Publications by authors named "J P Trevino"
Early pregnancy loss (EPL), also known as miscarriage or spontaneous abortion, makes up 15-20% of all clinically recognized pregnancies. EPL is a broad term that includes intrauterine pregnancies (IUPs) with findings that suggest the pregnancy may not progress or definitely will not progress; pregnancies with a gestational sac (GS) in the lower endometrial cavity or endocervical canal in the process of expulsion; residual pregnancy tissue or persistent GS; and complete passage of the GS without residual tissue. This document addresses medication management of EPL in which the complete passage of the GS has not yet occurred, including pregnancies concerning for and diagnostic of EPL (sometimes called "missed abortion") and EPL in progress.
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- The study investigates how cancer cells influence the fitness of surrounding tumor microenvironment (TME) cells through a mechanism involving a long non-coding RNA called Tu-Stroma, which alters the expression of Flower isoforms, impacting their growth advantage.
- The expression of Flower Win isoforms in cancer cells enhances their dominance over TME cells that express Flower Lose isoforms, leading to reduced fitness in the TME.
- Targeting Flower proteins with a humanized monoclonal antibody in mice has shown promising results, significantly reducing cancer growth and metastasis while improving survival rates and protecting organs from potential lesions.
KRAS G12C targeted therapies, such as sotorasib, represent a major breakthrough, but overall response rates and progression-free survival for patients with KRAS G12C lung cancer are modest due to the emergence of resistance mechanisms involving adaptive reactivation of ERK, which requires wild-type (WT) HRAS and NRAS membrane localization. Here, we demonstrate that the dual farnesyltransferase (FT) and geranylgeranyltransferase-1 (GGT-1) inhibitor FGTI-2734 inhibits WT RAS membrane localization and sotorasib-induced ERK feedback reactivation, and overcomes sotorasib adaptive resistance. The combination of FGTI-2734 and sotorasib is synergistic at inhibiting the viability and inducing apoptosis of KRAS G12C lung cancer cells, including those highly resistant to sotorasib.
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- Oncogenic KRAS signaling is vital in pancreatic ductal adenocarcinoma (PDAC), and previous treatments targeting MEK and BCL-xL were ineffective due to amplified EGFR signaling in patients.
- A new strategy using a triplet therapy involving trametinib (MEK inhibitor), DT2216 (BCL-xL degrader), and afatinib (EGFR inhibitor) showed improved results in killing PDAC cells both in lab tests and in mouse models.
- The combination produced significantly better tumor growth reduction compared to double treatments and highlighted EGFR's role, suggesting this triplet approach warrants clinical testing for PDAC patients.
Despite many decades of research, pancreatic ductal adenocarcinoma (PDAC) remains one of the most difficult cancers to diagnose and treat effectively. Although there have been improvements in the 5-year overall survival rate, it is still very low at 12.5%.
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