Academic literature on the topic 'Fl 525 B C -508 B C'

Abstract Abstract 4199 Background: The pre-B cell receptor promotes differentiation of normal pre-B cells and couples the immunoglobulin μ-chain to activating tyrosine kinases (e.g. SYK) via linker molecules (e.g. BLNK). We recently established that the pre-B cell receptor functions as a tumor suppressor in pre-B acute lymphoblastic leukemia (ALL) including ALL cells carrying the BCR-ABL1 oncogene (Trageser et al., J Exp Med, 2009). In virtually all cases of BCR-ABL1 ALL, pre-B cell receptor function is compromised and its reconstitution induces rapid cell cycle arrest. Given that the SYK tyrosine kinase represents a critical signaling molecule in the pre-B cell receptor pathway, one would expect that SYK tyrosine kinase activity has a tumor suppressive effect. It therefore seems counterintuitive that pharmacologic targeting of SYK was recently proposed as a new treatment approach for pre-B ALL (Uckun et al., Br J Haematol. 2010). While there is solid evidence for a role of Syk as a target in B cell lymphoma (Friedberg et al., Blood 2010) and B cell lineage CLL (Buchner et al., Blood 2010), where tonic B cell receptor signaling delivers critical survival signals, the role of Syk downstream of the pre-B cell receptor in ALL is unclear. Results: To clarify the role of SYK downstream of the pre-B cell receptor in pre-B ALL, we performed a genetic experiment to inducibly delete the Syk gene in pre-B ALL cells. To this end, pre-B cells from Syk-fl/fl mice were propagated in the presence of IL7 and then transformed with retroviral BCR-ABL1 or MLL-ENL oncogenes. After transformation, pre-B leukemia cells were transduced with 4-hydroxy-tamoxyfen (4-OHT)-inducible retroviral Cre-ERT2 or an ERT2 empty vector control. After puromycin-selection of Cre-ERT2 and ERT2 transduced leukemia cells, Cre-ERT2 or the ERT2 control were induced by addition of 4-OHT and deletion of Syk was studied at different time points. As assessed by Western blot and PCR, deletion of Syk was near complete after two days and undetectable after six days. We then studied changes in cell viability upon inducible deletion of Syk: Acute deletion of the Syk tyrosine kinase had no significant impact on the viability of pre-B ALL cells, even after prolonged cell culture over several weeks. We then reasoned that the effect of Syk-deletion may be subtle yet important, so we studied in BCR-ABL1-transformed Syk-fl/fl pre-B leukemia cells whether Syk-deletion sensitizes to Imatinib-treatment. Deletion of Syk was again confirmed by Western blot, yet the dose-response curves to Imatinib-treatment were superimposable for Syk-fl/fl and Syk-del/del pre-B leukemia cells. We conclude that SYK does not contribute important survival signals in our mouse model for pre-B ALL, nor does deletion of Syk sensitize BCR-ABL1-driven pre-B leukemia cells to Imatinib-treatment. We next investigated the counter-hypothesis that Syk functions as a tumor suppressor downstream of the pre-B cell receptor. To test this possibility, we tested the effect of forced pre-B cell receptor expression in the presence or absence of Syk. Syk-fl/fl and Syk-del/del pre-B leukemia cells were transduced with CD8/μ-chain or a CD8 empty vector control. The μ-chain represents the central component of the pre-B cell receptor. Forced expression of the CD8 empty vector control had no effect regardless of whether Syk was deleted or not. When pre-B cell receptor signaling was reconstituted in Syk-fl/fl cells by expression of CD/μ-chain, viability of the leukemia decreased by >80%. By contrast, deletion of Syk greatly attenuated the tumor suppressive effect of CD8/μ-chain expression and less than 25% of the leukemia cells underwent cell cycle arrest and cell death. Background: Genetic deletion of Syk unequivocally demonstrates that Syk does not deliver critical survival signals downstream of the pre-B cell receptor in ALL. This is unlike B cell lymphoma, where tonic signaling from the B cell receptor promotes cell survival via Syk (Friedberg et al., 2010; Buchner et al., 2010). On the contrary, in pre-B ALL, the Syk kinase mediates pre-B cell receptor-induced cell cycle arrest. These findings are in direct conflict with a recent report on the therapeutic usefulness of pharmacological inhibition of Syk in pre-B ALL cell lines (Uckun et al., Br J Haematol.; 149: 508-17; 2010). The compound (C-61) used in this study may have unrecognized off-target effects, which might account for the discrepancies. Disclosures: No relevant conflicts of interest to declare.

Targeted agents have greatly improved outcomes for patients (pts) with chronic lymphocytic leukemia (CLL) and other B cell lymphomas; however, single agents have been limited by intolerance, resistance and depth/durability of responses. Current novel targeted agent combinations may improve depth of response, but such "full dose" strategies have been associated with significant AEs, dose reductions/interruptions and discontinuations. Our in vitro & in vivo screening/optimization studies identified that concurrent inhibition of BTK & mTOR targets plus IMiD at low doses of each inhibitor can synergistically kill B-cell malignancies and may address drug-resistance. DTRM-555 is an optimized oral triplet combination of a novel BTK inhibitor DTRMWXHS-12 (DTRM-12) with everolimus (EV) & pomalidomide (POM). This once daily therapy was tested in a stepwise, phase I, US multicenter study in patients with highest unmet medical needs including r/r CLL, Richter's transformation (RT) of CLL, DLBCL, transformed B-cell lymphomas. We conducted a 3+3 design phase I, first human trial exploring DTRM-555 in pts ≥18 years, ECOG PS ≤1 with CLL, B-cell NHL, or Hodgkin lymphoma (HL) with no available standard therapy (NCT02900716). Our goal was to determine optimal doses for triplet combination therapy through 3 escalating phases of study: DTRM-12 in escalating doses (50, 100, 200, & 300 mg/day) in Part Ia, DTRM-12 at 200 mg or 300 mg & EV at 5 mg (doublet or DTRM-505) in Part Ib Arm A while DTRM-12 at 200 mg or 300 mg, EV at 5 mg & POM at 2 mg in Part Ib Arm B. For all arms, treatment was administered for 21 consecutive days of a 28-day cycle, until disease progression or unacceptable toxicity. Safety was the primary endpoint, and the dose-limiting toxicity (DLT) period was cycle 1. Secondary endpoints included response (iwCLL 2018 or Cheson 2014), progression free survival, duration of response and pharmacokinetics. Intra-patient migration between arms (Mono to doublet to triplet) was permitted if subsequent doses were tolerated. The trial commenced 9/27/2016 and completed enrollment 7/25/2019. Thirty-three pts were enrolled, including 2 screen failures and 4 intra-cohort migrations, with r/r DLBCL (n=8), CLL/SLL (n=5), RT (n=6), FL (n=5), MCL (n=4), MZL/LPL (n=3), HL (n=2). 30 of 31 treated pts were evaluated: 8 pts participated in phase Ia (DTRM-12) while 23 pts were treated on phase Ib combinations (DTRM-505 & DTRM-555). Baseline characteristics: 70% male (n=23), median age 70 years (range 46-94) and 94% white. Median prior therapies were 3 (range 1-10), 53% had been treated with ≥1 prior targeted agent (i.e., CD19/CD3 bispecific antibody, obtinutuzumab, pembrolizumab, nivolumab, ibrutinib, venetoclax, PI3k-i), CAR-T or HSCT. 35% pts were previously treated with ibrutinib. Table 1 describes Grade (Gr) 3 and 4 AEs (all causality, stratified by treatment arm). Regarding safety, AEs were manageable, with a total of 5 DLTs were observed: 2 (Gr 3 febrile neutropenia, URI) in part Ib arm A, 3 (Gr 4 thrombocytopenia, Gr 3 diarrhea, G3 febrile neutropenia) in Part Ib arm B. No MTD was reached for the mono & doublet arms, with the MTD of the triplet determined to be DTRM-12 200 mg, EV 5 mg, & POM 2 mg. Spider plot (Figure 1a) shows the clinical response for individual CLL and lymphoma pts treated with mono, doublet and triplet therapies. Depth and durability of response improved with combination therapies (vs. mono). Of note, 48% of all patients had a ≥50% reduction in sum of the products of lymph node diameters. Representative PET-CT scans are in Figure 1b-c. Responses in multi-refractory pts are ongoing (including 15+ mos in a pt with r/r DLBCL and 5+ mos PR in a pt aged > 90 yrs with r/r DLBCL; 4+ & 13+ mos PRs in two pts with RT). DTRM-12 plasma concentrations were unaffected by EV & POM (Once Daily Oral Therapies) in Figure 1d. The clinical trial met its primary endpoint as the triple combination DTRM-555 had an acceptable safety profile. Dose dependent drug levels with minimal inter-pt variations were observed in all arms, supporting once daily oral administration of this low-dose combination therapy. Encouraging clinical activity was observed in several high-risk, multi-refractory CLL and lymphoma pts, including those previously treated with ibrutinib. Thus synthetic lethality is a viable treatment approach. A phase II US expansion study is underway targeting pts with transformed lymphomas (follicular or prior CLL) and r/r DLBCL cohorts. Table 1. Disclosures Mato: AbbVie: Consultancy, Research Funding; Sunesis: Consultancy, Research Funding; Genentech: Consultancy, Research Funding; Johnson & Johnson: Consultancy, Research Funding; Celgene: Consultancy; AstraZeneca: Consultancy, Research Funding; Pharmacyclics: Consultancy, Research Funding; Gilead: Research Funding; Acerta: Consultancy; Janssen: Consultancy; TG Therapeutics: Consultancy, Other: DSMB member , Research Funding; LOXO: Consultancy, Research Funding; DTRM Biopharma: Research Funding. Schuster:DTRM Biopharma: Research Funding. Foss:Mallinckrodt: Consultancy; Acrotech: Consultancy; miRagen: Consultancy; Seattle Genetics: Consultancy, Other: fees for non-CME/CE services ; Eisai: Consultancy; Spectrum: Other: fees for non-CME/CE services . Isufi:Novartis: Consultancy; Astra Zeneca: Consultancy; Celgene: Consultancy. Ding:Merck: Research Funding; DTRM Biopharma: Research Funding. Brander:Novartis: Consultancy; MEI: Research Funding; Pharmacyclics LLC, an AbbVie Company: Consultancy; BeiGene: Research Funding; AstraZeneca: Consultancy, Research Funding; Acerta: Research Funding; Tolero: Research Funding; AbbVie: Consultancy, Honoraria, Research Funding; Genentech: Consultancy, Honoraria, Research Funding; Teva: Consultancy, Honoraria; TG Therapeutics: Consultancy, Honoraria, Research Funding; DTRM Biopharma: Research Funding. Tun:Mundi-pharma: Research Funding; TG Therapeutics: Research Funding; Curis: Research Funding; DTRM Biopharma: Research Funding; Celgene: Research Funding; BMS: Research Funding. He:DTRM Biopharma: Employment, Equity Ownership. Kearney:DTRM Biopharma: Employment, Equity Ownership. Gui:DTRM Biopharma: Employment, Equity Ownership. Anderson:Theradex: Employment. Roeker:AbbVie: Equity Ownership; Abbott Laboratories: Equity Ownership. Huntington:Bayer: Consultancy, Honoraria; AbbVie: Consultancy; Celgene: Consultancy, Research Funding; Genentech: Consultancy; Pharmacyclics: Honoraria; DTRM Biopharm: Research Funding. OffLabel Disclosure: Everolimus in B cell lymphomas and CLL Pomalidomide in B cell lymphomas and CLL

Работа посвящена микроскопическим синхротронным исследованиям морфологии, атомного и электронного строения массива пор субмикронного размера в слое SiO2 на кремнии, cформированного с использованием ионно-трековой технологии в комбинации с последующим за облучением химическим травлением. Методом исследования являлась фотоэмиссионная электронная микроскопия с использованием синхротронного излучения высокой интенсивности. Метод использовался в двух режимах. Использование химически селективной электронноймикроскопии позволило получить морфологическую информацию об изучаемом массиве пор. Рентгеноспектральный режим спектроскопии ближней тонкой структуры края синхротронного излучения рентгеновского диапазона позволил получить информацию о специфике локального окружения атомов заданного сорта от микроскопических областей нанометровых и субмикронных участков полученных микроскопических изображений. Поры имеют достаточно резкие границы, без переходного слоя. Дном пор является подложка - кристаллический кремний, покрытый естественным оксидом, толщина которого составляет величины около 2-3 нм. Облучение ионами ихимическое травление не оказывают существенного влияния на структурно-фазовые характеристики пористой матрицы оксида кремния. Не наблюдается существенного разупорядочения в кремнии, доступном на дне отдельных пор. Технологические загрязнения отсутствуют. Показана эффективность использования ионно-трековой технологии в комбинации с последующим за облучением химическим травлением для формирования массивов обособленных пор близких размеров субмикронного диапазона. Полученные результаты демонстрируют эффективность в применении метода фотоэмиссионной электронной микроскопии с использованием синхротронного излучениявысокой интенсивности для изучения с высокой точностью и в микроскопическом масштабе широкого ряда объектов композитной структурно-фазовой природы поверхности. ЛИТЕРАТУРА Sinha D., Petrov A., Fink D., Fahrner W. 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As maloclusões são classificadas como o terceiro maior problema de saúde bucal no mundo, perdendo apenas para cárie e doença periodontal. A mordida cruzada posterior é definida como a relação anormal vestíbulo-lingual de um ou mais dentes da maxila, com um ou mais dentes da mandíbula, quando os arcos dentários estão em relação cêntrica, podendo ser uni ou bilateral. Objetiva-se Realizar uma revisão de literatura sobre a mordida cruzada posterior. Foi feita uma seleção de artigos científicos a partir das bases de dados Lilacs e Scielo utilizando os descritores “Mordida Cruzada” e “Diagnóstico de Mordida Cruzada”. Foram incluídos trabalhos publicados entre 2000 a 2018. Dos 694 artigos encontrados e delimitados pelos critérios inclusivos, foram selecionados 49 artigos como amostra, que apresentaram a temática elencada para a pesquisa e que foram discutidos nos seguintes tópicos: a) Epidemiologia; b) Etiologia; c) Diagnóstico; d) Tratamento. As causas da mordida cruzada posterior são multifatoriais e seu diagnóstico precoce é fundamental uma vez que, a literatura mostra resultados satisfatórios, através de medidas interceptativas com um prognostico favorável quando o tratamento ocorre precocemente. O tratamento da mordida cruzada posterior de origem funcional, por contato prematuro em dentes decíduos, dentoalveolar e esquelético consiste, respectivamente, em desgaste seletivo, expansão dentoalveolar e disjunção maxilar.Descritores: Ortodontia; Aparelhos Ortodônticos; Má Oclusão; Odontopediatria.ReferênciasAlmeida MR, Pereira ALP, Almeida RR, Almeida-Pedrin RR, Silva Filho OG. Prevalência de má oclusão em crianças de 7 a 12 anos de idade. Dental Press J Orthod. 2011;16(4):123-31.Janson G, Barros SEC, Simão TM, Freitas MR. Variáveis relevantes no tratamento da má oclusão de Classe II. Rev Dental Press Ortodon Ortop Facial. 2009;14(1):149-57.Sousa RV, Pinto-Monteiro AKA, Martins CC, Granville-Garcia AF, Paiva SM. Maloclusion and socioeconomic indicators in primay dentition. Braz Oral Res. 2014;28(1):54-60.Carvalho CM, Carvalho LFPC, Forte FDS, Aragão MS, Costa LJ. Prevalência de mordida aberta anterior em crianças de 3 a 5 anos em Cabedelo/PB e relação com hábitos bucais deletérios. Pesq Bras Odontoped Clin Integr. 2009;9(2):205-10.Sousa RV, Clementino MA, Gomes MC, Martins CC, Graville-Garcia AF, Paiva SM. Maloclusion and quality of life in Brazilian preschoolers. Eur J Oral Sci. 2014;122(3):223-29.Bittencourt MA, Machado AW. Prevalência de má oclusão em crianças entre 6 e 10 anos: um panorama brasileiro. Dental Press J Orthod. 2010;15(6):113-22.Stahl F, Grabowski R, Gaebel M, Kundt G. Relationship between occlusal findings and orofacial myofunctional status in primary and mixed dentition. Part II: Prevalence or orofacial dysfunctions. J Orofac Orthop. 2007;68(2):74-90. Grabowski R, Stahl F, GaebeL M, Kundt G. 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