BEAM (BCNU, etoposide, cytarabine, melphalan) is the most widely used high dose chemotherapy regimen for autologous transplant in lymphoid malignancies. We report our early experience with an alternative regimen LEAM where BCNU was replaced with the oral analogue CCNU (lomustine) to tide over the non-availability of BCNU. Fifty one patients of relapsed or refractory lymphoma who received BEAM (n= 34) and LEAM (n= 17) from September 2001 to February 2012 were analyzed. From October 2009 onwards LEAM was used as the conditioning regimen instead of conventional BEAM. Patients in the LEAM group had more chemorefractory disease (35% vs 9%, p = 0.045) and high risk comorbidity score (24% vs 0%, p = 0.019). Grade 3 and 4 oral mucositis (67.6% vs. 64.7%, p = 0.834) and diarrhea (47% vs. 41.1%, p = 0.691) were similar. No difference was noted between the two groups in terms of engraftment, documented infections, antibiotic use, cumulative toxicity risk, length of hospital stay and 100 day transplant related mortality. The estimated 2 year overall survival (61.7% vs. 62.7%, p = 0.928) and event free survival (44.6% vs. 41.1%, p = 0.510) of the regimens BEAM and LEAM respectively were comparable. Thus LEAM appeared equivalent to BEAM in terms of toxicity and efficacy and can be used as an alternative to BEAM.

The British Journal of Haematology publishes original research papers in clinical, laboratory and experimental haematology. The Journal also features annotations, reviews, short reports, images in haematology and Letters to the Editor.

What is known and objective Variable response to docetaxel‐based neo‐adjuvant chemotherapy (NACT) in breast cancer patients had been reported. Genetic polymorphisms in the ABCB1 gene coding for the efflux transporter MDR1 (P‐glycoprotein, P‐gp) could result in altered tumour response. Hence, this study was proposed to assess the effect of single nucleotide polymorphisms (SNPs) of ABCB1 gene on tumour response in locally advanced breast cancer patients (LABC) of South India who have a distinct genetic makeup. Methods Out of 162 LABC patients recruited, 129 patients were included for the final analysis. DNA was extracted by “phenol‐chloroform extraction method” from the WBCs, and genotyping for SNPs rs1045642 (C3435T) and rs1128503 (C1236T) in ABCB1 gene was performed with real‐time PCR system using validated TaqMan^® SNP genotyping assay method. Tumour response was assessed by RECIST criteria based on the MRIs taken before and after completion of four cycles of docetaxel therapy. Results and discussion A total of 102 (79.1%) patients were found to be responders and 27 (20.9%) patients were found to be non‐responders to docetaxel therapy. Patients with “CT/TT” genotypes (response rate: 83.3%) of ABCB1 (C1236T) gene showed better tumour response than those with “CC” genotype (response rate: 16.6%) [OR = 2.94 (CI: 1.15‐7.52); P = 0.03]. However, on performing binary logistic regression, neither the studied SNPs nor the non‐genetic factors like age, BMI, postmenopausal status, laterality of the tumour, ER status, PR status and Her‐2/neu status were found to be associated with tumour response to docetaxel (P > 0.05). What is new and conclusion The tumour response to docetaxel was significantly influenced by the SNP C1236T of ABCB1 gene coding for the P‐gp. However, when adjusted for other non‐genetic factors, neither of the ABCB1 variants were found to be associated with tumour response to docetaxel‐based NACT in LABC patients of South India.

Background Treatment protocols for acute lymphoblastic leukemia (ALL) have evolved over time to give excellent cure rates in children and moderate outcomes in adults; however, little is known how delays in chemotherapy affect long-term survival. Objectives To find the association of delays during different treatment phases on the survival outcomes. Materials and Methods Data from 149 ALL cases treated between 2009 and 2015 were retrospectively analyzed. Treatment course in commonly used protocols was divided into three phases—induction, consolidation (postremission), maintenance, and also a combined intensive phase (induction plus consolidation) for the purpose of analysis, and delay in each phase was defined based on clinically acceptable breaks. Analysis was done to find the impact of treatment delay in each phase on the survival outcomes. Results The median age was 12 years (range, 1–57). Multi-center Protocol-841 (MCP-841) was used for 72%, German Multicenter Study Group for Adult ALL (GMALL) for 19%, and Berlin, Frankfurt, Muenster, 95 protocol (BFM-95) for 9% of patients. Delay in induction was seen in 52%, consolidation in 66%, and during maintenance in 42% of patients. The median follow-up was 41 months, and 3-year survival outcomes for the entire cohort were event-free survival (EFS)—60%, relapse-free survival (RFS)—72%, and overall survival (OS)—68%. On univariate analysis, delay in induction adversely affected EFS (hazard ratio [HR] = 1.78, p = 0.04), while delay in intensive phase had significantly worse EFS and RFS (HR = 2.41 [p = 0.03] and HR = 2.57 [p = 0.03], respectively). On separate analysis of MCP-841 cohort, delay in intensive phase affected both EFS (HR = 3.85, p = 0.02) and RFS (HR = 3.42, p = 0.04), whereas delay in consolidation significantly affected OS with (HR = 4.74, p = 0.04) independently. Conclusion Treatment delays mostly in intensive phase are associated with worse survival in ALL; attempts should be made to maintain protocol-defined treatment intensity while adequately managing toxicities.