Progesterone is essential for pregnancy maintenance, but its effects on complications like intrauterine growth restriction (IUGR), preeclampsia, prelabor rupture of membranes (PROM), preterm birth, and placental abruption are still debated. This review investigates the effects of progesterone supplementation on Doppler ultrasound indices and pregnancy outcomes. To assess the efficacy of progesterone supplements in reducing pregnancy complications during the first and second trimesters using Doppler ultrasound indices. Databases such as PubMed, Embase, the Cochrane Library, MEDLINE, Web of Science, Scopus, and Google Scholar were searched from inception to March 2024. Cohort, case–control, and clinical trials on progesterone supplementation in early to mid-pregnancy were included in the review. The primary outcomes were Doppler ultrasound indices, with secondary outcomes including preterm birth, IUGR, preeclampsia, PROM, and placental abruption. Nine studies with 2282 women were examined. Independent reviewers extracted data and assessed its quality, resolving discrepancies through consensus. Progesterone supplementation had varying effects on Doppler indices. There was no significant difference in uterine or umbilical artery Doppler indices, but some studies reported changes in fetal middle cerebral artery flow. Furthermore, there were no significant improvements in the rates of IUGR, preeclampsia, or PROM. Progesterone supplementation in early and mid-pregnancy may benefit certain subgroups, particularly those at risk of preterm birth. However, its overall effectiveness in improving clinical outcomes is unclear. More research using standardized progesterone regimens is needed to better understand its role in pregnancy management. Progesterone supplementation may help prevent preterm birth in high-risk populations, such as women with a short cervix. However, Doppler ultrasound findings should not be the sole factor in guiding its use. However, its role in improving other clinical outcomes, such as IUGR and preeclampsia, remains uncertain. Obstetricians should consider progesterone use as part of individualized treatment plans, particularly for women at high risk for preterm birth.

Hematological malignancies, including multiple myeloma (MM), leukemia, and lymphoma, represent a major global health burden, accounting for approximately 6.6% of all cancer cases and contributing to significant mortality. The evolutionary conserved WNT/β-catenin signaling pathway is a critical regulator of normal hematopoietic stem cell homeostasis, and its dysregulation is a hallmark of various hematological malignancies. Aberrant activation through mutations, overexpression of ligands, or disruption of the destruction complex drives uncontrolled proliferation, impaired differentiation, and therapeutic resistance to therapy in acute and chronic leukemias, lymphomas, and multiple myeloma. Therapeutic interventions targeting this pathway, such as GSK-3 inhibitors, β-catenin antagonists, and small molecules like CWP291 and salinomycin, have demonstrated promising antitumor effects. Furthermore, combining WNT/β-catenin inhibition with targeted or epigenetic therapies, such as venetoclax and chidamide, can produce synergistic antitumor effects and overcome chemoresistance. Despite this potential, clinical translation is hampered by on-target toxicities in healthy tissues, pathway complexity, and a lack of predictive biomarkers. We conclude that the future of WNT-directed therapy lies in developing biomarker-selective agents, advanced drug delivery systems to improve specificity, and exploring novel combinations with immunotherapy to harness the anti-tumor immune response.

Dysregulation of the c-Myc oncogene is a pivotal event in leukemia pathogenesis and therapy resistance. This review synthesizes current evidence, illustrating that c-Myc drives leukemogenesis by enhancing proliferation, inhibiting apoptosis, and upregulating immune checkpoints like PD-L1. Its overexpression is linked to poor treatment outcomes across various leukemia subtypes. Directly targeting c-Myc remains challenging; however, indirect epigenetic modifiers (BET inhibitors), transcriptional disruption (CDK9 inhibitors), and combination therapies emerge as promising strategies to suppress its oncogenic activity and overcome resistance, paving the way for improved clinical management.