Flow cytometry (FCM) is a widespread and useful technique that rapidly analyzes the immunophenotype of hematological neoplasms. 1 Although the detection of surface immunoglobulin light chain restriction (iLCR) by FCM reflects the monoclonality of mature B-cell lymphoma, hematologists and pathologists sometimes encounter cases of histologically confirmed malignant B-cell lymphoma lacking iLCR. Diffuse large B-cell lymphoma (DLBCL) is the most common subtype of B-cell non-Hodgkin lymphoma (NHL) accounting for 30%-50% of all adult NHL. 2 Previous reports demonstrated that 7%-19% of B-cell NHL and 22%-30% of DLBCL do not exhibit iLCR on FCM. [3][4][5][6] The loss of iLCR can be explained by (i) the lack of or decreased expression of surface immunoglobulin light chain on lymphoma cells; (ii) frequent cell necrosis, apoptosis, and mitosis (pathological features associated with the high proliferation of tumor cells); or (iii) sampling or mechanical errors during the procedure of FCM. [6][7][8][9] However, little evidence is available for the clinical prognosis associated with pathological features in iLCR-negative DLBCL.Our study examined the clinicopathological features of iLCR-negative DLBCL in comparison with iLCR-positive DLBCL treated mainly with rituximab-containing multiagent chemotherapy. MATERIALS AND METHODS Patient selectionWe retrospectively reviewed the medical records and selected consecutive patients who underwent dual-color FCM and were newly diagnosed with DLBCL at Osaka City

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We report a case of rhabdoid tumor predisposition syndrome with a renal tumor developing 10 years after a brain tumor, which demonstrated an unexpectedly favorable outcome. A 2‐year‐old boy underwent gross total resection of a brain tumor located in the fourth ventricle, and received adjuvant chemotherapy and radiotherapy. At the age of 11 years, a renal tumor was found and nephrectomy was performed. He is currently alive without evidence of disease over 2 years without postoperative therapy. Histologically, rhabdoid cells were observed in both brain and renal tumors. Loss of SMARCB1 (also known as INI1) expression was found in the nucleus of both tumor cells. Genetic testing revealed pathogenic variants of SMARCB1 exon 5 in the renal tumor and SMARCB1 exon 9 in the brain tumor. In addition, heterozygous deletion of 22q11.21‐q11.23 containing the SMARCB1 locus was shared by both tumors and this deletion was identified in normal peripheral blood. Considering the histopathological and genetic findings, our case was considered to be rhabdoid tumor predisposition syndrome with atypical teratoid/rhabdoid tumor and late‐onset rhabdoid tumor of the kidney.