Publications by authors named "Mustafa Emre Gedik"
Article Synopsis
- Tamoxifen is a common treatment for a type of breast cancer, but some patients can become resistant to it, meaning the medicine doesn't work anymore.
- A long non-coding RNA called LINC00152 stops cells from dying in a specific way when tamoxifen is used, which makes the cancer harder to treat.
- Researchers discovered that blocking LINC00152 can help make tamoxifen work better by changing how certain proteins and chemicals behave in the cancer cells, leading to more effective treatment.
Tamoxifen has been the mainstay therapy to treat early, locally advanced, and metastatic estrogen receptor-positive (ER+) breast cancer, constituting around 75% of all cases. However, emergence of resistance is common, necessitating the identification of novel therapeutic targets. Here, we demonstrated that long-noncoding RNA LINC00152 confers tamoxifen resistance via blocking tamoxifen-induced ferroptosis, an iron-mediated cell death.
View Article and Find Full Text PDFEffectiveness of metformin for the reversal of cold-ischemia-induced damage in hepatosteatosis.
Clin Res Hepatol Gastroenterol
April 2024
Background: Primary dysfunction and rejection are more common in donor liver tissues with steatosis. AMP-activated protein kinase (AMPK) assumes organ-protective functions during ischemia. Metformin was used for the activation of AMPK in hepatocytes.
View Article and Find Full Text PDFUnlabelled: Trastuzumab emtansine (T-DM1) was the first and one of the most successful antibody-drug conjugates (ADC) approved for treating refractory HER2-positive breast cancer. Despite its initial clinical efficacy, resistance is unfortunately common, necessitating approaches to improve response. Here, we found that in sensitive cells, T-DM1 induced spindle assembly checkpoint (SAC)-dependent immunogenic cell death (ICD), an immune-priming form of cell death.
View Article and Find Full Text PDFArticle Synopsis
- Immunogenic cell death (ICD) is a special type of cell death that helps the immune system fight cancer, and it can be triggered by some cancer treatments.
- A drug called T-DM1 can lead to ICD in cancer cells, but some patients don't respond to it because they have a higher level of a protein called TACC3.
- Blocking TACC3 can help T-DM1 work better by making the immune system recognize and attack cancer cells more effectively.
Background: Intriguingly, liver regeneration after injury does not induce uncontrolled growth and the underlying mechanisms of such a "hepatostat" are still not clear. Endocan, a proteoglycan, was implicated in liver regeneration. It can support the function of hepatocyte growth factor/scatter factor in tissue repair after injury.
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