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• W2073276394 abstract "Targeting of the potent anti-tubulin agent, monomethyl auristatin E (MMAE), directly to CD30 positive tumor cells using brentuximb vedotin (BV) has recently proven to be quite eff ective for patients with relapsed and refractory (rel/ref ) Hodgkin lymphoma (HL) and anaplastic large cell lymphoma (ALCL). Before the entry of BV, these patients had very limited treatment options at their disposal, and the introduction of BV has undoubtedly prolonged many lives. However, the full extent of its impact on HL and ALCL still remains to be determined. Clinical trials evaluating BV in the front-line setting in HL and ALCL are under way and may lead to dramatic changes in our treatment strategies for these malignancies. Following its success in HL and ALCL, the logical next step was to determine which other patient categories might benefi t from BV. Other non-Hodgkin lymphomas are known to express CD30 at varying rates, but whether this would translate into sensitivity to BV was still unknown. It was also unclear at this point what constitutes CD30 positivity and what percentage of CD30 positive cells is required to regard a tumor as positive or whether there was a particular cut-off suffi cient for BV activity. Ongoing studies are beginning to provide an answer to these questions, although some of the answers given may not be what we would have expected. Considerable single-agent activity has been reported for BV in other CD30 positive B cell lymphomas and systemic T cell lymphomas, as well as mycosis fungoides (MF) (Table I) (1 - 3). Contrary to what we may have predicted, in each of these analyses, the level of CD30 expression did not cor- relate with response to BV, and in fact, responses were even observed among patients determined by immunohis- tochemical (IHC) staining to have no CD30 expression in their tumors. Th e reason for this is as yet not known; how- ever, it is possible that a very low level of CD30 expression is indeed suffi cient for BV effi cacy due to the action of free MMAE on neighboring CD30-negative cells at the time of its release from dying CD30-positive cells within tumors. Fur- thermore, standard IHC may not be sensitive enough to detect very low levels of CD30 expression. Among patients with MF treated with BV, Krathen and colleagues were able to detect CD30 expression using quantitative image analysis on biop- sies from 12 patients that were initially deemed negative by routine IHC. Even with this more sophisticated technique for evaluating CD30 expression, though, no correlation between CD30 expression and sensitivity to BV was found (3). While these fi ndings clearly raise questions regarding mechanisms of resistance to BV and the issues of biomarkers of sensitivity" @default.
• W2073276394 created "2016-06-24" @default.
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• W2073276394 date "2014-11-19" @default.
• W2073276394 modified "2023-09-25" @default.
• W2073276394 title "New frontiers for brentuximab vedotin for lymphomas" @default.
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• W2073276394 doi "https://doi.org/10.3109/10428194.2014.974050" @default.
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