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1. Hairy cell leukemia and pregnancy

Author

L S Al-radi, T N Moiseeva, S Yu Smirnova, and R G Shmakov

Subjects
hairy cell leukemia, pregnancy, interferon-α, cladribine, Medicine
Abstract

The paper presents experience in following up and treating hairy cell leukemia (HCL) during pregnancy. The combination of HCL and pregnancy was observed in 5 patients. The patients’ median age was 35 years (range, 28—42 years). The diagnosis of HCL was based on a conventional examination protocol: clinical blood analysis with the morphological assessment of lymphocytes, a myelogram and trepanobiopsy, immunophenotypic analysis of lymphocytes or bone marrow (in all the patients), cytochemical determination of tartrate-resistant acid phosphatase in 3 patients, and identification of BRAFV600E mutation in 3 patients. Three pregnant women were treated for HCL in the postpartum period. In one patient with HCL, pregnancy was seen in remission after treatment with cladribine. In one patient with HCL detected at 11 weeks’ gestation, interferon-α therapy during the second trimester of pregnancy was performed for increased cytopenia, which was followed by cladribine therapy after delivery. Pregnancy and delivery were uncomplicated in all the patients; 3 patients had vaginal delivery and 2 patients underwent cesarean section. All infants were healthy, with no developmental abnormalities during a follow-up period of 6—140 months (median 30 months). All the patients with HCL are currently in remission: 4 patients in first remission at a follow-up of 10 to 48 months (median 15 months) and one patient in second remission at a follow-up of 88 months. Possible observational tactics is possible when HCL is detected during pregnancy. Treatment of HCL during pregnancy is necessary in cases of deep or progressive cytopenia and/or splenomegaly. The use of interferon-α or splenectomy is preferable.

Published
2017
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2. Hepatosplenic T-cell lymphoma: The problems of diagnosis and treatment

Author

N G Chernova, H L Julhakyan, Yu E Vinogradova, Yu V Sidorova, N V Ryzhikova, S M Korzhova, M N Sinitsyna, D S Tikhomirov, E V Naumova, T N Obukhova, V N Dvirnyk, A B Sudarikov, A M Kovrigina, S K Kravchenko, A L Melikyan, L A Kuzmina, I V Galtseva, S Yu Smirnova, E G Gemdzhian, E E Zvonkov, E N Parovichnikova, and V G Savchenko

Subjects
hepatosplenic t-cell lymphoma, immunohistochemical examination, clonal rearrangements, molecular study, morphology, flow cytometry, cytogenetic testing, Medicine
Abstract

In the past decade, a notable advance has been made in the understanding of the pathogenesis of NK/T-cell lymphomas; however, their diagnosis remains difficult because of their rarity and clinical and morphological variabilities. The paper generalizes the ten-year experience of the Hematology Research Center, Ministry of Health of Russia, in diagnosing and treating hepatosplenic T-cell lymphoma (HSTL), considers the problems of differential diagnosis with other hematological diseases occurring with similar clinical and laboratory symptoms, and lays down current approaches to the diagnosis and treatment of this condition. A clinician’s view of the problem of diagnosis and treatment of this disease is given. HSTL is shown to be a heterogeneous group of diseases differing in a T-cell receptor chain gene rearrangement, the clinical course of the disease, and overall survival (OS). According to our data, 3-year OS was 12%; the median survival was 26 months. Two-year OS for γδ and αβ HSTL was equal to 25 and 70%, respectively. The difference in OS for the variants of HSTL failed to reach statistical significance (because the sample might be insufficient).

Published
2016

3. QUANTITATIVE RHOA Gly17Val ALLELE-SPECIFIC POLYMERASE CHAIN REACTION AND T-CELL CLONALITY ANALYSIS IN ANGIOIMMUNOBLASTIC T-CELL LYMPHOMA

Author

Yu. V. Sidorova, N. G. Chernova, I. A. Yakutik, S. Yu. Smirnova, N. V. Ryzhikova, E. E. Nikulina, M. Yu. Aleksenko, M. N. Sinitsyna, A. M. Kovrigina, T. N. Moiseeva, E. E. Zvonkov, and A. B. Sudarikov

Subjects
аngioimmunoblastic t-cell lymphoma, clonality, point mutation, allele-specific polymerase chain reaction, rhoa gly17val, Diseases of the blood and blood-forming organs, RC633-647.5
Abstract

Introduction. Аngioimmunoblastic T-cell lymphoma (AITL) is a T-cell lymphoma, characterized by abundant polymorphocellular infiltrate of lymph nodes with the small number of tumor CD4+ T-cells. AITL could often be misdiagnosed as reactive processes and other lymphomas, including Hodgkin’s lymphoma. Molecular methods of determining clonality are used to confirm the diagnosis. TCR gene rearrangements detected in the lymph nodes may not coincide with those detected in the bone marrow (BM), blood or skin, that makes their interpretation difficult. Recently discovered point somatic RHOA (Ras homolog gene family, member A) Gly17Val mutation is present in 53–71 % of angioimmunoblastic T-cell lymphomas.The aim of the study was to evaluate the number of RHOA Gly17Val mutated cells in different tissues of AITL patients and to correlate it with corresponding T-cell clonality results.Materials and methods. TCRG and TCRB gene rearrangements were PCR-amplified according to BIOMED-2 standardized protocol and analyzed by capillary electrophoresis on ABI Prism 3130. Gly17Val mutation was analyzed by quantitative allele-specific (qAS) TaqMan Real-Time PCR assay. Lymph nodes (LN) and skin biopsies, blood and BM samples were studied for 40 patients with AITL.Results. The clonal TCR gene rearrangements were found in 37 (92 %) of 40 patients in LN and in 26 (96 %) of 28 patients in BM, but they were not matched in length in LN and BM in 12 (46 %) of 26 patients. RHOA (Gly17Val) mutation in LN was revealed in 60 % (24 of 40) patients. Number of cells with RHOA mutation was highest in the LN (in average 26.7 % of the total cells), while in the BM RHOA mutation were undetectable (in 7 patients), or detected in 10 patients in a low quantity (in average 2 % of the total cells). Skin, blood and BM samples with the T-cell clonality peaks that differ from those found in the LN were also negative for the presence of cells having RHOA Gly17Val mutation. Also, in four patients we showed that clonal products in BM and blood that do not coincide with LN refer to CD8+ lymphocytes.Conclusions. The results of the study demonstrate that the quantitative determination of cells with the mutation of RHOA Gly17Val must be taken into account in staging the disease and interpreting the results of T-cell clonality assay. Clonal cells with rearrangements not matching those identified for the LN should be considered reactive.

Published
2018
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4. Interim results of the PML-16, PML-19 protocols for primary mediastinal large B-cell lymphoma therapy

Author

N. G. Gabeeva, D. A. Koroleva, S. A. Tatarnikova, A. K. Smolianinova, D. S. Badmazhapova, S. Yu. Smirnova, E. E. Nikulina, A. V. Belyaeva, E. G. Gemdzhian, V. A. Lapin, E. R. Moskalets, I. E. Kostina, Y. K. Mangasarova, S. A. Shutov, B. V. Biderman, A. B. Sudarikov, T. N. Obukhova, A. M. Kovrigina, G. M. Galstyan, and E. E. Zvonkov

Subjects
Hematology
Abstract

Introduction. Primary mediastinal lymphoma (PML) is an aggressive lymphoid tumor treatment success of which is determined by induction therapy. To date, none of the standard chemotherapy regimens (CT) have demonstrated an advantage in efficacy. Intensive therapy programs are associated with high toxicity.Aim — to evaluate the efficacy and toxicity of two pilot prospective treatment protocols PML-16 and PML-19 as well as the possibility of using the analysis of freely circulating tumor DNA (ctDNA) to assess MRD in patients with PML.Materials and methods. From January 2016 to January 2022, 34 previously untreated PML patients were included in the study; average age — 32; stage > I — in 60 %; extramediastinal lesions — in 14.7 %; bulky disease — in 73.5 % of patients. Positron emission tomography combined with computed tomography (PET-CT) was performed; ctDNA was determined to assess the completeness of remission.Results. Eighteen patients received treatment according to the PML-16 protocol (6 courses of chemotherapy; 2 blocks of RmNHL-BFM-90 + 4 courses of R-EPOCH). After the end of therapy, all 18 patients achieved PET-negative remission. The next 16 patients received treatment according to the PML-19 protocol (4 courses of chemotherapy; 2 blocks of R-mNHL-BFM-90 + 2 courses of R-EPOCH) in combination with lenalidomide. After the end of therapy, 9 (56 %) patients achieved PET-negative remission; 7 (44 %) retained pathological activity (D4–5 points). After 3 and 6 months 15 (94 %) patients achieved normalization of metabolic activity. Considering the high frequency of false-positive results in patients with PML, a ctDNA study was performed to determine the depth of remission in 15 patients. After the end of therapy, all 15 patients had complete elimination of ctDNA. Of these, 5 (33 %) remained PET-positive at the end of treatment. During further observation, after 3–6 months, in 4 patients the level of metabolic activity decreased to physiological without the use of consolidating therapy. After the end of therapy, one patient suffered the new coronavirus infection, COVID-19. A month later, residual formation of SUVmax 14.2 remained in the mediastinum. The patient is currently under observation. With a median follow-up of 36 months (9 to 76 months) all 34 patients are in remission.Conclusion. The effectiveness of PML-16 made it possible to abandon the consolidation therapy and refuted the idea of the need for 6 courses of CT. The combination of programs based on the application of the principle of high-dose shortpulse induction of remission (R-mNHL-BFM-90) in combination with the prolonged administration of medium doses (R-EPOCH) was crucial in achieving a successful result. The inclusion of lenalidomide in the “PML-19” program made it possible to achieve complete remission in 100 % of cases after 4 courses. The possibility of using DNA analysis to assess MRD in patients with PML was shown.

Published
2022
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5. Influence of different chromosomal abnormalities in Ph-positive bone marrow cells on the chronic myeloid leukemia course during tyrosine kinase inhibitors therapy

Author

O. Yu. Vinogradova, E. A. Aseeva, A. V. Vorontsova, A. G. Turkina, A. L. Neverova, O. V. Lazareva, E. Yu. Chelysheva, G. A. Gusarova, T. I. Kolosheinova, L. Yu. Kolosova, S. R. Goryacheva, M. V. Vakhrusheva, S. M. Kulikov, I. A. Tishchenko, L. V. Dyachenko, A. I. Udovichenko, G. A. Alimova, E. V. Kleina, L. A. Grebenyuk, M. L. Konnova, S. Yu. Smirnova, N. D. Khoroshko, and E. V. Domracheva

Subjects
chronic myeloid leukemia, additional chromosomal abnormalities, Ph+-cells, Diseases of the blood and blood-forming organs, RC633-647.5
Abstract

The additional molecular and chromosomal abnormalities (ACA) in Phositive cells usually considered as a genetic marker of chronic myeloid leukemia (CML) progression. 457 patients in different CML phases received tyrosine kinase inhibitors (1st and 2nd generation) were studied. During therapy 50 cases with additional chromosomal abnormalities in Ph+ clone (22 of them in chronic CML phase) were revealed (median follow-up from CML diagnosis – 117 months, median imatinib therapy – 62 months). 86 % of patients in chronic phase with Ph+- cell abnormalities were cytogenetic resistance, and their 5-years overall survival was 80 % which was significantly lower than in patients without ACA (p < 0.005). The treatment results depend on chromosomal abnormalities detected. In patients with additional chromosome 8 imatinib therapy is effective, although complete cytogenetic response (CCR) is achieved only in the later therapy stages. In patients with additional translocations CCR also achieved with imatinib or 2nd generation TKI. Only a third of patients with additional Ph-chromosome or BCR/ABL amplification achieved complete suppression of Ph+ clone using 2nd generation TKI. The presence of additional chromosome 7 abnormalities and complex karyotype disorders involving isochromosome i(17)(q10) are poor prognostic factors of TKI treatment failures.

Published
2014

6. Photon reconstruction in the ATLAS Inner Detector and Liquid Argon Barrel Calorimeter at the 2004 Combined Test Beam

Author

Abat, E. Abdallah, J. M. Addy, T. N. Adragna, P. and Aharrouche, M. Ahmad, A. Akesson, T. P. A. Aleksa, M. and Alexa, C. Anderson, K. Andreazza, A. Anghinolfi, F. and Antonaki, A. Arabidze, G. Arik, E. Atkinson, T. Baines, J. Baker, O. K. Banfi, D. Baron, S. Barr, A. J. and Beccherle, R. Beck, H. P. Belhorma, B. Bell, P. J. and Benchekroun, D. Benjamin, D. P. Benslama, K. Kuutmann, E. Bergeaas Bernabeu, J. Bertelsen, H. Binet, S. Biscarat, C. Boldea, V. Bondarenko, V. G. Boonekamp, M. Bosman, M. and Bourdarios, C. Broklova, Z. Chromek, D. Burckhart and Bychkov, V. Callahan, J. Calvet, D. Canneri, M. Garrido, M. Capeans Caprini, M. Sas, L. Cardiel Carli, T. and Carminati, L. Carvalho, J. Cascella, M. Castillo, M. V. and Catinaccio, A. Cauz, D. Cavalli, D. Sforza, M. Cavalli and Cavasinni, V. Cetin, S. A. Chen, H. Cherkaoui, R. and Chevalier, L. Chevallier, F. Chouridou, S. Ciobotaru, M. and Citterio, M. Clark, A. Cleland, B. Cobal, M. Cogneras, E. Muino, P. Conde Consonni, M. Constantinescu, S. and Cornelissen, T. Correard, S. Radu, A. Corso Costa, G. and Costa, M. J. Costanzo, D. Cuneo, S. Cwetanski, P. Da Silva, D. Dam, M. Dameri, M. Danielsson, H. O. Dannheim, D. Darbo, G. Davidek, T. De, K. Defay, P. O. and Dekhissi, B. Del Peso, J. Del Prete, T. Delmastro, M. and Derue, F. Di Ciaccio, L. Di Girolamo, B. Dita, S. and Dittus, F. Djama, F. Djobava, T. Dobos, D. Dobson, M. and Dolgoshein, B. A. Dotti, A. Drake, G. Drasal, Z. and Dressnandt, N. Driouchi, C. Drohan, J. Ebenstein, W. L. and Eerola, P. Efthymiopoulos, I. Egorov, K. Eifert, T. F. and Einsweiler, K. El Kacimi, M. Elsing, M. Emelyanov, D. and Escobar, C. Etienvre, A. I. Fabich, A. Facius, K. and Fakhr-Edine, A. I. Fanti, M. Farbin, A. Farthouat, P. and Fassouliotis, D. Fayard, L. Febbraro, R. Fedin, O. L. and Fenyuk, A. Fergusson, D. Ferrari, P. Ferrari, R. and Ferreira, B. C. Ferrer, A. Ferrere, D. Filippini, G. and Flick, T. Fournier, D. Francavilla, P. Francis, D. and Froeschl, R. Froidevaux, D. Fullana, E. Gadomski, S. and Gagliardi, G. Gagnon, P. Gallas, M. Gallop, B. J. and Gameiro, S. Gan, K. K. Garcia, R. Garcia, C. Gavrilenko, I. L. Gemme, C. Gerlach, P. Ghodbane, N. Giakoumopoulou, V. Giangiobbe, V. Giokaris, N. Glonti, G. Goettfert, T. and Golling, T. Gollub, N. Gomes, A. Gomez, M. D. and Gonzalez-Sevilla, S. Goodrick, M. J. Gorfine, G. Gorini, B. and Goujdami, D. Grahn, K-J. Grenier, P. Grigalashvili, N. and Grishkevich, Y. Grosse-Knetter, J. Gruwe, M. Guicheney, C. Gupta, A. Haeberli, C. Haertel, R. Hajduk, Z. and Hakobyan, H. Hance, M. Hansen, J. D. Hansen, P. H. Hara, K. Harvey, Jr., A. Hawkings, R. J. Heinemann, F. E. W. and Correia, A. Henriques Henss, T. Hervas, L. Higon, E. and Hill, J. C. Hoffman, J. Hostachy, J. Y. Hruska, I. and Hubaut, F. Huegging, F. Hulsbergen, W. Hurwitz, M. and Iconomidou-Fayard, L. Jansen, E. Jen-La Plante, I. and Johansson, P. D. C. Jon-And, K. Joos, M. Jorgensen, S. and Joseph, J. Kaczmarska, A. Kado, M. Karyukhin, A. and Kataoka, M. Kayumov, F. Kazarov, A. Keener, P. T. and Kekelidze, G. D. Kerschen, N. Kersten, S. Khomich, A. and Khoriauli, G. Khramov, E. Khristachev, A. Khubua, J. and Kittelmann, T. H. Klingenberg, R. Klinkby, E. B. Kodys, P. and Koffas, T. Kolos, S. Konovalov, S. P. Konstantinidis, N. and Kopikov, S. Korolkov, I. Kostyukhin, V. Kovalenko, S. and Kowalski, T. Z. Krueger, K. Kramarenko, V. Kudin, L. G. and Kulchitsky, Y. Lacasta, C. Lafaye, R. Laforge, B. and Lampl, W. Lanni, F. Laplace, S. Lari, T. Le Bihan, A-C. and Lechowski, M. Ledroit-Guillon, F. Lehmann, G. Leitner, R. Lelas, D. Lester, C. G. Liang, Z. Lichard, P. and Liebig, W. Lipniacka, A. Lokajicek, M. Louchard, L. and Loureiro, K. F. Lucotte, A. Luehring, F. Lund-Jensen, B. and Lundberg, B. Ma, H. Mackeprang, R. Maio, A. Maleev, V. P. Malek, F. Mandelli, L. Maneira, J. Mangin-Brinet, M. and Manousakis, A. Mapelli, L. Marques, C. Marti i Garcia, S. Martin, F. Mathes, M. Mazzanti, M. McFarlane, K. W. and McPherson, R. Mchedlidze, G. Mehlhase, S. Meirosu, C. and Meng, Z. Meroni, C. Mialkovski, V. Mikulec, B. and Milstead, D. Minashvili, I. Mindur, B. Mitsou, V. A. and Moed, S. Monnier, E. Moorhead, G. Morettini, P. Morozov, S. V. Mosidze, M. Mouraviev, S. V. Moyse, E. W. J. and Munar, A. Myagkov, A. Nadtochi, A. V. Nakamura, K. and Nechaeva, P. Negri, A. Nemecek, S. Nessi, M. Nesterov, S. Y. Newcomer, F. M. Nikitine, I. Nikolaev, K. and Nikolic-Audit, I. Ogren, H. Oh, S. H. Oleshko, S. B. and Olszowska, J. Onofre, A. Aranda, C. Padilla Paganis, S. and Pallin, D. Pantea, D. Paolone, V. Parodi, F. Parsons, J. and Parzhitskiy, S. Pasqualucci, E. Passmored, S. M. Pater, J. Patrichev, S. Peez, M. Reale, V. Perez Perini, L. and Peshekhonov, V. D. Petersen, J. Petersen, T. C. Petti, R. and Phillips, P. W. Pilcher, J. Pina, J. Pinto, B. and Podlyski, F. Poggioli, L. Poppleton, A. Poveda, J. and Pralavorio, P. Pribyl, L. Price, M. J. Prieur, D. and Puigdengoles, C. Puzo, P. Ragusa, F. Rajagopalan, S. and Reeves, K. Reisinger, I. Rembser, C. de Renstrom, P. A. Bruckman Reznicek, P. Ridel, M. Risso, P. Riu, I. and Robinson, D. Roda, C. Roe, S. Rohne, O. Romaniouk, A. and Rousseau, D. Rozanov, A. Ruiz, A. Rusakovich, N. and Rust, D. Ryabov, Y. F. Ryjov, V. Salto, O. Salvachua, B. and Salzburger, A. Sandaker, H. Rios, C. Santamarina Santi, L. Santoni, C. Saraiva, J. G. Sarri, F. Sauvage, G. and Says, L. P. Schaefer, M. Schegelsky, V. A. Schiavi, C. and Schieck, J. Schlager, G. Schlereth, J. Schmitt, C. and Schultes, J. Schwemling, P. Schwindling, J. Seixas, J. M. and Seliverstov, D. M. Serin, L. Sfyrla, A. Shalanda, N. and Shaw, C. Shin, T. Shmeleva, A. Silva, J. Simion, S. and Simonyan, M. Sloper, J. E. Smirnov, S. Yu. Smirnova, L. and Solans, C. Solodkov, A. Solovianov, O. Soloviev, I. and Sosnovtsev, V. V. Spano, F. Speckmayer, P. Stancu, S. and Stanek, R. Starchenko, E. Straessner, A. Suchkov, S. I. and Suk, M. Szczygiel, R. Tarrade, F. Tartarelli, F. Tas, P. and Tayalati, Y. Tegenfeldt, F. Teuscher, R. Thioye, M. and Tikhomirov, V. O. Timmermans, C. J. W. P. Tisserant, S. and Toczek, B. Tremblet, L. Troncon, C. Tsiareshka, P. and Tyndel, M. Unel, M. Karagoez Unal, G. Unel, G. Usai, G. and Van Berg, R. Valero, A. Valkar, S. Valls, J. A. and Vandelli, W. Vannucci, F. Vartapetian, A. Vassilakopoulos, V. I. Vasilyeva, L. Vazeille, F. Vernocchi, F. and Vetter-Cole, Y. Vichou, I. Vinogradov, V. Virzi, J. and Vivarelli, I. de Vivie, J. B. Volpi, M. Anh, T. Vu Wang, C. Warren, M. Weber, J. Weber, M. Weidberg, A. R. and Weingarten, J. Wells, P. S. Werner, P. Wheeler, S. and Wiessmann, M. Wilkens, H. Williams, H. H. Wingerter-Seez, I. and Yasu, Y. Zaitsev, A. Zenin, A. Zenis, T. Zenonos, Z. and Zhang, H. Zhelezkobk, A. Zhou, N.

Subjects
Physics::Instrumentation and Detectors, High Energy Physics::Experiment
Abstract

The reconstruction of photons in the ATLAS detector is studied with data taken during the 2004 Combined Test Beam, where a full slice of the ATLAS detector was exposed to beams of particles of known energy at the CERN SPS. The results presented show significant differences in the longitudinal development of the electromagnetic shower between converted and unconverted photons as well as in the total measured energy. The potential to use the reconstructed converted photons as a means to precisely map the material of the tracker in front of the electromagnetic calorimeter is also considered. All results obtained are compared with a detailed Monte-Carlo simulation of the test-beam setup which is based on the same simulation and reconstruction tools as those used for the ATLAS detector itself.

Published
2011

7. Hepatosplenic T-cell lymphoma: The problems of diagnosis and treatment

Author

V N Dvirnyk, Eduard G. Gemdzhian, N G Chernova, Valery G. Savchenko, T N Obukhova, Hunan Julhakyan, Elena N. Parovichnikova, S M Korzhova, S Yu Smirnova, Tikhomirov Ds, Yu. V. Sidorova, Larisa A. Kuzmina, Alla M. Kovrigina, E V Naumova, M N Sinitsyna, Anait L. Melikyan, Kravchenko Sk, Andrey Sudarikov, Irina V. Galtseva, E E Zvonkov, Yu E Vinogradova, and N V Ryzhikova

Subjects
0301 basic medicine, Oncology, History, medicine.medical_specialty, Hepatosplenic T-cell lymphoma, Endocrinology, Diabetes and Metabolism, lcsh:Medicine, Disease, Lymphoma, T-Cell, Russia, immunohistochemical examination, 03 medical and health sciences, 0302 clinical medicine, Internal medicine, morphology, medicine, Humans, cytogenetic testing, clonal rearrangements, Hematology, Heterogeneous group, business.industry, flow cytometry, lcsh:R, Clinical course, General Medicine, Prognosis, medicine.disease, Lymphoma, 030104 developmental biology, molecular study, 030220 oncology & carcinogenesis, Immunology, Chain gene, Differential diagnosis, Family Practice, business, hepatosplenic t-cell lymphoma
Abstract

In the past decade, a notable advance has been made in the understanding of the pathogenesis of NK/T-cell lymphomas; however, their diagnosis remains difficult because of their rarity and clinical and morphological variabilities. The paper generalizes the ten-year experience of the Hematology Research Center, Ministry of Health of Russia, in diagnosing and treating hepatosplenic T-cell lymphoma (HSTL), considers the problems of differential diagnosis with other hematological diseases occurring with similar clinical and laboratory symptoms, and lays down current approaches to the diagnosis and treatment of this condition. A clinician's view of the problem of diagnosis and treatment of this disease is given. HSTL is shown to be a heterogeneous group of diseases differing in a T-cell receptor chain gene rearrangement, the clinical course of the disease, and overall survival (OS). According to our data, 3-year OS was 12%; the median survival was 26 months. Two-year OS for γδ and αβ HSTL was equal to 25 and 70%, respectively. The difference in OS for the variants of HSTL failed to reach statistical significance (because the sample might be insufficient).За последнее десятилетие достигнуты значительные успехи в понимании патогенеза NK/Т-клеточных лимфом, однако их диагностика остается затруднительной вследствие их редкости и клинико-морфологического разнообразия. В статье обобщен десятилетний опыт диагностики и лечения гепатолиенальной Т-клеточной лимфомы (ГЛТЛ) в ФГБУ 'Гематологический научный центр' Минздрава России, рассмотрены вопросы дифференциальной диагностики с другими гематологическими заболеваниями, протекающими со сходными клинико-лабораторными симптомами, сформулированы современные подходы к диагностике и лечению. Представлен взгляд клинициста на проблему диагностики и лечения данного заболевания. Показано, что ГЛТЛ - гетерогенная группа заболеваний, различающихся по реаранжировкам генов цепей Т-клеточного рецептора, клиническому течению заболевания, общей выживаемости (ОВ). По нашим данным, 3-летняя ОВ составила 12%, медиана продолжительности жизни - 26 мес. Для вариантов γδ и αβ ГЛТЛ 2-летняя ОВ равна 25 и 70% соответственно. Различие ОВ для вариантов ГЛТЛ не достигало статистической значимости (возможно, в силу недостаточного объема выборки).

Published
2016
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