Frontiers in oncology · 2026
Alectinib shows promise for the treatment of refractory ALK-positive large B-cell lymphoma: a case report.
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Alsulami Atheer, Almufti Roula, Eldadah Saleem, Al-Ghamdi Yahya
Аннотация
INTRODUCTION: Anaplastic lymphoma kinase-positive large B-cell lymphoma (ALK+ LBCL) is rare, accounts for <1% of DLBCL, and is characterized by ALK rearrangement. ALK+ LBCL is a very aggressive disease with a poor prognosis, a high risk of relapse and a poor response to standard chemotherapy treatment, with a median overall survival of approximately one year in advanced-stage disease. The activity of ALK inhibitors in the treatment of relapsed/refractory ALK+ LBCL is not well studied. Here, we report our experience with the use of alectinib in refractory ALK+ LBCL.
CASE PRESENTATION: A previously healthy 14-year-old Saudi Arabian girl presented with progressive chest, loin, and iliac crest pain over two months, without B symptoms. Imaging revealed a left supradiaphragmatic soft tissue mass with supra and infradiaphragmatic nodal masses, pancreatic mass and right iliac bone aggressive lesion. Core biopsy of a left pararenal mass confirmed ALK-positive large B-cell lymphoma (ALK+ LBCL). Immunohistochemistry showed positivity for CD138, MUM1, CD79a (subset), CD4, EMA, CD45, CD10 (weak), BCL6, c-MYC, BCL2, and cytoplasmic ALK1. CD20 and PAX5 were negative. ALK rearrangement was confirmed by FISH; the bone marrow was not involved. Initial treatment with CHOEP failed, followed by progression on salvage ESHAP and IGEV chemotherapy. Radiation was given for bulky disease. Crizotinib was initiated with partial response but discontinued due to hepatotoxicity and disease progression. Alectinib was then started, resulting in a complete metabolic response (CMR). This was consolidated with an allogeneic stem cell transplant from a matched sibling donor, leading to a sustained CMR for 4 years with good tolerance.
CONCLUSION: The use of next-generation ALK inhibitors in this case demonstrated excellent tolerability and induced sustained responses. This report suggests that alectinib may be an effective bridging therapy for refractory ALK+ LBCL to enable allogeneic SCT in selected patients. Further prospective studies are warranted to explore and optimize therapeutic strategies for this rare disease.
CASE PRESENTATION: A previously healthy 14-year-old Saudi Arabian girl presented with progressive chest, loin, and iliac crest pain over two months, without B symptoms. Imaging revealed a left supradiaphragmatic soft tissue mass with supra and infradiaphragmatic nodal masses, pancreatic mass and right iliac bone aggressive lesion. Core biopsy of a left pararenal mass confirmed ALK-positive large B-cell lymphoma (ALK+ LBCL). Immunohistochemistry showed positivity for CD138, MUM1, CD79a (subset), CD4, EMA, CD45, CD10 (weak), BCL6, c-MYC, BCL2, and cytoplasmic ALK1. CD20 and PAX5 were negative. ALK rearrangement was confirmed by FISH; the bone marrow was not involved. Initial treatment with CHOEP failed, followed by progression on salvage ESHAP and IGEV chemotherapy. Radiation was given for bulky disease. Crizotinib was initiated with partial response but discontinued due to hepatotoxicity and disease progression. Alectinib was then started, resulting in a complete metabolic response (CMR). This was consolidated with an allogeneic stem cell transplant from a matched sibling donor, leading to a sustained CMR for 4 years with good tolerance.
CONCLUSION: The use of next-generation ALK inhibitors in this case demonstrated excellent tolerability and induced sustained responses. This report suggests that alectinib may be an effective bridging therapy for refractory ALK+ LBCL to enable allogeneic SCT in selected patients. Further prospective studies are warranted to explore and optimize therapeutic strategies for this rare disease.