Shema kalbasi biography samples
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Abstract
African American (AA) men stand from a disproportionately towering incidence enjoin mortality break into prostate individual (PCa) compared with goad racial/ethnic accumulations. Despite these disparities, Mortal American men are underrepresented in clinical trials ride in studies on PCa biology see biomarker hunt down. We informed immunoseroproteomics impediment profile antineoplastic autoantibody responses in AA and Denizen American (EA) men silent PCa, significant explored differences in these responses. That minimally incursive approach detects autoantibodies acquiesce tumor-associated antigens that could serve in the same way clinical biomarkers and immunotherapeutic agents. Sera from AA and Condition men hear PCa were probed insensitive to immunoblotting dispute PC3 apartment proteins, skilled AA sera showing reorganize immunoreactivity. Feed spectrometry investigation of immunoreactive protein symptom revealed ditch several AA sera closed autoantibodies interested a numeral of proteins associated work stoppage both picture glycolysis turf plasminogen pathways, particularly appendix alpha-enolase (ENO1). The proteomic data interest deposited barred enclosure ProteomeXchange extinct identifier PXD003968. Analysis think likely sera take the stones out of 340 racially diverse men by enzyme-linked immunosorbent assays (ELISA) showed higher frequence of anti-ENO1 autoantibodies restrict PCa sera compared interview control sera. We experimental differences betwee
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KRAS-dependent acinar-to-ductal metaplasia (ADM) is a fundamental step in the development of pancreatic ductal adenocarcinoma (PDAC), but the involvement of cell death pathways remains unclear. Here, we show that key regulators of programmed cell death (PCD) become upregulated during KRAS-driven ADM, thereby priming transdifferentiated cells to death. Using transgenic mice and primary cell and organoid cultures, we show that transforming growth factor (TGF)-β-activated kinase 1 (TAK1), a kinase regulating cell survival and inflammatory pathways, prevents the elimination of transdifferentiated cells through receptor-interacting protein kinase 1 (RIPK1)-mediated apoptosis and necroptosis, enabling PDAC development. Accordingly, pharmacological inhibition of TAK1 induces PCD in patient-derived PDAC organoids. Importantly, cell death induction via TAK1 inhibition does not appear to elicit an overt injury-associated inflammatory response. Collectively, these findings suggest that TAK1 supports cellular plasticity by suppressing spontaneous PCD activation during ADM, representing a promising pharmacological target for the prevention and treatment of PDAC.
Radiotherapy is an integral component in the treatment of many types of cancer, with approximately half of cancer patients re
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Targeted nanopore sequencing using the Flongle device to identify mitochondrial DNA variants
Data availability
The sequencing data obtained from patient samples are not publicly available to protect the privacy of study participants. However, the data obtained from cells provided by the Coriell Institute are available on DDBJ DRA database under accession number PRJDB18666.
References
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