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Добірка наукової літератури з теми "BCL7"

Автор: Grafiati

Опубліковано: 21 грудня 2024

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Статті в журналах з теми "BCL7"

Dietrich, Nicholas, Kevin Trotter, James M. Ward, and Trevor K. Archer. "BRG1 HSA domain interactions with BCL7 proteins are critical for remodeling and gene expression." Life Science Alliance 6, no. 5 (February 17, 2023): e202201770. http://dx.doi.org/10.26508/lsa.202201770.

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The SWI/SNF complex remodels chromatin in an ATP-dependent manner through the subunits BRG1 and BRM. Chromatin remodeling alters nucleosome structure to change gene expression; however, aberrant remodeling can result in cancer. We identified BCL7 proteins as critical SWI/SNF members that drive BRG1-dependent gene expression changes. BCL7s have been implicated in B-cell lymphoma, but characterization of their functional role within the SWI/SNF complex has been limited. This study implicates their function alongside BRG1 to drive large-scale changes in gene expression. Mechanistically, the BCL7 proteins bind to the HSA domain of BRG1 and require this domain for binding to chromatin. BRG1 proteins without the HSA domain fail to interact with the BCL7 proteins and have severely reduced chromatin remodeling activity. These results link the HSA domain and the formation of a functional SWI/SNF remodeling complex through the interaction with BCL7 proteins. These data highlight the importance of correct formation of the SWI/SNF complex to drive critical biological functions, as losses of individual accessory members or protein domains can cause loss of complex function.

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Jadayel, Dalal M., Lucy R. Osborne, Lionel J. A. Coignet, Valter J. Zani, Lap-Chee Tsui, Stephen W. Scherer, and Martin J. S. Dyer. "The BCL7 gene family: deletion of BCL7B in Williams syndrome." Gene 224, no. 1-2 (December 1998): 35–44. http://dx.doi.org/10.1016/s0378-1119(98)00514-9.

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McBride, Amanda, Clare M. Adams, Ramkrishna Mitra, and Christine M. Eischen. "Bclw Overexpression Predicts Aggressive Disease in B-Cell Lymphomas." Blood 136, Supplement 1 (November 5, 2020): 29. http://dx.doi.org/10.1182/blood-2020-142545.

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B-cell lymphomas encompass a phenotypically and genetically heterogenous subgroup within hematologic malignancies. Despite this heterogeneity, the ability to evade apoptosis is a unifying feature across B-cell lymphomas, and alterations within the Bcl-2 family of apoptosis regulatory proteins is a key mechanism for this evasion. While overexpression of the anti-apoptotic Bcl-2 family member BCL2 has been widely described in multiple B-cell lymphomas, altered expression of other anti-apoptotic proteins within this family, including BCLX, MCL1, A1 and, in particular, BCLW has been under-investigated. This is highlighted by clinical trials of the BCL2 inhibitor, venetoclax, which found poor single agent activity in B-cell lymphomas that were thought to be highly BCL2-dependent. Therefore, we investigated the contributions of anti-apoptotic Bcl-2 proteins in B-cell lymphomas. Analysis of gene expression profiling datasets of patient samples of major B-cell lymphoma subtypes as compared to normal B-cells demonstrated differential overexpression of anti-apoptotic Bcl-2 proteins, with BCL2, BCLX and BCLW being significantly overexpressed in multiple B-cell lymphoma subtypes. Focusing on aggressive B-cell lymphoma subtypes, BCLW was consistently overexpressed across all major B-cell lymphoma subtypes. Notably, BCLW overexpression was maintained in high grade follicular lymphoma compared to low grade, whereas BCL2 levels decreased as grade increased. These findings indicate that BCLW overexpression is selected for in more aggressive B-cell lymphoma subtypes. BCLW overexpression in aggressive B-cell lymphoma cell lines conferred resistance to the non-specific BH3 mimetic navitoclax as well as to venetoclax. Further, analysis of diffuse large B-cell lymphoma (DLBCL) cell lines demonstrated that the combination of high BCLW/low BCL2 in GCB DLBCL and high BCLW/moderate BCL2 in non-GCB DLBCL is also associated with decreased navitoclax sensitivity, suggesting that high BCLW may confer treatment resistance. In accordance with this, analysis of patient outcomes in DLBCL demonstrates that patients exhibiting high BCLW levels with low BCL2 levels have poorer survival than those with low BCLW. Moreover, Cox regression analysis showed BCLW was an independent determinant of overall survival in DLBCL. Together, our results indicate that BCLW predicts for more aggressive disease in B-cell lymphomas and increased resistance to therapy. Disclosures Eischen: AbbVie Inc.:Research Funding.

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Kahraman, Dudu Solakoglu, Gulden Diniz, Cengiz Ceylan, Faruk Recep Ozalp, Yetkin Koca, Sumeyye Ekmekci, Duygu Ayaz, and Sevil Sayhan. "Prognostic impact of BCL2, BCL6 and MYC status in de novo diffuse large B-cell lymphoma: a regional study of 43 patients." International Journal of Research in Medical Sciences 7, no. 5 (April 26, 2019): 1720. http://dx.doi.org/10.18203/2320-6012.ijrms20191665.

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Background: Diffuse large B-cell lymphoma (DLBCL) is an aggressive non-Hodgkin lymphoma with marked biologic heterogeneity. We aimed to evaluate the status of MYC, BCL2, BCL6 in patients with DLBCL.Methods: Herein, we have investigated the prognostic relevance of MYC, BCL2 and BCL6 from 43 de novo DLBCL patients.Results: In this study, protein overexpression of BCL2 and BCL6 was encountered in 46.5% (n=20) and 27.9% (n=12) of the tumors, respectively. Rearrangements in MYC, BCL6, and BCL2 were detected in 9.3% (n=4), 25.6% (n=11), and 4.7% (n=2) of the cases, respectively. Any statistically significant difference could not be found between Bcl-2, Bcl-6 expression, C-MYC rearrangement and the survival.Conclusions: We concluded that C-MYC and BCL2 may contribute to aggressive transformation, so more mechanism-based therapy should be explored. A larger study is warranted to better understand the immunophenotypic and molecular features of DLBCL and their respective impact on patient survival.

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Sun, Guoxian, and Lya Montella. "Oncogene Amplification as an Incidental Finding in FISH Testing for Gene Rearrangements in Lymphoid Hematopoietic Neoplasms." Blood 118, no. 21 (November 18, 2011): 2505. http://dx.doi.org/10.1182/blood.v118.21.2505.2505.

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Abstract Abstract 2505 Oncogene amplification resulting in overexpression, although common in solid tumors, is rare in hematopoietic neoplasms. This is particularly true in lymphoid neoplasms compared to AML where MYC, MLL or RUNX1 (AML1) amplification has been mostly seen, and to CML where BCR/ABL fusion gene amplification has been also reported. Typically, lymphoid neoplasms are tested at diagnosis by FISH for specific reciprocal chromosome translocations that lead to overexpression of deregulated oncogenes such as BCL1, BCL2, BCL6 and MYC in B-cell lymphoma and myeloma or BCR/ABL gene fusion in ALL. Nevertheless, we have unexpectedly seen oncogene amplification from time to time in our FISH lab. To study the incidence of gene amplification and its diagnostic and clinical implications, we retrospectively analyzed FISH results routinely performed on paraffin embedded lymphoma tissues, lymph nodes, bone marrow aspirates and peripheral bloods in the past three and half years using translocation probes for BCL2/IGH, BCL1/IGH, MYC/IGH and BCR/ABL and break apart probes for BCL6 and MYC. The highest amplification rate seen was in BCL2/IGH testing: 11 of the 1,710 cases were positive (0.643%). In 2 cases with follicular lymphoma (FL), BCL2 amplification presented as homogenously staining regions (hsr), one case with diffuse large B-cell lymphoma (DLBCL) showed double minutes (dmin), and two cases with FL had a pattern of combined hsr and dmin. Five cases with low grade FL intriguingly showed a similar pattern of BCL2/IGH translocation and concomitant amplification of the rearranged BCL2 as a small hsr. The remaining case diagnosed as Burkitt lymphoma (BL) was positive for MYC/IGH translocation and for BCL2 amplification present as large hsr. BCL6 amplification was observed in 4 of 1,537 cases tested (0.26%). In all these cases, amplification presented as hsr. One case diagnosed as EBV+ DLBLC was positive for MYC/IGH translocation and 3' BCL6 high level amplification. Another case with FL showed BCL6 rearrangement and 5' BCL6 amplification. BCL1 amplification with translocation was seen as hsr in 1 case with mantle cell lymphoma out of 2,898 tested. BCL1 amplification was observed in another case with plasma cell myeloma as hsr out of 3,413 tests performed. MYC gene amplification was positive in 3 of 2,186 (0.137%). One case with BL showed MYC rearrangement with a concomitant 3' deletion and 5' amplification. The second case diagnosed as B-cell lymphoma with features intermediate between DLBCL and BL showed highly amplified MYC gene as hsr. The third case was DLBCL with 15–50 copies of MYC gene per cell as dmin. Among 530 BCR/ABL tests ordered for acute leukemia or ALL, 2 (0.377%) cases with T cell lymphoblastic leukemia/lymphoma (T-ALL/LBL) showed ABL amplification as episomes (4–8 copies in one case; 6–30 in another). Both were abnormal by cytogenetics analysis, but negative for t(9;22)(q34;q11.2) and without dmin or hsr identified. Although detection rates of oncogene amplification seem to be very low with limited specific translocation probes applied to lymphoid neoplasms, they may well be higher when FISH signal patterns are analyzed more carefully. In our study, 5 of the 11 FL cases tested for IGH/BCL2 showed a peculiar pattern positive for the t(14;18)-IGH/BCL2 and a concomitant red signal amplification of BCL2, the size of which is usually small and may be overlooked under microscope. All these 5 cases had low grade FL, suggesting that oncogene amplification can be an early genomic event in lymphomagenesis. MYC gene amplification is generally considered a late stage genomic alteration. When MYC is rearranged, amplification of BCL2, BCL6 or BCL1 may need to be taken into consideration for disease stratification, or vice versa. For instance, so called “double-hit” or “triple-hit” lymphomas currently require two or three concurrent translocations for diagnosis. Oncogene amplification, equally important for deregulation/overexpression as a translocation, should be considered as a second or a third hit in diagnosis and differential diagnosis of B-cell lymphoma unclassifiable with features intermediate between DLBCL and BL. FISH is a very useful tool to identify episomal oncogene amplification. Episomes, unlike cytogenetically evident dmin and hrs, are invisible by chromosome analysis, but their detection is important as reported for integration of targeted tyrosine kinase inhibitors into chemotherapeutic regimens. Disclosures: No relevant conflicts of interest to declare.

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González de Villambrosia, Sonia, Mercedes Colorado, Andres Insunza, Ana Batlle, Brenda López-Pereira, Guillermo Martin, Paloma Ibarrondo, Santiago Montes-Moreno, and Eulogio Conde. "B Cell Lymphoma Unclassifiable, with Features Intermediate Between Diffuse Large B Cell Lymphoma and Burkitt Lymphoma and Diffuse Large B Cell Lymphoma NOS with Doble/Triple Translocations: Immunophenotypic Analysis." Blood 126, no. 23 (December 3, 2015): 5037. http://dx.doi.org/10.1182/blood.v126.23.5037.5037.

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Abstract Background: Diffuse large B-cell lymphoma (DLBCL) is a clinically and molecularly heterogeneous disease. We can identify two subgroups with aggressive clinical course and higher risk of treatment failure after standard therapy: B cell lymphoma unclassifiable (BCLU) with features intermediate between DLBCL and Burkitt lymphoma (BL) and B-cell lymphomas with double/triple translocation (DHL/THL). Previous reports suggest that these types of lymphomas may show a common immunophenotype, providing another tool in the challenge of their diagnosis. Objetives: To analyze the immnunophenotype (IF) of BCLU and DH/TH lymphomas by multiparametric flow cytometry and compare it with the IF of a series of cases with DLBCL and BL. Methods: we analyzed the inmunophenotype (four-color flow cytometry on a FACSCalibur flow cytometer) and cytogenetic studies (FISH to detect MYC, BCL2 and/or BCL6 rearrangement) of cases diagnosed of BCLU and DH/TH lymphomas. Control cases of DLBCL and BL were consecutively collected from our database. Fisher`s Exact test was used to compare proportions between two groups. P-values <0.05 were considered statistically significant. Results: We analyzed 23 controls (14 DLBCL and 9 BL) and 17 cases: 9 DHL (8 BCL2/MYC+ and 1 BCL6/MYC+), 3 THL (BCL2/BCL6/MYC+) and 5 BCLU (1 IGH-MYC+, 3 MYC+ and 1 unknown). Six of the 17 cases (35.3%) had decreased expression of CD19 while this was exceptional in DLBCL (1/10 P=0.073) and BL (0/9 P=0.054). All of the cases were positive for CD20 but with different intensities: only 5.9% expressed high CD20 compared to 42.9% of DLBCL (p=0.021) and 55.6% of BL (P=0.010). Most of the cases (12/17) had intermediate expression of CD20 and only 4/17 had weak expression. CD10 expression was typical in BL (100%) and frequent in the cases (82.4%), while it was only present in 20% of DLBCL (P<0.0001). CD38 expression was high in 100% of BL, 6.3% of the cases and none of DLBCL. It was intermediate in 64.7% of the cases and in 35.7% of DLBCL (P=0.015). BCL2 overexpression was detected in 57.1% of the cases; neither DLBCL nor BL (P= 0.009) had BCL2 overexpression. Conclusions: We identify a common immunophenotype in DH/TH lymphomas and BCLU: decreased expression of CD19 and CD20, CD10 expression, overexpression of BCL2 and intermediate expression of CD38. This immuphenotype may be useful for identifying cases for confirmatory cytogenetic studies. Larger studies are needed to validate these results. Disclosures No relevant conflicts of interest to declare.

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Leski, Tomasz A., Clayton C. Caswell, Marcin Pawlowski, David J. Klinke, Janusz M. Bujnicki, Sean J. Hart, and Slawomir Lukomski. "Identification and Classification of bcl Genes and Proteins of Bacillus cereus Group Organisms and Their Application in Bacillus anthracis Detection and Fingerprinting." Applied and Environmental Microbiology 75, no. 22 (September 18, 2009): 7163–72. http://dx.doi.org/10.1128/aem.01069-09.

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ABSTRACT The Bacillus cereus group includes three closely related species, B. anthracis, B. cereus, and B. thuringiensis, which form a highly homogeneous subdivision of the genus Bacillus. One of these species, B. anthracis, has been identified as one of the most probable bacterial biowarfare agents. Here, we evaluate the sequence and length polymorphisms of the Bacillus collagen-like protein bcl genes as a basis for B. anthracis detection and fingerprinting. Five genes, designated bclA to bclE, are present in B. anthracis strains. Examination of bclABCDE sequences identified polymorphisms in bclB alleles of the B. cereus group organisms. These sequence polymorphisms allowed specific detection of B. anthracis strains by PCR using both genomic DNA and purified Bacillus spores in reactions. By exploiting the length variation of the bcl alleles it was demonstrated that the combined bclABCDE PCR products generate markedly different fingerprints for the B. anthracis Ames and Sterne strains. Moreover, we predict that bclABCDE length polymorphism creates unique signatures for B. anthracis strains, which facilitates identification of strains with specificity and confidence. Thus, we present a new diagnostic concept for B. anthracis detection and fingerprinting, which can be used alone or in combination with previously established typing platforms.

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Dupont, Thibault, Zhenghong Dong, ShaoNing Yang, Ari Melnick, and Leandro Cerchietti. "Combinatorial Targeting of BCL6 and Anti-Apoptotic Proteins in Diffuse Large B-Cell Lymphoma (DLBCL) and Follicular Lymphoma (FL)." Blood 120, no. 21 (November 16, 2012): 64. http://dx.doi.org/10.1182/blood.v120.21.64.64.

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Abstract Abstract 64 BCL6 represents a survival factor in DLBCL and FL since specific BCL6 inhibitors (i.e: the peptidomimetic RI-BPI and the small molecule 79-6) kill DLBCL and transformed FL (tFL) cell lines. Our group showed that BCL2 and other anti-apoptotic genes are transcriptionally repressed by BCL6 and could be reactivated upon treatment with RI-BPI or 79-6. We also showed that BCL6 and BCL2 control distinct and non-overlapping survival pathways in these lymphomas. This suggests that blocking the function of anti-apoptotic proteins might overcome any resistance that these proteins might mediate in response to BCL6 inhibition. In addition, constitutive expression of BCL2 has been observed in DLBCL and FL cases. We therefore hypothesized that targeting both BCL6 and BCL2 would eliminate two of the most potent survival mechanisms and would translate in synergistic killing of these lymphomas. In order to test this hypothesis, we examined the proteome-wide consequence of BCL6 inhibition in a DLBCL cell line (SU-DHL6) transfected with siBCL6 by phospho-protein arrays. We found that 280 unique proteins changed their abundance after siBCL6, 40 of them related to (pro and anti) apoptosis signaling (p<0.001). By means of pathway analysis bioinformatic tools, we then identified anti-apoptotic proteins with increased abundance after siBCL6 that could be therapeutically targeted. Among these druggable proteins we found BCL2, BCL-XL, MCL-1, NEDD8, PARP1 and several ubiquitin ligases. We confirmed in independent experiments that BCL6 knockdown induced mRNA (by qPCR) and protein up-regulation (by immunobloting) of these genes in 2 additional DLBCL and 2 tFL cell lines. Treatment of these siBCL6-transfected cell lines with small molecules inhibitors of BCL2 family members (ABT-737 and oblatoclax), NEDD8 activating enzyme (MLN4924), PARP (olaparib) and proteasome (bortezomib) showed increased killing compared to each treatment alone. In order to identify rational combinatorial therapies that could be potentially translated for use in clinical trials, we performed additional studies with the BCL6 inhibitor RI-BPI that is being developed for clinical use. We first analyzed the impact of RI-BPI on the apoptosome in a panel of 6 DLBCL (SU-DHL6, Ly1, Ly7, Ly3, Ly10, SU-DHL4) and 4 tFL (DoHH2, WSU-DLCL2, Granta452, SC-1) cell lines. RI-BPI induced a profile of up-regulated pro and anti-apoptotic proteins similar to siBCL6. Because ABT-737 and obatoclax are active in DLBCL cells where apoptotic BH3 activators are neutralized by BCL2 or BCL-XL and RI-BPI treatment changes the stoichiometry of pro and anti-apoptotic proteins, we determined the post-RI-BPI BH3 profiling accordingly to the amount of BIM sequestration (by co-immunoprecipitation). Accordingly, sequential treatment of DLBCL and tFL cell lines with RI-BPI and ABT-737 or obatoclax synergistically killed BCL2/BCL-XL dependent cells (but not MCL-1 dependent cells). This effect was independent of the mutational status of BCL2, MCL1, BCL6, MYC and TP53. Olaparib was not tested in combination since most cell lines were resistant to clinically achievable concentrations of this drug. Bortezomib and MLN4924 were synergistic in most cell lines when combined with RI-BPI (as determined by isobologram analysis). The synergistic killing was associated with increase in caspase 7/3 activation (by a plate-based assay) and NFkB inhibition (by p65 DNA binding assay). This effect was independent of the cell of origin classification of the cell line (i.e. ABC vs. GCB). We then tested the combination of RI-BPI with ABT-737, MLN4924 or bortezomib in Ly1 xenograft models (n=10 mice per combination). Ly1 represents a DLBCL with 3q27 and t(14,18). We found that after 10 days of treatment, each combinatorial treatment was more effective than their individual components (p=0.02, p=0.01 and p<0.01 for RI-BPI with ABT-737, MLN4924 and bortezomib, respectively; T-test, day 10). Detailed toxicity studies revealed no toxicity excess with these combinations. In sum, our work shows that pharmacologic targeting of anti-apoptotic pathways induced by inhibition of BCL6 activity successfully sensitized DLBCL and tFL cells to apoptosis. This effect was evident in cells in which the apoptosis resistant mechanism evolved as response to BCL6 inhibition and gene de-repression as well as those with constitutive overexpression of anti-apoptotic genes. Disclosures: No relevant conflicts of interest to declare.

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Pophali, Priyanka, Lisa M. Marinelli, Rhett P. Ketterling, Reid Gregory Meyer, Ellen D. McPhail, Paul J. Kurtin, Thomas M. Habermann, and Rebecca L. King. "High Level MYC Amplification in Aggressive B-Cell Lymphomas: Is It a Marker of Aggressive Disease?" Blood 132, Supplement 1 (November 29, 2018): 1693. http://dx.doi.org/10.1182/blood-2018-99-115484.

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Abstract MYC amplification (amp) is a marker of poor prognosis in many non-hematologic malignancies. While MYC translocations in B cell lymphoma (BCL) have been extensively studied, little is known about the significance of MYC amp. Recent studies describe increased MYC copy numbers (3-10 copies/cell) to be associated with more aggressive BCL. The WHO 2017 does not include MYC amp in the definition of high-grade BCL (HGBCL) with MYC and BCL2 and/or BCL6 rearrangement ("double-hit lymphoma", DHL). However, it also states that high-level MYC amp occurring together with a MYC rearrangement, and concurrent with BCL2 rearrangement likely has a similar clinical impact as classic DHL. Although increased MYC copy number is commonly identified by routine fluorescence in situ hybridization (FISH) testing in BCL, the experience of our large cytogenetics reference laboratory suggests that high-level MYC amp, defined as uncountable MYC signals, is far less common. Therefore, we sought to characterize the clinical, pathologic and cytogenetic features of patients with BCL showing high-level MYC amp. The Mayo Clinic cytogenetic database was retrospectively reviewed for all cases of BCL with high-level MYC amp seen by FISH from January 2010 - February 2018. All FISH studies reported as MYC amp were re-reviewed by a cytogeneticist to verify the level of amp and the MYC probes involved. Pathology was reviewed by two independent hematopathologists. Clinical information was collected through chart review. Survival analysis was performed using Kaplan-Meier curves and the Wilcoxon rank-sum test. FISH analysis for MYC aberrations identified 44/9715 (0.45%) cases with high-level MYC amp. Of cases with available H&E, the most common morphology was diffuse large BCL (DLBCL) (82%; 28/34), followed by HGBCL (15%; 5/34) and plasmablastic BCL (3%; 1/34). Hans cell of origin (COO) algorithm immunohistochemistry (IHC) identified 21/25 (84%) germinal center B-cell-like (GCB), and 4/25 (16%) non-GCB cases. 21/27 (78%) cases were BCL2+ by IHC. MYC+ by IHC was ≥40% in 21/28 (75%) and <40% in 7/28 (25%) cases. 9/17 (53%) were "double expressers" (DEL) by IHC. MYC amp probe signals appeared in a cloud-like distribution (CLD) in 31 (70%) or in a single homogenous staining region (HSR) in 13 (30%) [Figure 1A]. Among 38 cases with amp in a MYC break-apart probe, 21 (55%) had amp of 5' alone, 15 (40%) of intact and 2 (5%) of the 3' probe alone. 7/44 (16%) had MYC translocations (5 IGH; 2 non-IGH). BCL2 rearrangement was seen in 15/39 (38%) cases, and BCL6 rearrangement in 3/36 (8%). Only 2/44 (4%) cases met the current WHO 2017 definition of DHL. Clinical data was available for 20 cases. Median age at diagnosis was 64.5 (range 25-88) years with M:F of 1.5:1. Only 1/14 (7%) had bone marrow while 16/18 (88.8%) had other extranodal sites of involvement (8 gastrointestinal). The clinical presentation was heterogeneous: 13 de novo, 3 post-transplant, 3 transformed from low grade and 1 mediastinal BCL. 9/14 had an elevated LDH, median 387 (225 - 2063) U/L. R-CHOP was the most common first line therapy in 12/17 (70%). At median follow-up of 18.2 (range 0.4 - 88.9) months, 9 patients had died, 3 were in relapse and 8 remained in first complete remission. Lymphoma relapse/progression was the most common cause of death in 7/9 (78%). The median overall survival (OS) was 29.3 months [Figure 1B]. There was no statistically significant difference in OS by morphologic classification (DLBCL vs HGBCL, p=0.6), double expresser (Yes/No, p=0.19), COO (GCB vs non-GCB, p=0.08), MYC amp pattern (HSR vs CLD, p=0.48), MYC amp probe (3' vs 5' vs intact, p=0.31), MYC rearrangement (Yes/No, p=0.1), or MYC amp with concurrent BCL2/BCL6 rearrangement (Yes/No ,p=0.2). To our knowledge, this is the first study to characterize the clinical, pathologic and cytogenetic features of BCL with strictly-defined high level MYC amp identified by FISH. The 5' signal alone, or the intact MYC probe are most frequently amplified, and two distinct patterns of amp can be seen. Predominant extra nodal involvement is an important clinical observation. These cases are usually DLBCL, GCB type, and infrequently have concurrent MYC/BCL2/BCL6 rearrangement. Our study suggests that BCL with high-level MYC amp may have an aggressive disease course regardless of MYC, BCL2 and BCL6 gene rearrangement status. A larger series is necessary to further understand the clinical significance of high-level MYC amp in BCL. Figure 1. Figure 1. Disclosures No relevant conflicts of interest to declare.

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Pedersen, Mette Ølgod, Anne Ortved Gang, Tim Svenstrup Poulsen, Helle Knudsen, Anne F. Lauritzen, MajLis M. Talman, Signe Ledou Nielsen, and Peter H. Norgaard. "Concurrent BCL2 and MYC Translocations In a Prospective Cohort of Diffuse Large B-Cell Lymphomas." Blood 116, no. 21 (November 19, 2010): 319. http://dx.doi.org/10.1182/blood.v116.21.319.319.

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Abstract Abstract 319 Background: Concurrent chromosomal translocations involving the BCL2 and MYC protooncogenes, so-called double-hit, is found both in diffuse large B-cell lymphoma (DLBCL) and in a newly defined B-cell lymphoma category with features overlapping between DLBCL and Burkitt lymphoma (BCLU, 2008 WHO classification). Few studies have been published on series of double-hit B-cell lymphomas, and to our knowledge only retrospective series, reporting an average frequency of around 5%. Therefore some authors suspected that the frequency of double-hit translocations was underestimated. In addition to unanimous reports of highly aggressive clinical behaviour; poor outcome and resistance to chemotherapy, double-hit lymphomas had GCB immunophenotype (Hans), varying morphology from classical Burkitt like to DLBCL-NOS and mostly high proliferation rates (Ki-67). Purpose: We conducted a prospective study of DLBCL to evaluate the frequency of double-hit BCL2/MYC translocations in DLBCL. Secondly, we wanted to analyse if any pathologic and/or clinical features correlated with the presence of a double-hit in order to evaluate the need for routine genetic analysis of large B-cell lymphomas in prognostic stratification. Materials and methods: All patients diagnosed with DLBCL or BCLU at the Haematopathology Section at Copenhagen University Hospital in Herlev were prospectively collected throughout 2009. Tumours were classified according to their morphology (2008 WHO classification), immunohistochemistry (CD10, BCL6, MUM1, BCL2, Ki-67) and FISH (BCL2, BCL6 and MYC translocations). Clinical data were collected from patient files. Result: Double-hit BCL2/MYC translocations were detected in 9 of 93 cases (10%); 7 DLBCL, 1 BCLU, 1 unclassified. All double-hit DLBCL were GCB immunophenotype and showed varying morphology. Ki-67 index ranged from 15–95%. Interestingly, 2 double-hit cases were late relapses (primary double-hit). Characteristic clinical parameters included a high International Prognostic Index (IPI) score, a high stage and an extranodal presentation. Discussion and conclusion: In this prospective cohort of DLBCL patients the incidence of BCL2/MYC double-hit was 10%. This suggests that double-hit is more frequent in DLBCL than previously estimated. Double-hit lymphomas had GCB-immunophenotype but could not be identified by morphology or proliferation rate. Therefore if these patients should be identified due to an inferior prognosis (which we could not significantly establish due to limited observation time) routine FISH analysis for double-hit translocations should be performed in all patients with BCLU or DLBCL of GCB-subtype. Disclosures: No relevant conflicts of interest to declare.

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Дисертації з теми "BCL7"

Martin, Franck. "Structural and functional studies of chromatin remodeling complex mamalian SWI / SNF." Electronic Thesis or Diss., Strasbourg, 2024. http://www.theses.fr/2024STRAJ044.

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La chromatine est une structure dynamique régulée par différents mécanismes épigénétiques parmi lesquels le remodelage de la chromatine dépendant de l’ATP comme le SWI/SNF. Leur importance est telle que les mutations des protéines de remodelage de la chromatine sont fortement associées à plusieurs maladies dont le cancer. Par exemple les protéines BCL7, qui sont de nouvelles sous unité centrales récemment identifié du complexe SWI/SNF des mammifère, sont associées à différents types de cancers comme dans le Diffuse Large B-cell Lymphoma (DLBCL). Les informations sur les protéines BCL7 sont à ce jour très limitées. En utilisant des approches biochimiques et structurelles, ce projet vise à mieux comprendre la structure et la fonction de ces sous unités auxiliaires. Nous rapportons ici que les protéines se lient à l’acidique patch du nucleosome avec sa regions N-terminal qui comprend un motif d’ancrage arginines et que la mutation de l’une de ces arginines impacte directement la liaison au nucleosome. Nous apportons aussi une hypothèse sur la position au sein du complexe SWI/SNF de BCL7 qui interagit avec le module ARP et plus particulièrement avec ACTB par l'intermédiaire d'un motif 2W, et qu’elles sont directement des partenaires de liaisons avec BAF47. Nous avons aussi pu identifier qu’une fois sur les nucléosomes c’est BAF47 qui prend place sur l’acidique patch et l’hélice de BCL7A est déplacé
Chromatin is a dynamic structure regulated by various epigenetic mechanisms, including ATP-dependent chromatin remodeling such as SWI/SNF. Their importance is such that mutations in chromatin remodeling proteins are strongly associated with several diseases, including cancer. For example, BCL7 proteins, which are newly identified core subunits of the mammalian SWI/SNF complex, are associated with different types of cancer, such as Diffuse Large B-cell Lymphoma (DLBCL). To date, information on BCL7 proteins is very limited. Using biochemical and structural approaches, this project aims to better understand the structure and function of these auxiliary subunits. We report here that the proteins bind to the nucleosome with its N-terminal regions, which include an arginine anchoring motif, and that mutation of one of these arginines directly impacts binding to the nucleosome. We also hypothesize that the position within the SWI/SNF complex of BCL7, which interacts with the ARP module and more specifically with ACTB via a 2W motif, is directly linked to BAF47. We were also able to identify that once on the nucleosomes, BAF47 takes its place on the acidic patch and the BCL7A helix is displaced

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Barrans, Sharon Louise. "Immunophenotypic and molecular approaches to the classification of diffuse large B cell lymphoma." Thesis, Manchester Metropolitan University, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.366169.

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Li, Yue. "Investigating Selected Mechanisms of Modulation of BECN1-mediated Autophagy." Diss., North Dakota State University, 2019. https://hdl.handle.net/10365/29775.

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Autophagy is a lysosomal degradation pathway wherein cytoplasmic components not needed by or harmful to the cell are degraded and recycled. BECN homologs are key autophagy proteins consisting of an intrinsically disordered region (IDR), flexible helical domain (FHD), coiled-coil domain (CCD) and β-α repeated, autophagy-specific domain (BARAD). Diverse proteins modulate autophagy by binding BECN1. Understanding the mechanisms by which these proteins regulate BECN1-mediated autophagy is important for developing therapeutics targeting these proteins. Toward this goal, we have developed purification protocols for multi-domain BECN1 fragments to explore the conformational flexibility and interactions. We show that a BECN1 helix transitions between mutually exclusive packing states, wherein it either forms part of the CCD homodimer or packs against the BARAD, but predominantly packs against the BARAD. The same set of residues on this helix contribute to the CCD homodimer or packing with the BARAD, and mutation of these residues abrogates starvation-induced up-regulation of autophagy. Next, we show the equatorial groove of GAPR-1 may be responsible for binding BECN1. The five conserved residues lining the GAPR-1 equatorial groove are essential for the interaction, as mutation of these residues disrupts GAPR-1:BECN1 interaction. We also solved the structure of this pentad mutant, which indicates the changes in the equatorial groove and the improved dimerization of pentad mutant likely abrogates BECN1-binding. We then show that BH3D is not required for BECN1 to up-regulate autophagy, though it is required for binding BCL2 homologs. Therefore, we investigated the interactions between BH3D-containing BECN1 fragments and the BCL2 homolog, M11. BECN1 regions outside the BH3D increase binding to M11 by 5-10 fold. In addition, M11-binding increases flexibility of the nuclear export sequence (NES). Further, homodimerization and thermostability of BECN1 BH3D-FHD-CCD increases upon M11-binding. Lastly, the M11:BH3D-FHD-CCD complex appears to fluctuate between two major types of conformations, which may be mediated by the increased flexibility of BECN1 NES upon binding M11. Lastly, we investigated the interactions between BH3D-containing BECN1 fragments and Bcl-XL. Our results indicate that BECN1 regions outside the BH3D do not affect BECN1 interaction with Bcl-XL. Together, these studies are important for better understanding how proteins down-regulate BECN1-mediate autophagy.
NIH: RO3 NS090939, R15 GM122035, P20 RR015566, and R21 AI078198 (S.S). R15 GM113227, P30 GM103332-01, P41 GM103622, and P41 GM103403.; NSF: MCB-1413525 (S.S.); ND Dept. of Commerce: Award #14-11-J1-73 (S.S.)

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Thompson, Brian M. "Amino-terminal sequences of the bacillus anthracis exosporium proteins BCLA and BCLB important for localization and attachment to the spore surface." Diss., Columbia, Mo. : University of Missouri-Columbia, 2008. http://hdl.handle.net/10355/5700.

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Thesis (M.S.)--University of Missouri-Columbia, 2008.
The entire dissertation/thesis text is included in the research.pdf file; the official abstract appears in the short.pdf file (which also appears in the research.pdf); a non-technical general description, or public abstract, appears in the public.pdf file. "August 2008" Includes bibliographical references.

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Kunze, Doreen. "Small interfering RNA-vermittelte Hemmung der Apoptoseinhibitoren BCL2, BCL-XL, XIAP und Survivin in Zellkultur- und Mausmodellen des humanen Harnblasenkarzinoms." Doctoral thesis, Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2012. http://nbn-resolving.de/urn:nbn:de:bsz:14-qucosa-81888.

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Das Harnblasenkarzinom (BCa) stellt in Deutschland die vierthäufigste Tumorneuerkrankung und die zehnthäufigste krebsbedingte Todesursache bei Männern dar. Nichtmuskelinvasive BCa werden organerhaltend aus der Blasenwand entfernt und zur Rezidiv- und Progressionsprophylaxe mittels intravesikaler Chemo- oder Immuntherapien behandelt. Trotz dieser adjuvanten Therapien, die mit starken Nebenwirkungen verbunden sein können, ist nur eine bedingte Minimierung des Rezidivrisikos möglich. Besonders im fortgeschrittenen Stadium weisen Harnblasenkarzinome eine schlechte Prognose auf. Obwohl das BCa eine chemosensitive Erkrankung darstellt, wird das Ansprechen auf lokale oder systemische Chemotherapien häufig durch auftretende Resistenzmechanismen limitiert. Daher stehen sowohl die Verbesserung konventioneller Chemotherapien als auch die Suche nach neuartigen Behandlungsstrategien im Fokus der experimentellen BCa-Forschung. Die Apoptose, eine Form des programmierten Zelltodes, ist ein essenzieller, streng regulierter biologischer Prozess, welcher der Aufrechterhaltung der Gewebshomöostase und der gezielten, entzündungsfreien Eliminierung geschädigter Zellen dient. Fehlregulationen in den Apoptosesignalwegen stellen ein zentrales Ereignis in der Tumorgenese dar und tragen außerdem zur Entstehung von Chemo- und Radiotherapieresistenzen bei. Eine wichtige Rolle in der Apoptoseregulation spielen die Mitglieder der BCL2- und der Inhibitor of Apoptosis Protein (IAP)-Familien, deren wichtigste antiapoptotische Vertreter BCL2, BCL-XL, XIAP und Survivin häufig in Tumoren, einschließlich des BCa, überexprimiert sind. Unter Verwendung von small interfering RNAs (siRNAs), synthetischen Nukleinsäurekonstrukten zur selektiven Geninhibition, wurde im Rahmen der Arbeit in vitro und in vivo untersucht, ob die Hemmung der Apoptoseinhibitoren BCL2, BCL-XL, XIAP und Survivin – allein und in Kombination mit Chemotherapie – eine Therapieoption zur Behandlung des BCa darstellen könnte. Da zur Tumorentstehung und -progression eine Vielzahl von genetischen Veränderungen beitragen, erscheint der Angriff eines einzelnen Zielgens unzureichend für eine effektive Tumortherapie. Aufgrund dessen wurde untersucht, ob durch simultane Reduktion der ausgewählten Apoptoseinhibitoren in BCa-Zellen stärkere wachstumsinhibitorische Effekte erzielt werden können. In der vorliegenden Arbeit wurde gezeigt, dass insbesondere die siRNA-vermittelte Hemmung von BCL-XL und Survivin in den BCa-Zelllinien EJ28 und J82 antiproliferative Effekte hervorruft und diese Tumorzellen gegenüber einer nachgeschalteten Chemotherapie mit Mitomycin C oder Cisplatin sensitiviert. Hingegen bewirkte sowohl die transiente als auch die stabile RNAi-induzierte Hemmung von BCL2 und XIAP in den untersuchten BCa-Monolayerzellkulturen, möglicherweise infolge kontinuierlicher Versorgung der Tumorzellen mit Sauerstoff und Nährstoffen, keine Reduktion des Tumorwachstums. Eine gegenüber den Einzelbehandlungen deutliche Verstärkung der antitumoralen und insbesondere der chemosensitivierenden Effekte in den BCa-Zelllinien wurde durch simultane Hemmung von BCL-XL und Survivin erzielt. Beispielsweise stieg der Anteil apoptotischer Zellen von 64 % nach Survivin-siRNA+Cisplatin-Behandlung auf 94 % nach gleichzeitiger BCL-XL+Survivin-Inhibition in Kombination mit Cisplatin. Folglich stellt die simultane Inhibition von BCL-XL und Survivin in Kombination mit Chemotherapeutika eine äußert viel versprechende BCa-Therapieoption dar. Tierexperimentelle Studien belegen die wachstumsinhibitorische Wirkung der Survivin-Reduktion und der kombinierten BCL-XL-siRNA+Chemotherapie-Behandlung, so wurde das Tumorendvolumen im Vergleich zur Kontrollbehandlung um 43 % bzw. um 48 % reduziert.

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Mahn, Friederike Marie [Verfasser]. "Bruchereignisse in den Onkogenorten BCL2, BCL6 und MYC bei aggressiven B-Zell-Lymphomen im Kindesalter : molekularzytogenetische Analysen im Rahmen der NHL-BFM-Studie / Friederike Maria Mahn." Kiel : Universitätsbibliothek Kiel, 2010. http://d-nb.info/101998337X/34.

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Viant, Charlotte. "Régulation du développement et de la fonction des cellules innées lymphoïdes NKp46+." Thesis, Aix-Marseille, 2016. http://www.theses.fr/2016AIXM4018/document.

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Il existe différents groupes de cellules lymphoïdes innées (ILC) qui ont été caractérisées en fonction des facteurs de transcriptions indispensables à leur différenciation et des cytokines qu’elles sécrètent. Les ILC1, dont font partie les cellules Natural Killer (NK), expriment T-bet et produisent de l’IFN-γ. Les ILC2 sont caractérisées par GATA-3 et sécrètent de l’IL-5 et de l’IL-13. Quant aux ILC3, elles ont été identifiées par leur sécrétion d’IL-17 et d’IL-22 ainsi que par l’expression de RORγt.Mon travail de thèse m’a amené à étudier différents aspects de la biologie des cellules NK et ILC3 : leur tolérance, leur homéostasie et leur plasticité.Les cellules NK jouent un rôle dans l’élimination de cellules cancéreuses et des cellules infectées par des bactéries et des virus. J’ai mis en évidence le rôle de la phosphatase SHP-1 (Src homology region 2 domain-containing phosphatase-1) dans les mécanismes de tolérance et d’activation des cellules NK. J’ai également montré que la protéine anti-apoptotique Bcl2 (B-cell lymphoma 2) est importante pour l’homéostasie des cellules NK. Seules les cellules en cycle cellulaire peuvent compenser l’absence de Bcl2, notamment du fait de l’augmentation de l’expression d’une autre protéine anti-apoptotique, Mcl1 (Myeloid Cell Leukemia 1). Les ILC3 sont des cellules principalement localisées dans l’intestin et qui peuvent être classées en différents groupes en fonction des marqueurs qu’elles expriment. J’ai montré qu’il existe une plasticité entre les différentes populations d’ILC3, et que cette plasticité est régulée par des facteurs environnementaux tel que le TGF-β et le ligand de Notch, DL1
There are three groups of innate lymphoid cells (ILC), defined notably by the transcriptions factors essential to their differentiation and their cytokines secretion. ILC1, including natural killer (NK) cells, express T-bet and secrete IFN-γ. ILC2 are characterized by GATA3 expression and the production of IL-5 and IL-13. ILC3 secrete IL-17 and IL-22 and express RORγt.My PhD work dealt with different aspects of NK cells and ILC3: their tolerance, homeostasis and plasticity.NK cell are involved in killing tumor cells and bacteria- or virus-infected cells. I found that the phosphatase SHP-1 (Src homology region 2 domain-containing phosphatase-1) has a role in NK cell tolerance and activation.I also showed that the anti-apoptotic Bcl2 protein (B-cell lymphoma 2) is important for NK cell homeostasis. Only cycling NK cells could compensate the Bcl2 deficiency, due to the increase expression of another anti-apoptotic protein, Mcl1 (Myeloid Cell Leukemia 1).ILC3 are mainly located in the gut and are classified in different groups, depending on the markers that they expressed. I showed that there is plasticity between ILC3 populations and that this plasticity is regulated by environmental factors, including TGF-β and the Notch ligand, DL1

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Hakert, James Damian. "The crosstalk between notch1 and BCL6." Tallahassee, Fla. : Florida State University, 2010. http://purl.fcla.edu/fsu/lib/digcoll/undergraduate/honors-theses/2181936.

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Thesis (Honors paper)--Florida State University, 2010.
Advisor: Dr. Yoichi Kato, Florida State University, College of Arts and Sciences, Dept. of Chemistry and Biochemistry. Includes bibliographical references.

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Warner, Andrew. "Borylative cyclisation of alkynes using BCl3." Thesis, University of Manchester, 2017. https://www.research.manchester.ac.uk/portal/en/theses/borylative-cyclisation-of-alkynes-using-bcl3(7a4e56f3-e8c6-4c68-97ec-4596ef5e0ce2).html.

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Boron trichloride, a cheap and commercially available Lewis acid, has been demonstrated to activate alkynes possessing appropriate nucleophiles, facilitating borylative cyclisation. This reaction furnishes polycyclic compounds possessing a new C(sp2)-B bond externally to the newly formed ring (through concomitant C-C and C-B bond formation). The RBCl2 intermediates generated from cyclisation were esterified with pinacol to furnish air/moisture stable boronic esters. This methodology has been applied to the following classes of starting materials: 1,4-disubstituted but-1-ynes (including N- and O- linked analogues), 2-alkynylanisoles, 2-alkynylthioanisoles and 1,2-bis(alkynyl)benzenes. Thus, borylated scaffolds such as dihydronaphthalenes, dihydroquinolines, 2H-chromenes, benzofurans, benzothiophenes, dibenzopentalenes and benzofulvenes have been synthesised. A variety of functionalities (e.g. amines, esters, nitriles) were tolerated by the reaction, with a number of substrates cyclised on either a gram scale, or under ambient conditions, demonstrating the robust nature of this methodology. An oxidation reaction with [Ph3C][BF4] was carried out on some of the borylated dihydronaphthalene compounds to obtain borylated naphthalenes. Suzuki-Miyaura cross-coupling reactions were carried out on certain borylated cycles to furnish new C-C bonds and generate analogues of established pharmaceuticals such as Nafoxidine or Raloxifene, demonstrating the synthetic value of these borylated cycles. Additionally, a one-pot borylative cyclisation/Suzuki-Miyaura cross-coupling reaction was also developed. Throughout this investigation, alternative reactivity has been observed when using BCl3 to activate certain alkynes, including intermolecular 1,2-trans-carboboration and a rare example of N- and O-directed 1,2-trans-haloboration. Additionally, multiple borylative cyclisations have been carried out on an appropriate alkyne to obtain a B-doped polyaromatic hydrocarbon (PAH), which has potential material-based applications.

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Leal, Cristina Tavares. "Identificação da família BCL2 como alvo terapêutico no tratamento das neoplasias mieloproliferativas associadas à mutação da JAK2V617F." Universidade de São Paulo, 2017. http://www.teses.usp.br/teses/disponiveis/17/17154/tde-06042018-114114/.

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As neoplasias mieloproliferativas (NMPs) negativas para o rearranjo t(9;22)/BCRABL1, incluindo Policitemia Vera (PV), Trombocitemia Essencial (TE) e Mielofibrose Primária (MFP), são doenças hematopoéticas clonais e estão frequentemente associadas à mutação JAK2V617F. Apesar dos avanços no conhecimento da fisiopatologia após a descoberta da mutação JAK2V617F e do desenvolvimento de inibidores da JAK2, o tratamento permanece não curativo. Sabe-se que as célulastronco mais primitivas nas NMPs são responsáveis pela iniciação da doença e que a expansão dos precursores mieloeritróides contribui para o fenótipo clínico. Dados recentes obtidos com ensaios in vitro mostram que as proteínas da família BCL2, reguladoras da apoptose mitocondrial, desempenham um papel relevante na patogênese das NMPs. Acreditamos que a expressão anômala de BCL2 nas células progenitoras hematopoéticas (CPH) das NMPs pode contribuir para a patogênese desse grupo de doenças. Avaliamos a expressão gênica, por meio de PCR em Tempo Real, da família BCL2 (genes antiapoptóticos BCL-xL e BCL2 e o pró-apoptótico BIM) nas diferentes subpopulações de progenitores hematopoéticos murinos (de um modelo condicional knockin de expressão heterozigótica condicional da Jak2V617F) e de pacientes portadores de NMPs bem como sua contribuição para o fenótipo da doença e resposta ao inibidores da JAK2 (com a droga ruxolitinibe) e/ou inibição da família BCL2 (com o inibidor de BCL2 obatoclax). Não encontramos diferença de expressão basal dos genes BCL2, BCL-xL e BIM nas células CD34+ bem como nas subpopulações de células CD34+38-/+ de pacientes com NMPs, independente da presença da mutação JAK2V617F, em relação às células CD34+ e subpopulações CD34+38-/+ dos controles (p>0.05). Nas células CD34+ de pacientes com TE encontramos aumento de expressão de BCL2 em relação às células CD34+ pacientes com MFP (p=0.03). No modelo transgênico de camundongos Jak2 wt/VF (que apresentam uma NMP semelhante à PV) e Jak2 wt/wt (controles), comparamos a expressão diferencial dos genes da família Bcl2 em precursores hematopoéticos imaturos (LSKs) e progenitores mieloides mais maduros (MPs). A expressão do BclxL em MPs de camundongos wt/VF foi maior em relação à subpopulação de células LSKs e em relação as duas subpopulações de células dos controles (p=0.0011). Não houve diferença significativa de expressão do Bcl2 nas subpopulações de células LSKs e MPs de animais wt/VF e wt/wt (p=0.12). Observou-se menor expressão de Bim em LSKs em relação às células MPs dos animais mutados (p=0.026), diferença essa não observada entre os controles Jak2 wt/wt. O tratamento isolado com inibidor de JAK2 ou de BCL2 resultou em aumento de expressão do Bim nas CPH (LSKs e MPs) de camungongos Jak2 wt/VF em relação aos animais Jak2 wt/wt. Este aumento da expressão de Bim foi ainda mais evidente após o tratamento das células com a combinação das duas drogas quando comparadas às células não tratadas ou tratadas com um dos dois inibidores, sendo maior em animais doentes do que em animais controles (p<0.0001). A análise do efeito do tratamento com os inibidores de JAK2 e BCL2 na indução de apoptose por meio de citometria de fluxo (marcação com anexina/7-AAD) revelou que as células LSKs foram mais resistentes à apoptose tardia do que as células MPs independentemente da mutação da JAK2 (p<0.05). O tratamento com obatoclax resultou em indução de apoptose diferentemente do que foi observado com o tratamento com ruxolitinibe (p=0.594) nas células MPs de animais Jak2 wt/VF. Ademais, o tratamento combinado com ruxolitinibe e obatoclax resultou no aumento da apoptose nas células MPs dos animais com fenótipo de PV (Jak2 wt/VF) em relação aos animais Jak2 wt/wt (p=0.05). Em conclusão, demonstramos que a resistência à apoptose nas NMPs ocorre desde as CPH iniciadoras da doença. Nossos resultados sugerem que a modulação da apoptose mitocondrial pode ser uma nova estratégia terapêutica para pacientes com NMP em combinação aos inibidores de JAK2, na medida em que atua tanto nas CPH que iniciam a doença como nos MPs, responsáveis pelos sinais e sintomas de mieloproliferação.
Myeloproliferative Neoplasms (MPNs) negative for t(9;22)/BCR-ABL1 rearrangement, including Polycythemia Vera (PV), Essential Thrombocythemia (ET) and Primary Myelofibrosis (PMF), are clonal hematopoietic diseases and are often associated with the JAK2V617F mutation. Despite advances in the pathophysiology knowledge after the discovery of the JAK2V617F mutation and the development of JAK2 inhibitors, treatment remains non-curative. It is known that MPN primitive stem cells are essential for the initiation of the disease and that the expansion of the myeloeritroid precursors contributes to the clinical phenotype. Recent data, obtained with in vitro assays, showed that BCL2 family proteins, regulators of mitochondrial apoptosis, play a relevant role in the pathogenesis of MPNs. We believe that the anomalous expression of BCL2 in hematopoietic progenitor cells (HPCs) of MPNs may contribute to their pathogenesis. We evaluated BCL2 family (antiapoptotic genes BCL-xL and BCL2 and the pro-apoptotic BIM) gene expression by real-time PCR in different subpopulations of hematopoietic progenitors from a conditional Jak2V617F knockin murine model and from patients with MPNs as well as their contribution to the disease phenotype and response to JAK2 inhibitors (with ruxolitinib) and/or to the inhibition of the BCL2 family (with the BH3-mimetic obatoclax). We found no difference in the basal expression of the BCL2, BCL-xL and BIM in CD34+ cells as well as in subpopulations of CD34+ 38-/+ cells from patients with MPNs, regardless of the presence of the JAK2V617F mutation. In CD34+ cells obtained from patients with ET, we found an increase of BCL2 expression when compared to CD34+ cells with PMF (p=0.03). In the Jak2 wt/VF transgenic mice (that develop a MPN similar to PV) and Jak2 wt/wt controls, we compared the differential expression of Bcl2 family genes in immature hematopoietic precursors (LSKs) and more mature myeloid progenitors (MPs). Expression of Bcl-xL in MPs of wt/VF mice was greater when compared to LSKs and to the two progenitor subpopulations of control cells (p=0.0011). There was no significant difference in Bcl2 expression between the subpopulations of LSKs and MPs from wt/VF and wt/wt animals (p=0.12). Lower Bim expression in LSKs than in MPs was observed in samples from JAK2-mutated animals (p=0.026). Such difference was not observed between the Jak2 wt/wt subpopulations. Treatment with JAK2 or BCL2 inhibitors alone resulted in increased Bim expression in LSKs and MPs of the Jak2 wt/VF mice when compared to Jak2 wt/wt animals. This increase in Bim expression was even more evident when these cells were treated with the combination of the two drugs as compared to single treatment with one of the two inhibitors, being higher in mutaded than control animals (p<0.0001). The analysis of apoptosis by flow cytometry (annexin / 7-AAD labeling) revealed that LSK cells were more resistant to late apoptosis than MP cells regardless of the JAK2 mutation (p<0.05). Treatment with obatoclax resulted in greater apoptosis induction than it was observed with ruxolitinib treatment (p=0.594) on MP cells of Jak2 wt/VF animals. In addition, the combined treatment with ruxolitinib and obatoclax resulted in increased apoptosis in MP cells of animals with the PV phenotype (Jak2 wt/VF) as compared to the Jak2 wt/wt animals (p=0.05). In conclusion, we demonstrated that resistance to apoptosis in MPNs occurs at the level of the hematopoietic progenitors that initiate the disease. Our results suggest that modulation of mitochondrial apoptosis may be a new therapeutic strategy for MPN patients in combination with JAK2 inhibitors, as it acts on both the disease initiating and more mature progenitors, responsible for the clinical findings of myeloproliferation.

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Книги з теми "BCL7"

Gavathiotis, Evripidis, ed. BCL-2 Family Proteins. New York, NY: Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-8861-7.

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Hetz, Claudio, ed. BCL-2 Protein Family. New York, NY: Springer New York, 2010. http://dx.doi.org/10.1007/978-1-4419-6706-0.

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Guelachvili, G., ed. Linear Triatomic Molecules - BClH+ (HBCl+) - COSe (OCSe). Berlin/Heidelberg: Springer-Verlag, 1995. http://dx.doi.org/10.1007/b46104.

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Weil, Harry H. Structuring the smaller corporation under the BCL. [Harrisburg, Pa.] (P.O. Box 1027, Harrisburg 17108-1027): Pennsylvania Bar Institute, 1989.

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Catholic Church. National Conference of Catholic Bishops. Committee on the Liturgy. Thirty-five years of the BCL newsletter. Washington, D.C: United States Conference of Catholic Bishops, 2004.

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Beaton, Jennifer. Amplification and cloning of Bcl-xL and Bcl-xS to obtain in-vitro production of protein products. Sudbury, Ont: Laurentian University, 1995.

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United States. National Aeronautics and Space Administration., ed. The apparent strain stability and repeatability of a BCL3 resistance strain gage. [Washington, DC]: National Aeronautics and Space Administration, 1991.

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Tomlin, Jennifer Leigh. Novel biological approaches for detecting oncogenic cooperation with Bcl-2. Ottawa: National Library of Canada, 1999.

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Conference, British Comparative Literature Association. Literary representations of the self: Papers from the fifth triennial BCLA conference 1989. Oxford: Oxford University Press for the University of St Andrews, 1990.

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Wachek, Volker. Einfluss der BCL-2 Expression auf die Chemoresistenz des malignen Melanoms. [s.l.]: [s.n.], 1997.

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Частини книг з теми "BCL7"

Posypaiko, V. I., and E. A. Alekseeva. "BCl3." In Phase Equilibria in Binary Halides, 26. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4684-9024-4_10.

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Ruggiero, Marco, and John W. Anderson. "Bcl2." In Encyclopedia of Cancer, 1–7. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-27841-9_562-4.

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Ruggiero, Marco, and John W. Anderson. "Bcl2." In Encyclopedia of Cancer, 1–6. Berlin, Heidelberg: Springer Berlin Heidelberg, 2017. http://dx.doi.org/10.1007/978-3-642-27841-9_562-5.

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Brocke-Heidrich, Katja. "BCL3." In Encyclopedia of Cancer, 1–4. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-27841-9_565-2.

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Ruggiero, Marco, and John W. Anderson. "Bcl2." In Encyclopedia of Cancer, 447–52. Berlin, Heidelberg: Springer Berlin Heidelberg, 2017. http://dx.doi.org/10.1007/978-3-662-46875-3_562.

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Brocke-Heidrich, Katja. "BCL3." In Encyclopedia of Cancer, 452–55. Berlin, Heidelberg: Springer Berlin Heidelberg, 2017. http://dx.doi.org/10.1007/978-3-662-46875-3_565.

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Ruggiero, Marco. "Bcl2." In Encyclopedia of Cancer, 356–60. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-16483-5_562.

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Brocke-Heidrich, Katja. "BCL3." In Encyclopedia of Cancer, 361–63. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-16483-5_565.

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Saidak, Zuzana, Zakaria Ezzoukhry, Jean-Claude Maziere, Antoine Galmiche, Ken-Ichi Takemaru, Xingwang Chen, Feng-Qian Li, et al. "BAX (BCl2-Associated X Protein), BCL2L4 (BCL-2 Like 4)." In Encyclopedia of Signaling Molecules, 186. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_100109.

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Vini, Ravindran, Sreeja Sreekumar, Juberiya M. Azeez, and Sreeja Sreeharshan. "Pomegranate Extract Protects Endothelial Cells from TNF-α Associated Damage." In Proceedings of the Conference BioSangam 2022: Emerging Trends in Biotechnology (BIOSANGAM 2022), 276–89. Dordrecht: Atlantis Press International BV, 2022. http://dx.doi.org/10.2991/978-94-6463-020-6_27.

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AbstractPomegranates are known for being rich in polyphenols and are considered to have immense therapeutic potential. The present study investigates the hypothesis that the Methanolic Extract of Pomegranate (PME), a rich source of antioxidants, may reverse the adverse effects of TNF-α in endothelial cells. This was done by pre-treating the endothelial cells EA.hy926 with PME (80 µg/ml) before subjecting them to apoptotic stimuli, which was TNF-α in combination with cyclohexamide. PME was found to rescue a population of cells from apoptosis induced by TNF-α modulating the levels of BCL2 and BAX involved in intrinsic apoptotic pathway. PME was found to increase the BCL-2/BAX ratio and reverse the elevated levels of effector caspase and thus assist cells to escape from apoptotic stimuli. Also, the extract was found to attenuate oxidative stress by reducing the levels of Reactive Oxygen Species (ROS). Supplementing its anti-atherosclerotic potential, PME pre-treatment diminished the elevated levels of adhesion molecules like VCAM upon TNF-α treatment. PME may therefore have therapeutic implications in protecting the endothelium from TNF-α triggered atherosclerosis.

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Тези доповідей конференцій з теми "BCL7"

Salame, Jéssica Paola, Lucas Loss Cantele, Gabriela Gavasso, Beliza Loss, and Karla Patricia Casemiro. "LINFOMA DIFUSO DE GRANDES CÉLULAS B CUTÂNEO SECUNDÁRIO À DOENÇA TESTICULAR PRÉVIA, COM 4 ANOS DE INTERVALO - RELATO DE CASO." In I Congresso Brasileiro de Estudos Patológicos On-line. Revista Multidisciplinar em Saúde, 2022. http://dx.doi.org/10.51161/conbesp/18.

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Introdução: Linfomas cutâneos podem ser primários ou secundários. Os primários são os mais frequentes linfomas extra-nodais, com incidência em torno de 10 casos por milhão de habitantes por ano, sendo que destes, 20-30% são Linfomas cutâneos primários de células B. Embora idênticos morfologicamente, podem mostrar cursos clínicos bem distintos, sendo os primários geralmente mais indolentes em comparação com os secundários, que apresentam maiores taxas de doença disseminada e estadiamento avançado ao diagnóstico. Em um estudo, disseminação cutânea foi notada entre 0 e 46 meses após a doença primária, com média de 11 meses. Objetivo: Relatar um caso de linfoma difuso de grandes células B cutâneo secundário à doença testicular, com 4 anos de intervalo. Material e métodos: Paciente masculino, 64 anos, exibindo lesões cutâneas enduradas, com bordos definidos, não-pruriginosas, eritemato-violáceas, em membro inferior direito. Recebidas biópsias incisionais das lesões que foram submetidas ao exame histopatológico e ao exame imuno-histoquímica. Resultados: As amostras histologicamente apresentavam preservação da epiderme, e infiltrado dérmico intersticial, com predomínio de células de médio a grande porte, com escasso citoplasma e núcleos hipercromáticos, com ocasionais nucléolos. Ao exame imuno-histoquímico revelou positividade para CD20, BCL6, BCL2, MUM1, CMYC e KI67 de 80%, fechando o diagnóstico de Linfoma Difuso de Grandes Células B (LDGCB), do tipo não-centro germinativo. Após liberação do laudo, recebemos a informação de histórico de LDGCB testicular há 4 anos anteriores ao aparecimento das lesões cutâneas. Foram pesquisadas ainda mutações de BCL2, BCL6 e CMYC por método FISH, sendo todas negativas. Conclusão: O paciente no caso em questão apresentou doença cutânea secundária após cerca de 48 meses, sendo um longo tempo de intervalo entre os dois eventos. Envolvimento cutâneo secundário à LDGCB sistêmico indica uma progressão de doença, e desfechos mais sombrios do que o LDGCB convencional sendo um caso incomum, com grande importância prognóstica e alta morbi-mortalidade, podendo ser de difícil diagnóstico e com amplo espectro de diferenciais ao exame clínico das lesões cutâneas. Além disso, ressalta-se a importância do recebimento de dados clínicos e história prévia do paciente para correlação clínico-patológica, que neste caso foram fundamentais para o diagnóstico, prognóstico e tratamento do paciente.

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Hoppe, Michal, Shuangyi Fan, Patrick Jaynes, Phuong Mai Hoang, Liu Xin, Sanjay De Mel, Li Mei Poon, et al. "Abstract PO-35: Prognostic significance of MYC, BCL2, and BCL6 colocalization at single-cell resolution in DLBCL." In Abstracts: AACR Virtual Meeting: Advances in Malignant Lymphoma; August 17-19, 2020. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/2643-3249.lymphoma20-po-35.

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Zoeller, JJ, RT Bronson, D. Sampath, J. Leverson, and JS Brugge. "Abstract P4-14-02: Neutralization of BCL2/BCL-XL enhances the cytotoxicity of T-DM1 in vivo." In Abstracts: Thirty-Eighth Annual CTRC-AACR San Antonio Breast Cancer Symposium; December 8-12, 2015; San Antonio, TX. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.sabcs15-p4-14-02.

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Onen, Onursal, Alper Sisman, Patricia Kruk, and Rasim O. Guldiken. "An Urinary Biosensor for Early Stage Ovarian Cancer Detection: Experimental Characterization." In ASME 2012 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/imece2012-87850.

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In this study, an experimental characterization of a piezoelectric ultrasonic MEMS biosensor for detection of anti-apoptotic protein Bcl-2 in sub ng/ml scale is presented. Bcl-2 is demonstrated to be elevated at different stages of ovarian cancer in urine ranging from 0.5 to 12 ng/ml. Here, shear horizontal (SH) polarized surface acoustic waves (SAWs) were utilized by interdigital transducers (IDTs), which were micro fabricated on piezoelectric ST cut Quartz wafers. SH SAWs were generated and sensed by a pair of IDTs, separated by judiciously designed a delay path in-between with for most effective Bcl-2 capture. The Bcl-2 concentration is characterized with respect to the change in resonance frequency. The target sensitivity for diagnosis and quantifying the stage of ovarian cancer is achieved with successful detection of Bcl-2 levels as low as 0.5 ng/ml. The results are promising for the sensor system to be used in a lab-on-a-chip platform for point of care urinary ovarian cancer monitoring diagnosis.

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Brock, Benjamin, Aydın Buluç, and Katherine Yelick. "BCL." In ICPP 2019: 48th International Conference on Parallel Processing. New York, NY, USA: ACM, 2019. http://dx.doi.org/10.1145/3337821.3337912.

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Walters, Madeline A., Zhaoyan Fan, and Burak Sencer. "Data-Based Modeling for Reactive Ion Etching: Effectiveness of an Artificial Neural Network Model for Estimating Tungsten Silicon Nitride Etch Rate." In ASME 2020 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2020. http://dx.doi.org/10.1115/imece2020-23992.

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Abstract This paper presents a data-based approach for modeling a plasma etch process by estimating etch rate based on controlled input parameters. This work seeks to use an Artificial Neural Network (ANN) model to correlate controlled tool parameters with etch rate and uniformity for a blanket 1100 Å WSiN thin film using Cl2 and BCl3 chemistry. Experimental data was collected using a Lam 9600 PTX plasma metal etch chamber in an industrial cleanroom. The WSiN film was deposited over 3000 Å TEOS to ensure adhesion, with an 8-inch bare silicon wafer as the base layer. Controlled tool parameters were radio frequency (RF) upper electrode power, RF lower electrode power, Cl2 gas flowrate, BCl3 gas flowrate, and chamber pressure. The full factorial design of experiment method was used to select the combinations of experimental configurations. The ANN model was validated using a subset of the training data.

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Onen, Onursal, Patricia Kruk, and Rasim Guldiken. "Design of Urinary Biomarker Sensor for Early Ovarian Cancer Detection." In ASME 2011 International Mechanical Engineering Congress and Exposition. ASMEDC, 2011. http://dx.doi.org/10.1115/imece2011-62818.

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In this paper, our efforts on the design, surface functionalization and characterization of ultrasonic MEMS sensor for early ovarian cancer is presented. The sensor detects urinary anti-apoptotic protein Bcl-2 level that has been presented as being elevated for different stages of ovarian cancer. Our novel biosensor approach employs a pair of MEMS ultrasound transducers for generating and sensing surface acoustic waves and a delay path in-between with oriented Bcl-2 antibodies (C8C) attached. Piezoelectric surface acoustic wave devices are employed for sensor for their high coupling efficiency and ease of fabrication. The sensor quantifies the cancer progression by detecting mass loading change generated by adhesion of Bcl-2 molecules to antibodies on the sensor surface. The device is fabricated using common MEMS fabrication techniques and a multi-step surface functionalization is utilized for effective protein adhesion. As a result, our biosensor platform has various unique advantages such as: ultra-sensitive (sub pg/ml), low cost, and simple operation (reminiscent of a pregnancy test) not necessitating trained personnel.

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Huang, Zi-Xian, and Chuan-Xian Ren. "Rethinking Correlation Learning via Label Prior for Open Set Domain Adaptation." In Thirty-Third International Joint Conference on Artificial Intelligence {IJCAI-24}. California: International Joint Conferences on Artificial Intelligence Organization, 2024. http://dx.doi.org/10.24963/ijcai.2024/98.

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Open Set Domain Adaptation (OSDA) aims to transfer knowledge from a labeled source domain to an unlabeled target domain, where known classes exist across domains while unknown classes are present only in the target domain. Existing methods rely on the clustering structure to identify the unknown classes, which empirically induces a large identification error if the unknown classes are a mixture of multiple components. To break through this barrier, we formulate OSDA from the view of correlation and propose a correlation metric-based framework called Balanced Correlation Learning (BCL). BCL employs Hilbert-Schmidt Independence Criterion (HSIC) to characterize the separation between unknown and known classes, where HSIC is reformulated as the nodes’ relation on graph. By considering the label prior as variable, theoretical results are derived to analytically show a sufficient condition for desired learning direction for OSDA. Methodologically, the class-balanced HSIC is proposed to preserve domain-invariant and class-discriminative features. With the guarantee of correlation learning, the entropy-based principle can effectively identify the unknown classes via uncertainty. Empirically, extensive evaluations are conducted, where BCL achieves significant performance improvements.

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Martinez Torre, S., C. Carreño, L. Sordo, AE Llosa, J. Ousley, A. Waziri, R. Mathela, RD Umar, J. Usman, and MJ Sagrado. "Severity, symptomatology, and treatment duration for paediatric mental health disorders: A retrospective analysis from a conflict affected region of northern Nigeria." In MSF Paediatric Days 2022. NYC: MSF-USA, 2022. http://dx.doi.org/10.57740/88gr-bc57.

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Yue, Lok Man, David Hau Wing Chau, Wenying Piao, (Eric) Wai Choi Tse, and Yok Lam Kwong. "Abstract 2166: Arsenic trioxide targets BCL6 oncoprotein for degradation in BCL6-dependent diffuse large B-cell lymphoma." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-2166.

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Звіти організацій з теми "BCL7"

Machen, Terry. BCL-2, Ca, and Apoptosis in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, August 2000. http://dx.doi.org/10.21236/ada394121.

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Kim, Hyeong-Reh. Role of Bcl-2 in Breast Cancer Progression. Fort Belvoir, VA: Defense Technical Information Center, August 1999. http://dx.doi.org/10.21236/ada383052.

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Xu, Liang. Tumor-Targeted Silencing of Bcl-2/Bcl-xl by Self-Assembled Sirna-Nanovectors as a Novel Molecular Therapy for Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, August 2007. http://dx.doi.org/10.21236/ada475350.

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Marassi, Francesca M. Structural Basis for Bcl-2-Regulated Mitochondrion-Dependent Apoptosis. Fort Belvoir, VA: Defense Technical Information Center, April 2004. http://dx.doi.org/10.21236/ada429719.

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Jamerson, Matthew. Cooperation of Bcl-XL and c-Myc in Mammary Tumorigenesis. Fort Belvoir, VA: Defense Technical Information Center, August 2000. http://dx.doi.org/10.21236/ada396438.

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Shul, R. J., C. I. H. Ashby, C. G. Willison, L. Zhang, J. Han, M. M. Bridges, S. J. Pearton, J. W. Lee, and L. F. Lester. GaN etching in BCl{sub 3}Cl{sub 2} plasmas. Office of Scientific and Technical Information (OSTI), April 1998. http://dx.doi.org/10.2172/658195.

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Schor, Nina F. Exploiting BCL-2 Overexpression in the Chemotherapy of Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, June 1998. http://dx.doi.org/10.21236/ada350950.

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Jamerson, Matthew H. Cooperation of Bcl-xL and c-Myc in Mammary Tumorigenesis. Fort Belvoir, VA: Defense Technical Information Center, August 1999. http://dx.doi.org/10.21236/ada391341.

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Nunez, Gabriel. Molecular Analysis of Bcl-xs-Induced Apoptosis in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, July 2000. http://dx.doi.org/10.21236/ada384375.

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Kennedy, C. H., K. D. Kenyon, and J. Tesfaigzi. Transfection of normal human bronchial epithelial cells with the bcl-2 oncogene. Office of Scientific and Technical Information (OSTI), December 1995. http://dx.doi.org/10.2172/381812.

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