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David M. Menke

Researcher at Mayo Clinic

Publications -  96
Citations -  2869

David M. Menke is an academic researcher from Mayo Clinic. The author has contributed to research in topics: Lymphoma & Diffuse large B-cell lymphoma. The author has an hindex of 26, co-authored 95 publications receiving 2544 citations.

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Use of Rituximab for Periocular and Intraocular Mucosa-associated Lymphoid Tissue Lymphoma

TL;DR: The clinical efficacy of rituximab therapy in systemic mucosa-associated lymphoid tissue (MALT) lymphoma with both periocular and intraocular involvement is described.
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Comparable Efficacy of Reduced Dose Radiation Therapy for the Treatment of Early Stage Gastric Extranodal Marginal Zone Lymphoma of Mucosa-Associated Lymphoid Tissue

TL;DR: Lower dose RT achieved excellent complete response rates with minimal toxicity, comparable with standard dose RT (30-36 Gy), for gMALT, and incidence and severity of reported toxicities were similar between the 2 groups.
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Remission induction with lenalidomide in a patient with relapsed diffuse large B cell lymphoma of the leg type.

TL;DR: A 78-year-old, female patient was treated for DLBCL of the right breast with cyclophosphamide, doxorubicin, vincristine, and prednisone followed by chest wall/axillary radiation in the early 1980s and had since been in complete remission (CR), in which remission was achieved with lenalidomide-based therapy.
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Solitary pelvic nodule: diagnosis of metastatic prostate cancer by endoscopic ultrasound-guided, fine-needle aspiration

TL;DR: The following is a report of a single pelvic nodule that was determined to be metastatic prostate cancer by endoscopic ultrasound-guided, fine-needle aspiration.
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Mantle cell lymphoma with a novel t(11;12)(q13;p11.2): a proposed alternative mechanism of CCND1 up-regulation

TL;DR: It is suggested that, in the absence of the typical CCND1/IGH@ fusion, this rearrangement promotes MCL pathogenesis by eliminating miRNA interaction elements within the 3' untranslated region (UTR) of the CC ND1 mRNA transcript consequently resulting inCCND1 overexpression.