Human Bcl2 Modifying Factor Elisa Kit (BMF)
- Known as:
- Human Bcl2 Modifying Factor Elisa Kit (BMF)
- Catalog number:
- E01B0573
- Product Quantity:
- 96 Tests/kit
- Category:
- -
- Supplier:
- Other suppliers
- Gene target:
- Human Bcl2 Modifying Factor Elisa Kit (BMF)
Related genes to: Human Bcl2 Modifying Factor Elisa Kit (BMF)
- Gene:
- BCL2 NIH gene
- Name:
- BCL2 apoptosis regulator
- Previous symbol:
- -
- Synonyms:
- Bcl-2, PPP1R50
- Chromosome:
- 18q21.33
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-22
- Date modifiied:
- 2019-04-23
- Gene:
- BMF NIH gene
- Name:
- Bcl2 modifying factor
- Previous symbol:
- -
- Synonyms:
- FLJ00065
- Chromosome:
- 15q15.1
- Locus Type:
- gene with protein product
- Date approved:
- 2004-01-16
- Date modifiied:
- 2016-10-05
Related products to: Human Bcl2 Modifying Factor Elisa Kit (BMF)
Related articles to: Human Bcl2 Modifying Factor Elisa Kit (BMF)
- Primary leiomyosarcoma of the breast is an extremely rare malignancy, accounting for less than 1% of all breast tumors. Diagnosis is challenging because its morphology overlaps with that of other spindle cell lesions, and standardized treatment guidelines are currently unavailable. A 44-year-old woman presented with a rapidly enlarging, firm, 14.8 cm mass in the left breast. She had previously undergone surgery elsewhere, with diagnoses of leiomyoma and desmoid-type fibromatosis. Imaging demonstrated a lobulated mass without evidence of metastasis. Excision revealed pleomorphic spindle cells arranged in intersecting fascicles, with necrosis and dermal invasion. Primary breast leiomyosarcoma was confirmed by immunohistochemistry, which demonstrated smooth muscle actin and desmin positivity and negative staining for pancytokeratin, p63, S100, CD34, and BCL2. The patient underwent modified radical mastectomy followed by adjuvant radiotherapy and chemotherapy. Primary breast leiomyosarcoma is a rare entity that remains diagnostically challenging. Immunohistochemistry is essential for accurate diagnosis, and optimal management requires a dedicated multidisciplinary approach. - Source: PubMed
Publication date: 2026/06/15
Pitambra AshwiniRath AshutoshPradeep ImmanuelRamavath KrishnaRamalingam Chandramouli - Wang et al. Ibrutinib plus venetoclax for relapsed/refractory mantle cell lymphoma: Final analysis of the phase 3 SYMPATICO study. Br J Haematol (Online ahead of print). - Source: PubMed
Publication date: 2026/06/14
Eyre Toby A - Classic BCR::ABL1-negative myeloproliferative neoplasms (MPNs)-polycythaemia vera, essential thrombocythaemia, and primary myelofibrosis-are clonal haematopoietic stem cell disorders with marked heterogeneity in clinical phenotype, disease trajectory, and therapeutic response. Genomic stratification by driver and cooperating mutations only partially accounts for this variability, leaving gaps in predicting thrombotic risk, fibrotic progression, leukaemic transformation, and treatment benefit. Proteomics bridges this gap by providing function-proximal readouts of protein abundance, post-translational modifications, pathway activity, and intercellular signalling that genomics and transcriptomics cannot capture, positioning it as a theranostic platform in which the same molecular readouts simultaneously inform diagnostic stratification and therapeutic decision-making. We propose a five-stage translational framework spanning from discovery-scale mass spectrometry and affinity-based plasma profiling to targeted validation, multicentre standardisation, and machine learning-integrated clinical panels. Proteomic evidence is synthesised across the following four disease axes: clonal fitness in haematopoietic stem and progenitor cells; bone marrow microenvironmental remodelling and fibrosis; chronic inflammation and thrombosis; and leukaemic transformation. We further describe how phosphoproteomics reveals resistance mechanisms to JAK inhibitors, including AXL-MAPK bypass and PP2A-autophagy-mediated tolerance, and how protein-level biomarkers (BCL2-BCL-XL, RAS-ERK, CAMK2G, and ROCK1/2) can guide individualised therapeutic selection. Affinity-based platforms (Olink PEA and SomaScan) and spatially resolved technologies (CODEX and single-cell proteomics) complement discovery proteomics. At present, however, this evidence base is constrained by small and heterogeneous cohorts, limited cross-platform reproducibility, and a scarcity of independent external validation for candidate protein panels. Realising this vision will require multicentre standardisation, analytically validated panel assays, and prospective clinical studies that translate molecular findings into decision-grade tools for patients with MPNs. - Source: PubMed
Publication date: 2026/06/14
Zhang JingHan Yan-Qiu - The failure of second-generation antiandrogen drugs such as enzalutamide (ENZ) treatment indicates that prostate cancer (PCa) can progress to castration-resistant prostate cancer (CRPC). CRPC is considered the terminal stage of PCa and currently has no effective treatment options due to drug resistance. However, the underlying mechanism of ENZ- resistance in CRPC remains unclear. Here, we conducted a single-cell transcriptomic analysis in combination with a gene module clustering assessment to identify the regulatory genes enriched along the hormone-sensitive PCa and CRPC trajectories. This approach revealed that tripartite motif-containing 17 (TRIM17) is a specific time-dependent gene and key regulator that is expressed at significantly low levels in CRPC cells but at high levels in nonresistant epithelial PCa cells. Analysis of patient-derived clinical specimens and in vitro functional experiments demonstrated that TRIM17 low expression could promote CRPC progression and ENZ resistance. Moreover, TRIM17 activation markedly inhibited CRPC progression and enhanced the sensitivity of CRPC cells to ENZ. Mechanistically, TRIM17 binds to and ubiquitinates B-cell lymphoma-2 (BCL2) directly to mediate its degradation. On the other hand, TRIM17 represses BCL2 by inhibiting p53 degradation by TRIM28. The stabilization of p53 suppresses BCL2 expression and interferes with the abundance and signaling of BCL2 in CRPC cells, further inhibiting CRPC progression and conveying ENZ resensitivity. Importantly, the TRIM17 activator pioglitazone, a registered drug for type 2 diabetes, could synergize with ENZ to reverse ENZ resistance and amplify its cytotoxic effects on CRPC cells. In conclusion, this study identifies a previously undefined function of TRIM17 to modulate ENZ sensitivity and reveals that activation of TRIM17 has great potential as a promising therapeutic strategy for ENZ- resistant PCa, indicating that TRIM17 can serve as a biomarker to guide the treatment of CRPC. - Source: PubMed
Publication date: 2026/06/13
Shang ZhiLin GuowenYu LiuLiu ShiweiZhang YongqingZheng ShengfengHong ZongyuanHong ZheYe Dingwei - Although inflammation protects our bodies against harmful stimuli, uncontrolled inflammation drives serious chronic disorders. Malva parviflora L. (family Malvaceae) may represent a source for anti-inflammatory metabolites based on its potent anti-inflammatory activity. Its total ethanol extract demonstrated notable inhibition of cyclooxygenase-1/2 (COX-1/COX-2) and 5-lipoxygenase (5-LOX), with IC values comparable to those of the reference drugs indomethacin and zileuton, respectively. The hexane fraction was the most active fraction (lowest IC₅₀) among the solvent partitions (dichloromethane, ethyl acetate, and butanol). Subsequent column chromatography of the hexane fraction produced two compounds: Cassipourol, isolated for the first time from the Malvaceae family, and β-sitosterol. Their structures were confirmed by matching their NMR and mass spectrometry data with literature. Both were validated in vitro as dual COX/LOX inhibitors, exhibiting IC₅₀ values comparable to those of the standards. To uncover additional mechanisms, a compound-target-inflammation network was constructed using network pharmacology approaches, revealing 178 shared targets. Among these, tumor necrosis factor (TNF-α) and the antiapoptotic protein B-cell lymphoma 2 (BCL-2) emerged as central nodes linked to inflammatory pathways. Subsequent assays in human colon carcinoma (Caco-2) and lung adenocarcinoma (A549) cell lines showed that β-sitosterol suppressed TNF-α and BCL-2 by approximately 55%, whereas cassipourol displayed only modest inhibition (~20%). Molecular docking predicted moderate (ca. -4.5) and strong (> -5) binding affinities of both compounds to key inflammatory targets. Collectively, these results suggest that β-sitosterol from M. parviflora is a promising multitarget lead for inflammatory disorders, including cancer, whereas cassipourol requires further structural optimization and mechanistic investigation to improve its unfavorable physicochemical properties. - Source: PubMed
Publication date: 2026/06/13
Anwar Mohamed AEl Gedaily Rania AAboulthana Wael MElshewy AhmedKandil Zeinab AAbdel-Dayem Shymaa I A