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Turk J Hematol 2017;34:356-381LETTERS TO THE EDITORIn conclusion, prostatic lymphoma is clinically difficult todistinguish from benign prostatic hyperplasia and prostaticcarcinoma as it occurs in the same age group and presentswith similar symptoms; thus, the histopathological andimmunohistochemical findings in TUR-P material are important.Early and appropriate treatment improves the patient’s qualityand length of life.Keywords: Follicular lymphoma, Extranodal, ProstaticinvolvementAnahtar Sözcükler: Foliküler lenfoma, Ekstranodal, ProstatTutulumuConflict of Interest: The authors of this paper have no conflictsof interest, including specific financial interests, relationships,and/or affiliations relevant to the subject matter or materialsincluded.References1. Sarris A, Dimopoulos M, Pugh W, Cabanillas F. Primary lymphoma ofthe prostate: good outcome with doxorubicin-based combinationchemotherapy. J Urol 1995;153:1852-1854.2. Global Burden of Disease Cancer Collaboration, Fitzmaurice C, AllenC, Barber RM, Barregard L, Bhutta ZA, Brenner H, Dicker DJ, Chimed-Orchir O, Dandona R, Dandona L, Fleming T, Forouzanfar MH, Hancock J,Hay RJ, Hunter-Merrill R, Huynh C, Hosgood HD, Johnson CO, Jonas JB,Khubchandani J, Kumar GA, Kutz M, Lan Q, Larson HJ, Liang X, Lim SS, LopezAD, MacIntyre MF, Marczak L, Marquez N, Mokdad AH, Pinho C, PourmalekF, Salomon JA, Sanabria JR, Sandar L, Sartorius B, Schwartz SM, ShackelfordKA, Shibuya K, Stanaway J, Steiner C, Sun J, Takahashi K, Vollset SE, Vos T,Wagner JA, Wang H, Westerman R, Zeeb H, Zoeckler L, Abd-Allah F, AhmedMB, Alabed S, Alam NK, Aldhahri SF, Alem G, Alemayohu MA, Ali R, Al-Raddadi R, Amare A, Amoako Y, Artaman A, Asayesh H, Atnafu N, AwasthiA, Saleem HB, Barac A, Bedi N, Bensenor I, Berhane A, Bernabé E, Betsu B,Binagwaho A, Boneya D, Campos-Nonato , Castañeda-Orjuela C, Catalá-López F, Chiang P, Chibueze C, Chitheer A, Choi JY, Cowie B, Damtew S,das Neves J, Dey S, Dharmaratne S, Dhillon P, Ding E, Driscoll T, EkwuemeD, Endries AY, Farvid M, Farzadfar F, Fernandes J, Fischer F, G/Hiwot TT,Gebru A, Gopalani S, Hailu A, Horino M, Horita N, Husseini A, Huybrechts I,Inoue M, Islami F, Jakovljevic M, James S, Javanbakht M, Jee SH, KasaeianA, Kedir MS, Khader YS, Khang YH, Kim D, Leigh J, Linn S, Lunevicius R, ElRazek HMA, Malekzadeh R, Malta DC, Marcenes W, Markos D, Melaku YA,Meles KG, Mendoza W, Mengiste DT, Meretoja TJ, Miller TR, MohammadKA, Mohammadi A, Mohammed S, Moradi-Lakeh M, Nagel G, Nand D, LeNguyen Q, Nolte S, Ogbo FA, Oladimeji KE, Oren E, Pa M, Park EK, PereiraDM, Plass D, Qorbani M, Radfar A, Rafay A, Rahman M, Rana SM, Søreide K,Satpathy M, Sawhney M, Sepanlou SG, Shaikh MA, She J, Shiue I, Shore HR,Shrime MG, So S, Soneji S, Stathopoulou V, Stroumpoulis K, Sufiyan MB,Sykes BL, Tabarés-Seisdedos R, Tadese F, Tedla BA, Tessema GA, Thakur JS,Tran BX, Ukwaja KN, Uzochukwu BSC, Vlassov VV, Weiderpass E, WubshetTerefe M, Yebyo HG, Yimam HH, Yonemoto N, Younis MZ, Yu C, Zaidi Z, ZakiMES, Zenebe ZM, Murray CJL, Naghavi M. Global, regional, and nationalcancer incidence, mortality, years of life lost, years lived with disability,and disability-adjusted life-years for 32 cancer groups, 1990 to 2015: asystematic analysis for the Global Burden of Disease Study. JAMA Oncol2017;3:524-548.3. Chu PG, Huang Q, Weiss LM. Incidental and concurrent malignantlymphomas discovered at the time of prostatectomy and prostate biopsy: astudy of 29 cases. Am J Surg Pathol 2005;29:693-699.4. Eisenberger CF, Walsh PC, Eisenberger MA, Chow NH, Partin AW, Mostwin JL,Marshall FF, Epstein JI, Schoenberg M. Incidental non-Hodgkin’s lymphomain patients with localized prostate cancer. Urology 1999;53:175-179.5. Terris MK, Hausdorff J, Freiha FS. Hematolymphoid malignancies diagnosedat the time of radical prostatectomy. J Urol 1997;158:1457-1459.Address for Correspondence/Yazışma Adresi: Sinan DEMİRCİOĞLU, M.D.,Necmettin Erbakan University Meram Medicine Faculty, Department of Hematology, Konya, TurkeyPhone : +90 555 432 44 74E-mail : sinandemircioglumd@gmail.com ORCID-ID: orcid.org/0000-0003-1277-5105Received/Geliş tarihi: May 02, 2017Accepted/Kabul tarihi: June 30, 2017DOI: 10.4274/tjh.2017.0181365
LETTERS TO THE EDITOR Turk J Hematol 2017;34:356-381Coexistence of EZH2, NOTCH1, IL7R, and PHF6 Mutations in AdultT-cell Acute Lymphoblastic LeukemiaErişkin T-hücre Akut Lenfoblastik Lösemi’sinde EZH2, NOTCH1, IL7R ve PHF6Mutasyonlarının BirlikteliğiXilian Zhou 1 , Yan Gu 1 , Qi Han 1 , Mario Soliman 2 , Chunhua Song 2 , Zheng Ge 11Zhongda Hospital, Medical School of Southeast University Department of Hematology Nanjing, China2Pennsylvania State University, Department of Pediatrics, Pennsylvania, USATo the Editor,Enhancer of zestehomolog 2 (EZH2) mutations are reportedin solid tumors [1,2,3] as well as leukemia, and they aremost commonly detected in early T-cell precursor acutelymphoblastic leukemia (ETP-ALL) [4,5,6,7,8], which is anextraordinarily aggressive malignancy of enigmatic geneticbasis [9]. We screened EZH2 mutations in 146 Chinese adult ALLpatients, among which 24.7% (36/146) cases were T-cell acutelymphoblastic leukemia (T-ALL) and 12.9% (4/31) T-ALL caseswere identified as ETP-ALL. We found three EZH2 mutationsin two patients with T-ALL. One patient had Mu#1:D730fs*1,a truncation mutation that was previously reported in acutemyeloid leukemia, and the another patient had two new EZH2mutations, Mu#2:K466T and Mu#3:T467fs*>3 (Figure 1). Wealso screened the mutations in other genes (Table 1). Strikingly,the EZH2 mutations coexisted with mutations of NOTCH1, IL7R,and PHF6 in the two patients and they responded poorly tochemotherapy and experienced difficult clinical histories andinferior outcomes (Table 1). Patient 1 was diagnosed with T-ALLwith myeloid expression based on his bone marrow (BM) smearand immunophenotypes (Table 1). With the first inductivetherapy (Table 1), the patient achieved complete remission (CR)with 0.1% blasts in the peripheral blood (PB) and 0.8% in BM.One year later, the patient relapsed with 90.4% lymphoblasts inthe BM and 1.0% in the PB, and CR was achieved after the firstchemotherapy. During the following treatment, he underwentan intramedullary and an extramedullary relapse infiltrating hisleft tonsil and then endured three more relapses. On the fifthrelapse, the BM blast rate was 50.4%. Although the patient wastreated with nelarabine, no CR was achieved in the subsequenttreatments. Even though the BM blast rate was 5.2%, thepatient died of infection during the BM suppression periodafter he received the last chemotherapy. We examined theEZH2 mutational status in the BM samples of the 1 st relapse, 5 threlapse, and 6 weeks after his 5 th relapse; the EZH2 and NOTCH1mutation status remained the same as in the first diagnosis evenafter the nelarabine treatment (Figure 1D). Patient 2 presentedwith 80.0% lymphoblasts in the PB and 78.0% blasts in theBM (Table 1). Two somatic mutations, K466T and T467fs*>3 inFigure 1. Location and sequencing data of the EZH2 mutations.A) Mutation 1 (Mu#1:D730fs*1), located in exon 19, is a frameshift-creating insertion; on the protein level, it leads to atruncated protein with a length of 731 amino acids, which islocated in the conserved catalytic SET domain(amino acids 618-731). This domain is critical for the methyltransferase activity ofEZH2. The other two mutations (Mu#2:K466T; Mu#3:T467fs*>3)located within exon 11 are anon-synonymous single-nucleotidesubstitution and a frame shift-creating deletion, respectively; onthe protein level, they result in the substitution of EZH2 lysine466to tyrosine and a truncation of the EZH2 protein, respectively.Mu#2 and Mu#3 are novel EZH2 mutations; both of them arelocated in the SANT domain of the EZH2 protein (amino acids435-485), which is known to be incharge of the DNA binding.Mu#1 was detected in patient 1 and the other two in patient2. Blue, pink, and yellow bars correspond to exons encodingthe SANT domains, the cysteine-rich CXC domain, and the SETdomain, respectively. The red arrows show EZH2 mutations. B-F)The direct sequencing data of EZH2 mutations (B, D, F) and wildtype(C, E). B: c.2187_2188insT p.D730fs*1; C: EZH2 exon 19 wildtype;D: Mu#1 after nelarabine treatment; E: EZH2 exon 11 wildtype;F: c.1397A>C; 1399delA p.K466T; T467fs*>3.366
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