1098 - Crizotinib in ALK-positive diffuse large B-cell lymphoma: a case report

Date 28 September 2012
Event ESMO Congress 2012
Session Publication Only
Topics Anticancer Agents
Biological Therapy
Presenter Maxi Wass
Authors M. Wass, T. Behlendorf, U. Gläser, J. Rüssel, F. Güntsch, K. Jordan, H. Schmoll
  • Klinik Für Innere Medizin Iv, Universitätsklinikum Halle (Saale), 06120 - Halle/DE



Anaplastic lymphoma kinase (ALK)-positive diffuse large B-cell lymphoma (DLBCL) is a distinct variant of DLBCL characterized by very aggressive clinical course with an estimated median survival of only 11.0 months. Crizotinib, an ALK inhibitor, has demonstrated impressive clinical efficacy in patients with alk-rearranged tumors. The potential role of Crizotinib in ALK-positive DLBCL has not been established yet.

Case report

A 27-year-old female patient with ALK-positive DLBCL was primary refractory to 6 cycles of standard chemotherapy with CHOP. She was subsequently treated with salvage combination chemotherapy regimens including high-dose chemotherapy with autologous stem-cell transplantation. However, disease followed a very aggressive course. 6 weeks after transplantation patient presented with right cervical lymphadenopathy and multiple cutaneous lesions. CT scan revealed additional bilateral cervical, axillary, mediastinal and abdominal lymphadenopathy and involvement of lung and liver. LDH levels were exorbitant elevated (233 mmol/l). On an individual base, our patient received the ALK inhibitor Crizotinib 250 mg per os twice daily. No glucocorticoids or other drugs with antineoplastic activity were co-administered. Within 72 hours LDH levels were halved (89 mmol/l). On day 8 cervical palpable lymphadenopathy disappeared. Initial erythematous papular cutaneous lesion decreased from 4.0 x 2.5 cm to a residual hyperpigmented macule of 1.5 x 2.5 cm. On day 16 LDH levels were almost within normal limits (6 mmol/l). However, remission was not sustained and patient developed resistance to Crizotinib. By day 21 after beginning the treatment with Crizotinib LDH levels increased again and patient presented with a swollen left arm due to lymphatic obstruction, detected by CT scan, which showed a general progressive disease, causing death one month later.


To our knowledge, this is the first case which reports sensitivity in ALK-positive DLBCL to ALK inhibition with Crizotinib. Despite remission duration was short our results indicate a potential role of ALK in the pathogenesis of ALK-positive DLBCL and suggest ALK inhibition as a potential treatment modality in the therapy of this fatal disease.


All authors have declared no conflicts of interest.