Signalling Pathways and Inhibitors in Triple Negative Breast Cancer: Current Progress

Area of Science:

• Oncology
• Molecular Biology
• Genetics

Background:

• Triple Negative Breast Cancer (TNBC) is an aggressive breast cancer subtype, accounting for 15% of all breast cancer diagnoses.
• TNBC is characterized by the absence of HER2, estrogen, and progesterone receptors, limiting targeted treatment options and primarily affecting younger women.
• The disease's rapid progression, high recurrence rates, and propensity for metastasis contribute to a poor prognosis, necessitating novel therapeutic strategies.

Purpose of the Study:

• To review current and emerging therapeutic strategies for Triple Negative Breast Cancer.
• To highlight the potential of targeting dysregulated signaling pathways in TNBC.
• To discuss challenges and future directions in TNBC treatment.

Main Methods:

• Review of recent clinical and molecular research findings on TNBC treatment.
• Identification of dysregulated signaling pathways (PI3K/AKT/mTOR, JAK/STAT, Wnt/β-catenin, Notch, MAPK/ERK) as therapeutic targets.
• Evaluation of novel treatment modalities including immune checkpoint inhibitors and Antibody-Drug Conjugates (ADCs).

Main Results:

• Immune checkpoint inhibitors (e.g., Pembrolizumab) combined with chemotherapy show significant benefits in early-stage and metastatic TNBC.
• Antibody-Drug Conjugates (ADCs) like sacituzumab govitecan demonstrate efficacy in advanced TNBC by delivering cytotoxic agents and improving progression-free survival.
• Despite advancements, significant obstacles such as tumor heterogeneity and treatment resistance remain critical challenges.

Conclusions:

• Small molecule inhibitors and combination therapies offer beneficial effects for TNBC treatment.
• Targeting dysregulated signaling pathways presents a promising avenue for developing new TNBC therapies.
• Future research should focus on identifying predictive biomarkers and refining personalized treatment plans to improve outcomes for TNBC patients.