Context.— In the 2016 update of the World Health Organization (WHO) classification of hematopoietic neoplasms, BCR-ABL1–like B-acute lymphoblastic leukemia/lymphoma (B-ALL) is added as a new provisional entity that lacks the BCR-ABL1 translocation but shows a pattern of gene expression very similar to that seen in B-ALL with BCR-ABL1. Objective.— To review the kinase-activating alterations and the diagnostic approach for BCR-ABL1–like B-ALL. Data Sources.— We provide a comprehensive review of BCR-ABL1–like B-ALL based on recent literature and the 2016 update of the World Health Organization classification of hematopoietic neoplasms. Conclusions.— Several types of kinase-activating alterations (fusions or mutations) are identified in BCR-ABL1–like B-ALL. The main categories are alterations in the ABL class family of genes, encompassing ABL1, ABL2, PDGFRB, PDGFRA (rare), and colony-stimulating factor 1 receptor ( CSF1R) fusions, or the JAK2 class family of genes, encompassing alterations in JAK2, CRLF2, EPOR, and other genes in this pathway. These alterations determine the sensitivity to tyrosine kinase inhibitors. As a wide variety of genomic alterations are included in this category, the diagnosis of BCR-ABL1–like B-ALL is extremely complex. Stepwise algorithms and comprehensive unbiased testing are the 2 ways to approach the diagnosis of BCR-ABL1–like B-ALL.

Proliferation centres (PC) are the histological hallmark of chronic lymphocytic leukaemia/small lymphocytic lymphoma (CLL/SLL), and are thought to be important sites of B-cell receptor (BCR) signalling, driving cell proliferation (Stevenson et al, 2011;Krysov et al, 2012). A major downstream target of BCR signalling, at least partly via MEK1/2-ERK1/2, is the MYC proto-oncogene, which regulates a variety of proteins and microRNAs controlling cell cycle entry and cell growth (Stevenson et al, 2011;Dang, 2012;Krysov et al, 2012). MYC is expressed in various lymphomas due to rearrangements, gains/amplifications, or for other uncertain reasons (Dang, 2012;Chisholm et al, 2015).Gene expression profiling has indicated up-regulation of MYC and its target genes in lymph nodes involved by CLL/ SLL and Western blotting has shown increased MYC expression in lymph node-derived CLL cells (Herishanu et al, 2011;Krysov et al, 2012). Studies reporting MYC immunohistochemistry (IHC) in CLL/SLL are extremely limited, with staining described in 71-100% of cases (Krysov et al, 2012;Chisholm et al, 2015;Onaindia et al, 2015). Although one study noting MYC staining in PC of 7/8 CLL/SLL cases (88%) hypothesized that this pattern was consistent with induction from upstream signalling pathways, others have not indicated any type of preferential distribution with IHC (Krysov et al, 2012;Chisholm et al, 2015;Onaindia et al, 2015). MYC abnormalities are rare in CLL/SLL, but at least one study has shown an increased frequency of chromosomal abnormalities in PC compared to the surrounding lymphoma (Balogh et al, 2011;Brown et al, 2012;Put et al, 2012). Thus, the possibility that a MYC gene abnormality is responsible for its expression in PC could be considered, as it might not be present in a sufficient number of cells to be detected in whole lymph node studies. To investigate the overall frequency of MYC expression in a larger series of CLL/SLL, and to assess whether MYC rearrangements or gains/amplifications might play a role in MYC expression, 54 CLL/SLL tissue biopsies were stained for MYC and a subset studied with fluorescence immunophenotyping and interphase cytogenetics (FICTION) to assess MYC abnormalities in the MYC-positive and -negative cells.IHC for MYC (clone Y69, prediluted, Ventana Medical Systems, Tucson, AZ) was performed on formalin-fixed

Background: Radiological and intraoperative findings of xanthogranulomatous cholecystitis (XGC) mimic carcinoma gallbladder (CaGB) leading to extended surgical resections and increased morbidity. We reviewed the clinical and CECT findings of histopathologically proven XGC and compared them with those of CaGB. Methods: The clinical and CECT findings from 22 patients with XGC were compared with 15 patients with CaGB manifesting as diffuse wall thickening. Results: GB wall thickness was similar in both groups (XGC 12.4 ± 3 mm, CaGB 13.9 ± 6.5 mm; p = 0.61). Intramural hypoattenuating nodules occupying >60% of the GB wall were suggestive of XGC, while the absence of nodules suggested CaGB (p = 0.017). The mucosal lining was intact and enhancing in XGC (20/22) and disrupted in CaGB (10/15; p = 0.001). Among adjacent organ infiltration, bile duct invasion resulting in obstruction was a significant finding in patients with CaGB (p = 0.04). Among XGC patients, 11 patients underwent radical cholecystectomy, 10 had open cholecystectomy and frozen section and 1 underwent bypass. Conclusions: Though there is an overlap between XGC and CaGB, the presence of intramural hypoattenuating nodules occupying >60% of the diffusely thickened GB wall with intact mucosal line and the absence of obstructive features suggest XGC. In the presence of such imaging features, frozen biopsy should be done before proceeding with mutilating radical surgery.