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Triple-Negative Breast Cancer (TNBC) with Skin Involvement: Current Research Insights
Introduction to TNBC and Skin Involvement
Triple-negative breast cancer (TNBC) is a subtype of breast cancer characterized by the absence of estrogen and progesterone receptors and the lack of HER2 protein overexpression (ER–/PR–/HER2–). This subtype is known for its aggressive nature, poor prognosis, and limited treatment options due to the lack of targeted therapies. Skin involvement in TNBC, presenting as cutaneous metastases, is particularly distressing and challenging to treat.
Chemotherapy Combinations: Pegylated Liposomal Doxorubicin and Gemcitabine
Recent studies have explored the efficacy of combining pegylated liposomal doxorubicin (PLD) with gemcitabine in treating TNBC with skin involvement. This combination has shown promising results in cases with extensive cutaneous metastases. The use of PLD and gemcitabine has led to remarkable responses in some patients, suggesting that this regimen could be a viable option for managing skin-involved TNBC. However, further investigations are necessary to confirm these findings and establish standardized treatment protocols.
Genetic Heterogeneity and Early Metastasis in TNBC
TNBC is not only clinically aggressive but also exhibits significant genetic heterogeneity, which complicates treatment responses. Whole-exome sequencing of TNBC lesions has revealed extensive intrapatient and interpatient genetic diversity, with different mutational signatures at various stages of the disease. Notably, early metastasis to lymph nodes is a common feature in aggressive TNBC, often occurring before distant metastasis. Key genetic alterations, such as MCL1 amplifications and deletions in RB1 and PTEN, have been identified in metastatic lesions, providing potential targets for future therapies.
Bufotalin: A Potential Natural Compound for TNBC Treatment
Bufotalin, a natural compound derived from the toad Bufo gargarizan, has demonstrated significant anticancer properties in TNBC cell lines. Research indicates that bufotalin suppresses the proliferation and metastasis of TNBC cells by promoting apoptosis and inhibiting the STAT3/EMT signaling pathway. This compound effectively induces cell cycle arrest and caspase-mediated apoptosis, while also reducing the migration and invasion capabilities of TNBC cells by modulating key epithelial-mesenchymal transition (EMT) biomarkers and matrix metalloproteinases (MMPs). These findings suggest that bufotalin could be a promising candidate for developing new TNBC treatment strategies.
Conclusion
The management of TNBC, particularly with skin involvement, remains a significant challenge due to its aggressive nature and genetic complexity. The combination of pegylated liposomal doxorubicin and gemcitabine has shown potential in treating cutaneous metastases, while the genetic heterogeneity of TNBC underscores the need for personalized treatment approaches. Additionally, natural compounds like bufotalin offer new avenues for therapy by targeting specific molecular pathways. Continued research is essential to develop effective treatments and improve outcomes for patients with TNBC.
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