Brentuximab Vedotin in Frontline Therapy of Hodgkin Lymphoma in Patients with Significant Comorbidities Ineligible for Standard Chemotherapy (SGN35-015 Part E)

Bordoni, Rodolfo; Patel‐Donnelly, Dipti; Larson, Timothy; Goldschmidt, Jerome H.; Boccia, Ralph V.; Cline, Vivian Jean M.; Mamidipalli, Adrija; Liu, Jingmin; Beck, J.T.

doi:10.1182/blood-2022-156567

Cited by 2 publications

(1 citation statement)

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“…BV was also tested as a frontline therapy in older or unfit patients to reduce or avoid chemotherapy exposure. While BV monotherapy granted a high ORR but limited PFS and OS [71][72][73], the addition of reduced-intensity chemotherapy showed promising results. Evens et al [74] tested a sequential treatment modality with single-agent BV administered before and after AVD in previously untreated patients aged 60 or older.…”

Section: Bv Plus Chemotherapy Combinationsmentioning

confidence: 99%

Advances in Hodgkin Lymphoma Treatment: From Molecular Biology to Clinical Practice

Benevolo Savelli,

Bisio,

Legato

et al. 2024

Cancers

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Classical Hodgkin Lymphoma (cHL) is a highly curable disease, but around 20% of patients experience progression or relapse after standard frontline chemotherapy regimens. Salvage regimens followed by autologous stem cell transplants represent the historical treatment approach for these cases. In the last decade, with the increasing understanding of cHL biology and tumor microenvironment role in disease course, novel molecules have been introduced in clinical practice, improving outcomes in the relapsed/refractory setting. The anti-CD30 antibody-drug conjugated brentuximab vedotin and PD-1/PD-L1 checkpoint inhibitors represent nowadays curative options for chemorefractory patients, and randomized trials recently demonstrated their efficacy in frontline immune-chemo-combined modalities. Several drugs able to modulate the patients’ T-lymphocytes and NK cell activity are under development, as well as many anti-CD30 chimeric antigen receptor T-cell products. Multiple tumor aberrant epigenetic mechanisms are being investigated as targets for antineoplastic compounds such as histone deacetylase inhibitors and hypomethylating agents. Moreover, JAK2 inhibition combined with anti-PD1 blockade revealed a potential complementary therapeutic pathway in cHL. In this review, we will summarize recent findings on cHL biology and novel treatment options clinically available, as well as promising future perspectives in the field.

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