A5093645874- PARP inhibition in cancer therapy
- Ovarian cancer diagnosis and treatment
- Autophagy in Disease and Therapy
- Calcium signaling and nucleotide metabolism
- Colorectal Cancer Treatments and Studies
- Cell death mechanisms and regulation
- Intraperitoneal and Appendiceal Malignancies
- Genomics, phytochemicals, and oxidative stress
- Colorectal and Anal Carcinomas
The University of Texas MD Anderson Cancer Center
2024
Pancreatic ductal adenocarcinoma (PDAC) and low-grade ovarian cancer (LGSOC) are characterized by the prevalence of KRAS oncogene mutations. DIRAS3 is first endogenous non-RAS protein that heterodimerizes with RAS, disrupts RAS clustering, blocks signaling, inhibits cell growth. Here, we found DIRAS3-mediated inhibition induces ROS-mediated apoptosis in PDAC LGSOC cells mutations, but not wild-type KRAS, downregulating NFE2L2/Nrf2 transcription, reducing antioxidants, inducing oxidative...
Abstract Poly (ADP-ribose) polymerase inhibitors (PARPi) can encounter resistance through various mechanisms, limiting their effectiveness. Our recent research showed that PARPi alone induce drug by promoting autophagy. Moreover, our studies have revealed anaplastic lymphoma kinase (ALK) plays a role in regulating the survival of ovarian cancer cells undergoing Here, we explored whether ALK-inhibitor crizotinib could enhance efficacy targeting drug-induced autophagic cell and xenograft...
<div>Abstract<p>Poly (ADP-ribose) polymerase inhibitors (PARPi) can encounter resistance through various mechanisms, limiting their effectiveness. Our recent research showed that PARPi alone induce drug by promoting autophagy. Moreover, our studies have revealed anaplastic lymphoma kinase (ALK) plays a role in regulating the survival of ovarian cancer cells undergoing Here, we explored whether ALK-inhibitor crizotinib could enhance efficacy targeting drug-induced autophagic cell...
<div>Abstract<p>Poly (ADP-ribose) polymerase inhibitors (PARPi) can encounter resistance through various mechanisms, limiting their effectiveness. Our recent research showed that PARPi alone induce drug by promoting autophagy. Moreover, our studies have revealed anaplastic lymphoma kinase (ALK) plays a role in regulating the survival of ovarian cancer cells undergoing Here, we explored whether ALK-inhibitor crizotinib could enhance efficacy targeting drug-induced autophagic cell...
<p>Supplementary Figure S3 shows the viability of ovarian cancer cells treated with other PARPi in combination Olaparib</p>
<p>Supplementary Figure S2 shows dose response curves, colony formation assays and viability of Olaparib resistant cells treated with crizotinib</p>
<p>Supplementary Figure S7 shows the effect of knocking down ALK on sensitivity ovarian cancer cells to Olaparib/crizotinib combination</p>
<p>Supplementary Figure S5 shows induction of ROS, DNA damage and apoptosis after treatment with Olaparib crizotinib</p>
<p>Supplementary Figure S5 shows induction of ROS, DNA damage and apoptosis after treatment with Olaparib crizotinib</p>
<p>Supplementary Figure S4 shows induction of autophagy after treatment with the combination Olaparib and crizotinib</p>
<p>Supplementary Figure S3 shows the viability of ovarian cancer cells treated with other PARPi in combination Olaparib</p>
<p>Supplementary Figure S6 shows the effect of combination Olaparib and crizotinib in tumor growth</p>
<p>Supplementary Figure S7 shows the effect of knocking down ALK on sensitivity ovarian cancer cells to Olaparib/crizotinib combination</p>
<p>Supplementary Figure S4 shows induction of autophagy after treatment with the combination Olaparib and crizotinib</p>
<p>Supplementary Figure S6 shows the effect of combination Olaparib and crizotinib in tumor growth</p>
<p>Supplementary Figure S1 shows CI values and IC50 of Olaparib Olaparib/crizotinib</p>
<p>Supplementary Figure S1 shows CI values and IC50 of Olaparib Olaparib/crizotinib</p>
<p>Supplementary Figure S2 shows dose response curves, colony formation assays and viability of Olaparib resistant cells treated with crizotinib</p>
<h3>Background</h3> Appendiceal cancer's mucinous nature and scant cellularity significantly restrict traditional molecular analyses. Single cell sequencing overcomes technical challenges of bulk but lacks spatial information. To address this, we employed digital profiling to select regions interest exclusive mucin pools better isolate the tumor compartment. Specimens from patients in a recently completed trial combination immune checkpoint blockade (ICB) VEGF inhibition...