival and cytogenetic testing remains a key part of patient care in the management of CML, particularly early in response. Longerterm follow-up data will be required to confirm CCyR as a surrogate marker for survival in imatinib-resistant patients treated with the secondgeneration tyrosine kinase inhibitors, dasatinib and nilotinib.</p></div>","PeriodicalId":100272,"journal":{"name":"Clinical Lymphoma and Myeloma","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2009-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3816/CLM.2009.n.043","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"28242964","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Urinary Findings in Renal Light Chain–Derived Amyloidosis and Light Chain Deposition Disease","authors":"Gavin M. Melmed ,&nbsp;Andrew Z. Fenves ,&nbsp;Marvin J. Stone","doi":"10.3816/CLM.2009.n.046","DOIUrl":"10.3816/CLM.2009.n.046","url":null,"abstract":"<div><h3>Background</h3><p>Early recognition of light chain—derived (AL) amyloidosis and light chain deposition disease (LCDD) is essential for optimal therapy. However, clinical and laboratory manifestations of these unusual conditions often go unrecognized. Renal protein deposits in AL amyloidosis and LCDD can cause both heavy albuminuria and Bence Jones proteinuria. Absent separate etiologies, this combined finding is rare and provides a clue to the diagnosis of these conditions.</p></div><div><h3>Materials and Methods</h3><p>We retrospectively reviewed test results of urine immunoelectrophoreses and urine immunofixation electrophoreses performed at a single institution from 1977 to 2006. Patients with both heavy albuminuria and Bence Jones proteinuria were investigated further to determine whether these findings were predictive of renal AL amyloidosis or LCDD. We reviewed the patients' clinical histories, laboratory data, and pathology reports and included patients with biopsy-confirmed renal AL amyloidosis or LCDD in this series.</p></div><div><h3>Results</h3><p>We identified 6 patients with renal amyloidosis or LCDD who presented with the dual findings of Bence Jones proteinuria and heavy albuminuria. We report their demographic information, laboratory data, and case histories.</p></div><div><h3>Conclusion</h3><p>The simultaneous presence of heavy albuminuria and Bence Jones proteinuria justifies a workup for AL amyloidosis or LCDD. Prompt recognition of these rare conditions would permit earlier initiation of therapy and potentially limit organ dysfunction. In addition, patients might be spared unnecessary clinical investigation and unwarranted treatment.</p></div>","PeriodicalId":100272,"journal":{"name":"Clinical Lymphoma and Myeloma","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2009-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3816/CLM.2009.n.046","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"28242323","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"von Hippel–Lindau Methylation Status in Patients with Multiple Myeloma: A Potential Predictive Factor for the Development of Bone Disease","authors":"Eleftheria Hatzimichael ,&nbsp;George Dranitsaris ,&nbsp;Aggeliki Dasoula ,&nbsp;Leonidas Benetatos ,&nbsp;Justin Stebbing ,&nbsp;Tim Crook ,&nbsp;Konstantinos L. Bourantas","doi":"10.3816/CLM.2009.n.047","DOIUrl":"10.3816/CLM.2009.n.047","url":null,"abstract":"<div><p>It has been suggested that during multiple myeloma (MM) progression, a proangiogenesis stress response occurs, but the mechanistic basis of this has not been established. It is an attractive hypothesis that loss of expression of the von Hippel—Lindau (VHL) gene, resulting in constitutive activation of hypoxia-inducible factor—1α (HIF-1α), contributes to increased angiogenesis in MM. Because aberrant methylation in the VHL CpG island could cause downregulation of VHL transcription, we prospectively studied the methylation status of the VHL CpG island in 45 individuals with multiple myeloma (MM; 25 men, 20 women; mean age, 66.4 years) and in 10 individuals with borderline thrombocytopenia, who were proven to have no malignancy and served as controls. Methylation was found in 15 of 45 patients with MM at diagnosis (33.3%). The presence of methylation in the VHL CpG island was significantly associated with the development of bone disease (odds ratio, 7.5; <em>P</em> = .018). Patients with bone disease had an increased risk of death compared with those with no bone lytic lesions (hazard ratio [HR], 5.1; <em>P</em> = .13). VHL methylation was not a predictor of excess mortality (HR, 0.92; <em>P</em> = .91). Our data imply that methylation in the VHL CpG island is a frequent event in patients with MM and might be a potential biomarker of bone disease. Methylation in the VHL CpG island, leading to transcriptional silencing and hence decreased HIF-1α proteolysis, could be a possible mechanism of increased angiogenesis and altered bone marrow microenvironment that is more supportive for survival and growth of MM cells, contributing to MM bone disease. Whether it represents an early or late event of the disease merits additional study. Additional studies regarding the serum levels of HIF-1α and vascular endothelial growth factor would be mechanistically interesting.</p></div>","PeriodicalId":100272,"journal":{"name":"Clinical Lymphoma and Myeloma","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2009-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3816/CLM.2009.n.047","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"28242324","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The 50th Annual Meeting of the American Society of Hematology","authors":"Sonia Cunningham PhD,&nbsp;Sabeeha Muneer PhD,&nbsp;Sundar Jagannath MD,&nbsp;Sagar Lonial MD,&nbsp;Stefan Faderl MD,&nbsp;Stephan Stilgenbauer MD","doi":"10.3816/CLM.2009.n.041","DOIUrl":"10.3816/CLM.2009.n.041","url":null,"abstract":"","PeriodicalId":100272,"journal":{"name":"Clinical Lymphoma and Myeloma","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2009-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3816/CLM.2009.n.041","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"28242963","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}