What Causes Bruton Tyrosine Kinase Inhibitor Resistance in Mantle Cell Lymphoma and How Should We Treat Such Patients?

McCulloch, Rory; Eyre, Toby A.; Rule, Simon

doi:10.1016/j.hoc.2020.06.008

Cited by 1 publication

(2 citation statements)

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“…As mentioned above, these include not only the leukemic/non-nodal, SOX11-negative form but also rare, asymptomatic, nodal/extra-nodal forms with a low tumor burden, classical morphology on histopathology, low proliferation rate and an intact TP53 [ 51 , 76 ]. It was shown that these subsets may remain stable for years and that early treatment does not impact overall survival [ 77 , 78 ]. Therefore, it is currently recommended to keep these patients under surveillance, starting treatment only when symptoms or clear progression demands it.…”

Section: Mantle Cell Lymphoma (Mcl)mentioning

confidence: 99%

“…Targeted therapies approved for relapsed refractory MCL include the proteasome inhibitor Bortezomib, the immune modulator Lenalidomide and, in Europe, the mTOR inhibitor Temsirolimus [ 85 , 86 ]. However, very active BTK inhibitors (BTKi), of which Ibrutinib [ 78 , 85 , 87 ] and Acalabrutinib [ 88 ] are approved, currently dominate the therapeutic strategies. Numerous clinical trials are testing the combination of new agents with chemotherapy at the first line, the addition of lenalidomide or bortezomib to maintenance regimens and the use of new agents in comparison to chemotherapy [ 72 , 76 ].…”

Section: Mantle Cell Lymphoma (Mcl)mentioning

confidence: 99%

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How to Diagnose and Treat CD5-Positive Lymphomas Involving the Spleen

et al. 2021

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Patients with CD5-expressing lymphomas presenting with splenomegaly are frequently diagnosed with chronic lymphocytic leukemia. The most important differential diagnosis is mantle cell lymphoma, both in its classical and leukemic, non-nodal forms, given its prognostic and therapeutic implications. Other small B-cell neoplasms that frequently involve the spleen and occasionally express CD5 include the splenic marginal zone lymphoma, hairy cell leukemia and, rarely, lymphoplasmacytic lymphoma. The frequency of CD5 positivity depends in part on the sensitivity of the detection methods employed. Usually, a combination of morphological, immunophenotypic and molecular findings allows for a precise sub-classification of CD5-positive, low-grade B-cell lymphomas of the spleen. Some of these tumors may display a mixture of small and larger B cells, raising the possibility of more aggressive lymphomas, such as diffuse large B-cell lymphomas (DLBCL). Approximately 5–10% of DLBCL are CD5-positive and some may manifest as primary splenic lesions. When available, the morphology of DLBCL in the splenic tissue is distinctive and a leukemic picture is very rare. In conclusion, the appropriate morphological and clinical context assisted by flow cytometry panels and/or immunohistochemistry allows the differential diagnosis of CD5-positive, non-Hodgkin, B-cell lymphomas involving the spleen.

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