Satyendra Kumar Rajput1*, Vishal Kumar Dubey2, Shalini Singh1 and Swati Madan3
Bartogenic Acid (BA) is a natural triterpenoid compound found in several plants, including Barleria lupulina, Croton tiglium, and Euphorbia hirta. It has been shown to exhibit a wide range of pharmacological activities, including anti-inflammatory, anti-cancer and anti-oxidant properties. BA has been shown to exhibit promising anti-cancer properties in various studies. In particular, BA is effective against a variety of cancer cell lines, including breast, lung, and colon cancer. Its ability to induce apoptosis, inhibit cell proliferation, and suppress tumor angiogenesis makes it a potential therapeutic agent for various cancers. BA has been demonstrated to induce apoptosis in cancer cells through various mechanisms, including activation of the caspase cascade, downregulation of Bcl-2, and upregulation of Bax. It also inhibits cell proliferation by arresting cell cycle progression at the G1/S checkpoint. Additionally, BA suppresses tumor angiogenesis by inhibiting the expression of Vascular Endothelial Growth Factor (VEGF). The molecular mechanisms underlying BA's anti-cancer effects are not fully elucidated, but several potential pathways have been identified. BA has been shown to interact with various signaling molecules, including nuclear factor-κB (NF-κB), Mitogen-Activated Protein Kinase (MAPK), and phosphatidylinositol 3-kinase/Akt (PI3K/Akt) pathways. BA is also a potent inhibitor of topoisomerase I and II, which are enzymes that are involved in DNA replication which suggests that BA may be able to prevent cancer cells from replicating and dividing. This review summarizes the current understanding of BA's anti-cancer effects and its possible mechanisms of action. Further research is warranted to fully elucidate the molecular mechanisms underlying BA's anti-cancer effects and to evaluate its potential for clinical development.
Hala Ahmed Zaghloul1,2*, Lulwah Abduljabbar2, Karim Abdel Halim3 and Miral Mashhour4
Purpose: To depict Progesterone Receptor (PR) expression exerted modulations on Oncotype-DX Recurrence Scores (RS) in immunehistochemically determined node-negative luminal-B-like breast cancers with Ki67 between ≥ 14% and <30% alongside their potentials in forecasting the outcome.
Methods: The impact of PR variations on Oncotype-Dx RS alongside their implications to the different prognosticators, including adjuvant chemotherapy, local and distant Recurrence-Free Survival (RFS) were scrutinized. Additionally, the concordance of the Hormone Receptor (HR) quantifying approaches devising immune staining and Reverse Transcriptase-Polymerase Reaction (RT-PCR) were statistically particularized.
Results: We selected 250 surgically treated node-negative Luminal-B1 (Ki67 ≥ 14%-<20%) and Luminal-B2(Ki67 ≥20%-<30%) breast cancers who had Oncotype-DX RS analyzed. The PR ≤ 20% was linked to high-grades tumors (P=0.013, 0.012) and accentuated Oncotype-DX RS (P=0.003, 0.001) in both Luminal-B1and B2. Multivariate regression revealed that PR ≤ 20% was a substantial forecaster of the enhanced RS and the adjuvant chemotherapy use (P<0.0001, 0.002), respectively. The Cox regression divulged that the accentuated Oncotype-Dx RS alongside the PR ≤ 20% were independently attributed to lower RFS, with a hazard ratio of 1.84 (95% confidence interval [CI], 3.67-8.14) and 2.53 (95% CI, 2.62-6.12), respectively. Furthermore, ER and PR characterized by immune staining and RT-PCR were concordant in 98.2% and 86.7% of cases.
Conclusion: In node-negative luminal-B with Ki67 between ≥14% and <30% breast cancers, PR ≤ 20% was a robust prognosticator of enhanced RS and adjuvant chemotherapy. The accentuated RS and PR ≤ 20% were independently attributed to reduced recurrence-free survival. Furthermore, a substantial concordance was attained between HR status defined by immune staining and RT-PCR that mounted up to 98.2% and 86.7% for ER and PR, respectively.