Shema kalbasi biography samples

  • African American (AA) men suffer from a disproportionately high incidence and mortality of prostate cancer (PCa) compared with other racial/ethnic groups.
  • To elucidate the mechanisms of TAM-mediated early cellular repopulation and transcriptional programs that precede detectable changes in tumor.
  • Samples evaluated were taken immediately prior to 1) commencing initial chemotherapy, 2) prior to the second infusion (for the first 6 patients only), 3) prior.

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    Abstract

    African American (AA) men suffer from a disproportionately high incidence and mortality of prostate cancer (PCa) compared with other racial/ethnic groups. Despite these disparities, African American men are underrepresented in clinical trials and in studies on PCa biology and biomarker discovery. We used immunoseroproteomics to profile antitumor autoantibody responses in AA and European American (EA) men with PCa, and explored differences in these responses. This minimally invasive approach detects autoantibodies to tumor-associated antigens that could serve as clinical biomarkers and immunotherapeutic agents. Sera from AA and EA men with PCa were probed by immunoblotting against PC3 cell proteins, with AA sera showing stronger immunoreactivity. Mass spectrometry analysis of immunoreactive protein spots revealed that several AA sera contained autoantibodies to a number of proteins associated with both the glycolysis and plasminogen pathways, particularly to alpha-enolase (

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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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    3. P Grady, J. et al. mtDNA heteroplasmy level and copy number indicate disease burden in m.3243A > G mitochondrial disease. EMBO Mol. Med.https://doi.org/10.15252/emmm.201708262 (2018).

    4. Wei, W

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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 fängelse 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 s

    5. shema kalbasi biography samples