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Amplification of 9p24.1 Associated With Advanced Stage and Poorer Outcome in Classic Hodgkin Lymphoma

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Key Points

  • Concordant amplification of the PD-L1/PD-L2 loci was found in 36% of cases of classic Hodgkin lymphoma.
  • Amplification of 9p24.1 was associated with advanced-stage disease and poorer progression-free survival.

In a study reported in the Journal of Clinical Oncology, Roemer et al identified PD-L1 (programmed cell death ligand 1) and PD-L2 genetic alterations in patients with classic Hodgkin lymphoma, finding that 9p24.1 amplification was common and associated with advanced-stage disease and poorer outcome.

Study Details

In the study, a fluorescent in situ hybridization assay was used to evaluate CD274/PD-L1 and PDCD1LG2/PD-L2 alterations in 108 biopsy specimens from patients with newly diagnosed disease who had received the Stanford V regimen and had long-term follow-up.

Alterations

Overall, concordant alterations of the PD-L1 and PD-L2 loci were found in 97% of cases, consisting of polysomy in 5%, copy gain in 56%, and amplification in 36%. Decreased residual 9p24.1 disomy was significantly associated with increased PD-L1 expression (P = .005). Assessment of progression-free survival by 9p24.1 alteration showed significantly poorer outcome with amplification (P < .001), and the incidence of amplification was higher among patients with advanced-stage disease (50%) vs those with early-stage favorable (24%) or early-stage unfavorable disease (34%; P = .024).

The investigators concluded: “PD-L1/PD-L2 alterations are a defining feature of [classical Hodgkin lymphoma]. Amplification of 9p24.1 is more common in patients with [advanced stage] disease and associated with shorter [progression-free survival] in this series. Further analyses of 9p24.1 alterations in patients treated with standard … induction regimens or checkpoint blockade are warranted.”

The study was supported by the National Institutes of Health and the Miller Family Fund.

Margaret A. Shipp, MD, of the Dana-Farber Cancer Institute, is the corresponding author of the Journal of Clinical Oncology article.

The content in this post has not been reviewed by the American Society of Clinical Oncology, Inc. (ASCO®) and does not necessarily reflect the ideas and opinions of ASCO®.


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