Blastoid or pleomorphic mantle cell lymphoma (B/P-MCL) is characterized by high invasiveness and unfavorable outcomes, which is still a challenge for treating MCL. This retrospective study was performed to comprehensively analyze the clinical, genomic characteristics and treatment options of patients with B/PMCL from multicenter in China. Data were obtained from 693 patients with B/PMCL from three centers in China between April 1999 and December 2019. Seventy-four patients with BMCL ( n = 43) or PMCL ( n = 31) were included in the analysis. The median age of the cohort was 60.0 years with a male-to-female ratio of 2.89:1. The 3-year progression-free survival (PFS) and overall survival (OS) rates were 44.1% and 46.0%, respectively. Mutations of TP53 , ATM , NOTCH1 , NOTCH2 , NSD2 , SMARCA4 , CREBBP , KMT2D , FAT1 , and TRAF2 genes were the most common genetic changes in B/P-MCL. Progression of disease within 12 months (POD12) could independently predict the poor prognosis of patients with blastoid and pleomorphic variants. Patients with POD12 carried a distinct mutation profile ( TP53 , SMARCA4 , NSD2 , NOTCH2 , KMT2D , PTPRD , CREBBP , and CDKN2A mutations) compared to patients with non-POD12. First-line high-dose cytosine arabinoside exposure obtained survival benefits in these populations, and BTKi combination therapy as the front-line treatment had somewhat improvement in survival with no significant difference in the statistic. In conclusion, B/P-MCL had inferior outcomes and a distinct genomic profile. Patients with POD12 displayed a distinct mutation profile and a poor prognosis. New therapeutic drugs and clinical trials for B/P-MCL need to be further explored.

Primary testicular lymphoma (PTL) is a rare lymphoma predominantly occurring in the elderly male population. It is characterized by a limited response to treatment and a heightened tendency towards relapse. Histologically, approximately 90% of PTL cases are classified as diffuse large B-cell lymphomas (DLBCL). Genetic features of PTL were delineated in a limited scope within several independent studies. Some of the articles which analyzed the genetic characterization of DLBCL have incorporated PTL samples, but these have been constrained by small sample sizes. In addition, there have been an absence of independent molecular typing studies of PTL. This report summarizes the common mutational features, copy number variations (CNVs) and molecular typing of PTL patients, based on whole-exome sequencing (WES) conducted on a cohort of 25 PTL patients. Among them, HLA, CDKN2A and MYD88 had a high mutation frequency. In addition, we found two core mutational characteristics in PTL including mutation in genes linked to genomic instability (TP53 and CDKN2A) and mutation in immune-related genes (HLA, MYD88, CD79B). We performed molecular typing of 25 PTL patients into C1 subtype with predominantly TP53 mutations and C2 subtype with predominantly HLA mutations. Notably, mutations in the TP53 gene predicted a poor outcome in most types of lymphomas. However, the C1 subtype, dominated by TP53 mutations, had a better prognosis compared to the C2 subtype in PTL. C2 subtype exhibited a worse prognosis, aligning with our finding that the mechanism of immune escape in PTL was primarily the deletions of HLA rather than PD-L1/PD-L2 alterations, a contrast to other DLBCLs. Moreover, we calculated the tumor mutation burden (TMB) and identified that TMB can predict prognosis and recurrence rate in PTL. Our study underscores the significance of molecular typing in PTL based on mutational characteristics, which plays a crucial role in prognostication and guiding therapeutic strategies for patients.

Histiocytic sarcoma (HS) is a rare hematopoietic neoplasm with an aggressive clinical course and a poor response to conventional chemotherapy. Currently, no standard treatment paradigms are available. Herein, we present a case of de novo HS treated with pembrolizumab combined with a GDP regimen (gemcitabine, cisplatin, and dexamethasone) that resulted in sustained complete remission with progression-free survival exceeding 4 years. Immunohistochemical analysis demonstrated significant overexpression of programmed death ligand 1 (PD-L1) on biopsy samples. Additionally, fluorescence in situ hybridization (FISH) with a JAK-2 probe indicated 9p24.1 amplification, suggesting reliance on the JAK-STAT pathway. Polymerase chain reaction (PCR) analysis did not reveal any BRAF-V600 mutations. Consequently, an immune checkpoint inhibitor (ICI) was administered alongside chemotherapy, resulting in sustained complete remission and progression-free survival for over 4 years. Our findings suggest that a combination of ICI and chemotherapy could represent a promising therapeutic approach for HS.

Aims:The differential diagnosis between ALK-negative anaplastic large cell lymphoma (ALK- ALCL) and peripheral T-cell lymphoma, not otherwise specified (PTCL, NOS) with high expression of CD30 (CD30high) are essential. However, no reliable biomarker is available in daily practice except CD30. STAT3 is characteristically activated in ALCL. We aimed to investigate whether the status of STAT3 phosphorylation could help the differential diagnosis.Methods:The status of phosphorylation of STAT3 was examined using two antibodies against pSTAT3-Y705 and pSTAT3-S727 by immunohistochemistry in ALK+ ALCL (n=33), ALK- ALCL (n=22) and PTCL, NOS (n=34). Ten PTCL, NOS with diffuse CD30 expression were defined as CD30high PTCL, NOS. Flowcytometric analysis were performed to evaluate the expression of pSTAT3-Y705/S727 in PTCL, NOS (n=3).Results:The median H-scores of pSTAT3-Y705 and S727 were 280 and 260 in ALK+ ALCL, 250 and 240 in ALK- ALCL, and 45 and 75 in CD30high subgroup, respectively. Using H score of 145 as the cutoff value, pSTAT3-S727 alone distinguished between ALK- ALCL and CD30high PTCL, NOS with a sensitivity of 100% and specificity of 83%. Additionally, pSTAT3-S727, but not pSTAT3-Y705, was also expressed by background tumor-infiltrating lymphocytes (S727TILs) in PTCL, NOS. PTCL, NOS patients with high S727TILs H score had a favorable prognosis than those with no TILs (3-year OS rate: 43% vs. 0, p=0.013) or low S727TILs (3-year OS rate: 43% vs. 0, p=0.099). Flowcytometric analysis revealed that of the three patients investigated, two had enhanced pSTAT-S727 signals in neoplastic cell populations, and all three patients were negative for pSTAT3-Y705 expression in both tumor cells and background lymphocytes.Conclusions:pSTAT3-Y705/S727 can be used to help distinguish ALK- ALCL from CD30high PTCL, NOS and pSTAT3-S727 expression by TILs predicts the prognosis of a subset of PTCL, NOS.

ALK-positive anaplastic large-cell lymphoma (ALK + ALCL) is characterized by expression of ALK and CD30. The current World Health Organization (WHO) classification recognizes five morphologic patterns: common, small-cell, lymphohistiocytic, Hodgkin-like, and composite. There are few reports about the morphologic transformation of ALK + ALCL. Today, we report an intriguing case of presumed transformation from common-pattern to composite-pattern (lymphohistiocytic and small-cell pattern) ALK + ALCL, with CD30 expression changing from positive to negative. This case expands understanding of morphologic transformation between different subtypes of ALK + ALCL and highlights common diagnostic pitfalls, including atypical morphology and negative CD30. Morphologic transformation of ALK + ALCL should be assigned importance, and comprehensive clinical history, histologic and immunophenotypic evaluation are vital to rendering the correct diagnosis of ALK + ALCL.

Background/purpose:Lymphoepithelial sialadenitis (LESA), Sjögren's syndrome (SS), and salivary MALT lymphoma are diseases characterized by lymphoepithelial lesions, and the differential diagnosis between them in the salivary glands is challenging. This study aimed to explore clinicopathological and genetic characteristics of the three diseases. Materials and methods:We retrospectively analyzed the clinical features, the histomorphology, immunohistochemistry, and genetic profiling by polymerase chain reaction (PCR) and next-generation sequencing (NGS). Results:There included 68 LESAs, 25 SSs, and 62 MALT lymphomas. Ten cases relapsed in total, and 3 of MALT lymphomas died due to high-level transformation. Immunohistochemical double staining showed FCRL4 cells co-expressed Pax-5 and Ki-67, suggesting FCRL4 cells were proliferative B-cells. The expression level of the FCRL4 was significantly higher in MALT lymphoma than LESA and SS. The detection rates of clonal IGH, IGK, and IGL gene rearrangements in MALT lymphoma with a sensitivity of 83.33%. Monoclonal immunoglobulin gene rearrangements were confirmed in five suspected patients by NGS (100%). Conclusion:FCRL4 B cells might play an important role in the formation of lymphoepithelial lesions and might be as a diagnostic positive marker of salivary MALT lymphoma. The application of multiple detection methods could significantly improve the diagnostic accuracy for MALT lymphomas from LESA and SS.

BackgroundX-linked immunodeficiency with magnesium defect and Epstein-Barr virus infection and neoplasia (XMEN) disease is an X-linked genetic disorder of immune system caused by loss-of-function mutation in gene encoding Magnesium transporter 1 (MAGT1). Individuals with XMEN disease are prone to developing Epstein Barr Virus (EBV)-associated lymphomas. Herein, we report the first known case of an EBV+ EMZL associated with XMEN disease.Case presentationThe patient was an 8-year-old Chinese boy who suffered from recurrent infections from birth. Six months before, the patient presented with a painless mass on his upper lip and excisional biopsy revealed an EBV-positive extra-nodal marginal zone lymphoma (EBV+ EMZL). Furthermore, molecular investigations with next-generation sequencing identified a novel germline mutation in MAGT1 (c.828_829insAT) in the patient. The c.828_829insAT variant was predicted to cause premature truncation of MAGT1 (p.A277M.fs*11) and consequently was defined as likely pathogenic. The mutation was inherited from his asymptomatic heterozygous carrier mother. Hence the patient was diagnosed with an XMEN disease both clinically and genetically.ConclusionOur results expand the genetic spectrum of XMEN disease and also the clinical spectrum of EBV+ EMZL. We highlight the importance of the genetic etiology underlying EBV+ lymphoma in the pediatric population.

N-6-methyladenosine (m(6)A) is the most abundant eukaryote mRNA modification, modulated by regulators known as epigenetic writers, erasers and readers, which are known to serve crucial roles in mRNA metabolism. However, the role of m(6)A during B-cell development and B-cell tumorigenesis remains poorly understood. By analyzing the gene expression profile of 123 mantle cell lymphoma cases from the Gene Expression Omnibus database, the present study demonstrated that one-half of the m(6)A regulators were able to predict patient survival in mantle cell lymphoma, notably the m(6)A.index. The expression levels of the m(6)A regulators were regarded as good classifiers in mantle cell lymphoma. The m(6)A.index-low mantle cell lymphoma type exhibited a poor patient survival and lower mRNA levels from the total transcriptome. The m(6)A regulators may be associated with the cell division and the RNA metabolic pathways, which may result in poor survival of patients with mantle cell lymphoma.

Objective To analyze the cases that are easily misdiagnosed as diffuse large B-cell lymphoma (DLBCL),and to explore the diagnosis,differential diagnosis and clinicopathological features of DLBCL.Methods The clinicopathological data of 431 cases preliminarily diagnosed as DLBCL in the Department of Pathology,School of Basic Medical Science,Peking University from October 2016 to December 2017 were retrospectively analyzed.Further immunohistochemical staining and molecular biological tests were performed if necessary.Results The diagnostic accuracy rate of DLBCL was 88.86％ (383/431).Misdiagnosis mainly occurred in follicular lymphoma (36 cases,8.35％),high-grade B-cell lymphoma (HGBL) with gene rearrangement of c-myc and bcl-2 or bcl-6 (4 cases,0.93％),atypical lymphoid tissue hyperplasia (3 cases,0.70％),mantle cell lymphoma (3 cases,0.70％),classic Hodgkin lymphoma (CHL) (1 case,0.23％) and composite lymphoma (DLBCL and CHL) (1 case,0.23％).Except the poor quality of sections,the lack of immunohistochemical markers,the poor knowledge of the diagnosis of DLBCL and high-grade FL as well as HGBL were the main reasons of misdiagnosis.Conclusions The diagnosis and differential diagnosis of DLBCL is based on morphology,and it needs to combine with the corresponding immunohistological markers and molecular biological detection when necessary.The recognition of clinical and pathological features of various types of misdiagnosed lymphomas should be strengthened.

目的 观察结节性淋巴细胞为主型霍奇金淋巴瘤(nodular lymphocyte-predominant Hodgkin lymphoma,NLPHL)伴少见免疫结构变异即富于T细胞/组织细胞大B细胞淋巴瘤(T-cell/histiocyte-rich large B cell lymphoma,THRLBL)样转化的NLPHL的临床病理学特征,以提高对NLPHL免疫结构变异的认识、诊断及鉴别诊断.方法 回顾性分析1例伴有THRLBL样转化的NLPHL的临床病理学特征及免疫表型.行EB病毒相关性和Ig/TCR基因克隆性检测,并复习相关文献.结果 患者男性,58岁,腹股沟区无痛性淋巴结肿大.腹股沟淋巴结活检组织学观察可见淋巴结结构破坏,低倍镜下见浅染区和深染区交替分布,以浅染区为主,两种区域均可见散在分布的异型大细胞.免疫表型:大细胞一致强表达全B细胞标记(CD20、PAX5)、不表达CD30;CD21显示深染区内不规则滤泡树突细胞网结构,而浅染区内缺如.此外,两种结构背景细胞组成也存在明显差异.深染区背景细胞富于小B细胞,并可见PD1阳性细胞围绕大细胞形成花环样结构;浅染区背景细胞则以小T细胞和组织细胞为主,小B细胞基本缺如,且PD1阳性细胞量及强度均显著下降.EB病毒原位杂交检测两种结构内均无阳性细胞,Ig和TCR基因重排检测均未发现克隆性重排.结论 伴有THRLBL样转化的NLPHL具有特殊形态学和免疫结构特征,易被误诊为原发性THRLBL,了解NLPHL免疫结构变异并结合细致全面的组织学观察和免疫组化检测有助于其诊断和鉴别诊断.

Drug resistance is one of the major obstacles to breast cancer therapy. However, the mechanisms of how cancer cells develop chemoresistance are still not fully understood. In the present study, we found that expression of TM9SF4 proteins was much higher in adriamycin (ADM)-resistant breast cancer cells MCF-7/ADM than in its parental line wild-type breast cancer cells MCF-7/WT. shRNA-mediated knockdown of TM9SF4 preferentially reduced cell growth and triggered cell death in chemoresistant MCF-7/ADM cells compared with MCF-7/WT cells. Knockdown of TM9SF4 also reduced cell growth and triggered cell death in chemoresistant MDA-MB-231/GEM cells. Mechanistic studies showed that TM9SF4 knockdown increased protein misfolding and elevated endoplasmic reticulum (ER) stress level in MCF-7/ADM cells, as indicated by aggresome formation and upregulated expression of ER stress markers, the effect of which was reversed by a small molecule chaperone 4-phenybutyric acid. In an athymic nude mouse model of ADM-resistant human breast xenograft tumor, knockdown of TM9SF4 decreased the growth of tumor xenografts. In chemoresistant breast cancer patients, chemotherapy increased the expression of TM9SF4 proteins in breast tumor samples. Taken together, these results uncovered a novel role of TM9SF4 proteins in alleviating ER stress and protecting chemoresistant breast cancer cells from apoptotic/necrotic cell death. These results highlight a possible strategy of targeting TM9SF4 to overcome breast cancer chemoresistance.

In order to explore whether NF-κB activation correlates to the prognosis, chemoresistance, and sex hormone receptors status in ovarian serous carcinoma, we analyzed the expression of NF-κB, ER, and PR by immunohistochemistry in 72 cases of ovarian serous carcinoma, investigated the association among these markers, and evaluated their relations to clinicopathologic factors and prognosis. The positive rates were 88.9% for NF-κB cytoplasmic expression, 45.8% for NF-κB nuclear expression, 41.7% for ER, and 29.2% for PR. NF-κB nuclear expression was positively correlated with the 4th edition WHO grade (P=0.045) and tumor stage (P=0.001). NF-κB cytoplasmic expression was associated with preoperative serum CA125 level (P=0.015) and ascites (P=0.042). Neither cytoplasmic nor nuclear staining of NF-κB showed any association with survival. PR expression was correlated with tumor stage (P=0.023) and omental metastasis (P=0.022). Omental metastasis occurred more frequently in ER−/PR− tumors (P=0.009). No correlation between NF-κB expression and ER, PR expression was observed. In conclusion, in ovarian serous carcinoma, NF-κB nuclear expression correlated with the 4th edition WHO grade and PR was a favorable prognostic factor for ovarian serous carcinoma.

Objective To study the frequency of diffuse large B-cell lymphoma (DLBCL) with multi-genetic alteration, and its correlation with c-myc, bcl-2 and bcl-6 protein expression. Methods 50 cases diagnosed with DLBCL from January 2012 to December 2016 were collected. The expression of c-myc, bcl-2 and bcl-6 was analyzed by immunohistochemistry. Interphase fluorescence in situ hybridization (I-FISH) analysis was performed to identify the genetic alteration of c-myc, bcl-2 and bcl-6. Results In all cases, there were 27 males and 23 females with a median age of 50 years (range: 3-85 years). 23 (46.00 %) cases were defined as primary nodal DLBCL and 27 (54.00 %) cases were primary extra-nodal DLBCL, with gastrointestinal tract (48.15 %, 13/27) being the most common site of involvement. c-myc protein expression was detected in 94.00 % (47/50) cases, in which 82.00 % (41/47) cases exhibited high levels of c-myc expression with positive nuclear staining observed in over 40.00 % of tumor cells. The positive rate of bcl-2 protein was 84.00 % (42/50), 76 % (38/50) cases presented with high-level bcl-2 expression. Concurrent high expression of c-myc and bcl-2 were presented in 18 cases (36.00%). FISH analysis demonstrated c-myc gene rearrangement in 7 cases (14.00 %) and amplification in 2 cases (4.00 %). bcl-2 gene rearrangement was detected in 6 cases (12.00 %) and 4 cases (8.00 %) exhibited gene amplification. bcl-6 gene rearrangement was identified in 8 cases (16.00%), amplification in 3 cases (6.00%), and 1 case concomitantly harbored the rearrangement and amplification of bcl-6. Multi-genetic alterations were defined in 4 cases with 3 cases fulfilling the criteria for double-hit lymphoma (DHL) and 1 case for triple-hit lymphoma (THL). For the cases with concomitant high-level expression of c-myc and bcl-2 proteins, 3 cases (16.67 %) was detected with multi-genetic alterations, including 2 cases for DHL and 1 case for THL. Conclusions The proportion of DLBCL with multi-genetic alterations is 8.00 % in this study. The genetic alterations are not consistently correlated with the protein expression. The molecular genetic testing is reliable for the identification of DHL.

OBJECTIVE:To evaluate the correlation between MicroRNA-191 (miR-191) and T lymphoblastic leukemia/lymphoma (T-ALL/LBL) to probe its underlying molecular mechanism.METHODS:The expression of miR-191 was examined by real-time PCR (RT-PCR) in 20 T-ALL/LBL tissue samples and 20 lymphoid reactive hyperplasia (LRH) tissue samples. The correlation between miR-191 and the clinicopathological feature of T-ALL/LBL was analyzed. Antisense miR-191 lentiviral vectors was constructed and transfected into T-ALL/LBL Jukat cells. After transfection, the expression of miR-191 was examined by RT-PCR. The cell activity was evaluated by CCK-8 asssy. The cell cycle and apoptosis were determined by flow cytometry.RESULTS:Compared with LRH samples, the results of RT-PCR showed significant upregulation of miR-191 in 20 T-ALL/LBL tissue samples (1.875±0.079 vs 1.000, P<0.05). The expression level of miR-191 was negatively associated with prognosis. Compared with LV-NC-GFP and control groups, the expression of miR-191 significantly decreased after transfection of antisense miR-191 lentiviral vectors (0.578±0.012 vs 1.011±0.053 and 1.000, P<0.05), the percentages of apoptotic cells and the cell in G0/G1 phase significantly increased (P<0.05).CONCLUSIONS:miR-191 might play a significant role in the development of T-ALL/LBL, implicating a new target for therapy.

Objective:To investigate pathological characteristics and prognosis of patients with Epstein-Barr virus (EBV) positive gastric diffuse large B-cell lymphoma (DLBCL). Methods:Through retrospective study, we collected 75 cases of patients with DLBCL that oc-curs in the stomach. The patients were divided into two groups consisting of 60 cases of EBV negative control group and 15 cases of EBV positive group. To analyze the pathological characteristics and prognosis of patients with EBV positive gastric DLBCL, immunohisto-chemical and Epstein-Barr encoding region (EBER) in situ hybridization methods were used to detect Bcl-2, c-myc protein expression, and EBV-encoded RNA (EBER). Results:In certain aspects of clinical manifestations, such as age, gender, and origin, the comparison be-tween EBV-positive and EBV-negative groups had no statistically significant difference. The same results were obtained for Bcl-2 and c-myc protein expression. However, a statistically significant difference (P=0.01) was observed under the R-CHOP regimen where the me-dian overall survival (OS) of the EBV-positive and EBV-negative groups were 15.1 and 31.4 months, respectively. Conclusion:In pa-tients with DLBCL of the stomach, the EBV infection had no obvious effects in terms of clinical manifestation, origin, morphology, and protein expression of tumor cells. EBV-positive DLBCL was not limited to elderly patients. Under the R-CHOP regimen, the prognosis of EBV-positive patients was worse than that of EBV-negative patients.

患者女,42岁.面、躯干及四肢皮疹2年.皮肤科情况:面、颈、胸、背、四肢近端多发浸润性暗红色丘疹和结节,伴高γ球蛋白血症.皮损组织病理及免疫组化示浆细胞增多症,增生细胞κ多数+,λ个别+.系统检查无明显异常,诊断:皮肤浆细胞增多症.

1病例资料患者，女性，61岁，因左胸背部疼痛1年入院。1周前外院查胸椎MRI平扫示胸7椎管内占位。为进一步手术治疗，转入我院。入院时体格检查：左侧胸6~9水平条带状区域针刺觉减退；神经功能Frankel评级E级。入院后复查胸椎MRI平扫+增强示：胸7~9水平椎管髓外硬膜下可见两个占位性病变（图1A）。入院诊断：胸椎管内多发脊膜瘤？在全麻下行后正中入路胸椎管肿瘤切除术，术中探查见胸7水平肿瘤位于椎管左侧髓外硬膜下，灰红色，大小约1.5 cm×1.5 cm，基底部与椎管左侧硬脊膜粘连紧密，靠近硬脊膜处有钙化，余肿瘤部分质地较脆，先瘤内减体积后再完整切除肿瘤；胸8~9水平肿瘤位于椎管右侧髓外硬膜下，大小约1.0 cm×1.0 cm，黄白色，葫芦状，与神经根粘连紧密，无法游离载瘤神经，故将载瘤神经及肿瘤一并切除（图1B）。术后1周，患者左侧季肋部及左后背灼烧样疼痛基本消失，右下肢肌力恢复至Ⅳ+，能自主下床活动，伤口愈合良好，复查胸椎MRI平扫+增强示两个肿瘤均全切（图1C）。术后1月随访，双下肢肌力基本对称，能自主行走、活动及负重，左侧季肋部及左背部烧灼感基本消失。术后病理结果：胸7水平病灶为脑膜皮细胞型脑膜瘤（WHOⅠ级）（图1D）；胸8~9水病灶为神经鞘瘤（图1E）。

Objective To investigate the clinicopathological and prognosis features of enteropathy-associated T-cell lymphoma (EATL).Methods 21 cases of EATL,6 cases of peripheral T-cell lymphoma (PTCL) and 11 cases of natural-killer/T-cell lymphoma (NKTCL) were collected from January 2008 to May 2015.The immunophenotype of the tumor cell was tested by EnVision and as well as EBV-EBER for EB virus.Some patients were performed with follow-up data.Results 21 EATL patients included 14 males,7 females and the middle age was 55 years old (40-79 years old).15 patients affected the small bowel,4 cases affected colon,2 cases affected more than one site.18 cases were mono-morpholohic EATL while 3 cases were classical EATL.The expression rates of neoplastic cells for CD3ε,CD4,CD8,CD56,Granzyme B,TIA-1 were 95.24 ％ (20/21),20.00 ％ (3/15),73.68 ％ (14/19),85.71％ (18/21),64.71％ (11/17),88.89 ％ (16/18) respectively.The expression of EBER in EATL patients (0,0/21) was obviously lower than that in NKTCL patients (100 ％,11/11).17 EATL patients had follow-up data,and the middle survival time was 15 months.No different prognosis was found in the three kinds of T-NHL (P =0.697).Conclusions EATL usually occurs in elder male and jejunum.The diagnosis of EATL needs a lot of information,including clinical history,endoscopy,histomorphology,immunophenotype and EBV-EBER result.EATL has low mobidity and high malignancy,it still lacks impactful therapeutic regimen.

OBJECTIVE:To summarize the clinicopathological features of testicular lymphomas (TL).METHODS:The medical records of 65 patients diagnosed with TL between 2008.1.1 and 2014.11.30 were retrospectively reviewed.RESULTS:TL was classified as primary (PTL) when there's no prior diagnosis of an extara-testicular lymphoma/leukemia and no concurrent widespread disease, except for the concomitant involvement of ipsilateral inguinal lymph nodes; otherwise it was classified as secondary (STL). Of our patients group, 46 (70.8%) cases were classified primary TL as and the other 19 (29.2%） cases were secondary TL. All patients presented with painless testicular swelling. The median age of STL was significantly younger than that of PTL [65 (12-88) ys vs 13 (1-75) ys, P<0.001]. Additionally, a striking difference in the distribution of histological subtypes was observed between the PTL and STL patients group.CONCLUSION:Primary TLs were more common than secondary. Striking differences in the distribution of patients'age and histology were found between STL and PTL.