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Laubach, Jacob

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Laubach

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Jacob

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Laubach, Jacob

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2011 - 201932020 - 20211

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Author's Publications: search.filters.isAuthorOfPublication.42106bca-5597-4303-9ae2-121897cd7980

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Now showing 1 - 4 of 4
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    Lenalidomide for the Treatment of Relapsed and Refractory Multiple Myeloma
    (Dove Medical Press, 2012) Görgün, Güllü; Nijhof, Inger S; Raymakers, Reinier A; Lokhorst, Henk M; Groen, Richard W.j.; Jakubikova, Jana; Mitsiades, Constantine; Hideshima, Teru; Laubach, Jacob; Richardson, Paul; Anderson, Kenneth; van de Donk, Niels WCJ
    Lenalidomide is an amino-substituted derivative of thalidomide with direct antiproliferative and cytotoxic effects on the myeloma tumor cell, as well as antiangiogenic activity and immunomodulatory effects. Together with the introduction of bortezomib and thalidomide, lenalidomide has significantly improved the survival of patients with relapsed and refractory myeloma. The most common adverse events associated with lenalidomide include fatigue, skin rash, thrombocytopenia, and neutropenia. In addition, when lenalidomide is combined with dexamethasone or other conventional cytotoxic agents, there is an increase in the incidence of venous thromboembolic events. There is now evidence that continued treatment with lenalidomide has a significant impact on survival by improving the depth and duration of response. This highlights the value of adverse event management and appropriate dose adjustments to prevent toxicity, and of allowing continued treatment until disease progression. In this review, we will discuss the different lenalidomide-based treatment regimens for patients with relapsed/refractory myeloma. This is accompanied by recommendations of how to manage and prevent adverse events associated with lenalidomide-based therapy.
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    The Medical Research Council Myeloma IX Trial: The Impact on Treatment Paradigms
    (Blackwell Publishing Ltd, 2011) Richardson, Paul; Laubach, Jacob; Schlossman, Robert Lawrence; Ghobrial, Irene; Mitsiades, Constantine; Rosenblatt, Jacalyn; Mahindra, Anuj; Raje, Noopur; Munshi, Nikhil; Anderson, Kenneth
    Osteolytic bone disease is a hallmark of symptomatic multiple myeloma. Bisphosphonates have been the mainstay of treatment to preserve skeletal integrity and prevent skeletal-related events in patients with myeloma-related bone disease. Recently, the MRC Myeloma IX trial demonstrated for the first time improved survival and delayed disease progression with the use of an intravenous amino-bisphosphonate, zoledronic acid, vs. an oral agent, clodronate, with intensive and non-intensive anti-myeloma treatment regimens in patients with newly diagnosed multiple myeloma. These results validate a large body of preclinical, translational and other clinical data suggesting anti-myeloma effects of amino-bisphosphonates. In addition, this trial also provided the first head-to-head evidence for superiority of one bisphosphonate over another (zoledronic acid vs. clodronate) for reducing skeletal morbidity in patients with multiple myeloma, as well as a prospective comparison of toxicities. Despite the use of non-bortezomib containing anti-myeloma treatment regimens in the MRC Myeloma IX trial, these results are encouraging and provide an impetus to continue to evaluate current treatment guidelines for myeloma-associated bone disease.
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    Dynamic Transcriptional Reprogramming Leads to Immunotherapeutic Vulnerabilities in Myeloma
    (Springer Science and Business Media LLC, 2021-10-21) Frede, Julia; Anand, Praveen; Sotudeh, Noori; Pinto, Ricardo A.; Nair, Monica S.; Stuart, Hannah; Yee, Andrew J.; Vijaykumar, Tushara; Waldschmidt, Johannes M.; Potdar, Sayalee; Kloeber, Jake A.; Kokkalis, Antonis; Dimitrova, Valeriya; Mann, Mason; Laubach, Jacob; Richardson, Paul; Anderson, Kenneth; Raje, Noopur; Knoechel, Birgit; Lohr, Jens
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    Ibrutinib in Previously Treated Waldenström’s Macroglobulinemia
    (Massachusetts Medical Society, 2015-04-09) Treon, Steven; Tripsas, Christina K.; Meid, Kirsten; Warren, Diane; Varma, Gaurav; Green, Rebecca; Argyropoulos, Kimon V.; Yang, Guang; Cao, Yang; Xu, Lian; Patterson, Christopher J.; Rodig, Scott; Zehnder, James L.; Aster, Jon; Harris, Nancy; Kanan, Sandra; Ghobrial, Irene; Castillo, Jorge; Laubach, Jacob; Hunter, Zachary; Salman, Zeena; Li, Jianling; Cheng, Mei; Clow, Fong; Graef, Thorsten; Palomba, M. Lia; Advani, Ranjana H.
    Background: MYD88(L265P) and CXCR4(WHIM) mutations are highly prevalent in Waldenström's macroglobulinemia. MYD88(L265P) triggers tumor-cell growth through Bruton's tyrosine kinase, a target of ibrutinib. CXCR4(WHIM) mutations confer in vitro resistance to ibrutinib. Methods: We performed a prospective study of ibrutinib in 63 symptomatic patients with Waldenström's macroglobulinemia who had received at least one previous treatment, and we investigated the effect of MYD88 and CXCR4 mutations on outcomes. Ibrutinib at a daily dose of 420 mg was administered orally until disease progression or the development of unacceptable toxic effects. Results: After the patients received ibrutinib, median serum IgM levels decreased from 3520 mg per deciliter to 880 mg per deciliter, median hemoglobin levels increased from 10.5 g per deciliter to 13.8 g per deciliter, and bone marrow involvement decreased from 60% to 25% (P<0.01 for all comparisons). The median time to at least a minor response was 4 weeks. The overall response rate was 90.5%, and the major response rate was 73.0%; these rates were highest among patients with MYD88(L265P)CXCR4(WT) (with WT indicating wild-type) (100% overall response rate and 91.2% major response rate), followed by patients with MYD88(L265P)CXCR4(WHIM) (85.7% and 61.9%, respectively) and patients with MYD88(WT)CXCR4(WT) (71.4% and 28.6%). The estimated 2-year progression-free and overall survival rates among all patients were 69.1% and 95.2%, respectively. Treatment-related toxic effects of grade 2 or higher included neutropenia (in 22% of the patients) and thrombocytopenia (in 14%), which were more common in heavily pretreated patients; postprocedural bleeding (in 3%); epistaxis associated with the use of fish-oil supplements (in 3%); and atrial fibrillation associated with a history of arrhythmia (5%). Conclusions: Ibrutinib was highly active, associated with durable responses, and safe in pretreated patients with Waldenström's macroglobulinemia. MYD88 and CXCR4 mutation status affected responses to this drug.