RESUMO
T-DM1 (Trastuzumab Emtansine) belongs to class of Antibody-Drug Conjugates (ADC), where cytotoxic drugs are conjugated with the antibody Trastuzumab to specifically target HER2-positive cancer cells. Platelets, as vital components of the blood system, intricately influence the immune response to tumors through complex mechanisms. In our study, we examined platelet surface proteins in the plasma of patients before and after T-DM1 treatment, categorizing them based on treatment response. We identified a subgroup of platelets with elevated expression of CD63 and CD9 exclusively in patients with favorable treatment responses, while this subgroup was absent in patients with poor responses. Another noteworthy discovery was the elevated expression of CD36 in the platelet subgroups of patients exhibiting inadequate responses to treatment. These findings suggest that the expression of these platelet surface proteins may be correlated with the prognosis of T-DM1 treatment. These indicators offer valuable insights for predicting the therapeutic response to T-DM1 and may become important references in future clinical practice, contributing to a better understanding of the impact of ADC therapies and optimizing personalized cancer treatment strategies.
Assuntos
Ado-Trastuzumab Emtansina , Plaquetas , Neoplasias da Mama , Humanos , Feminino , Plaquetas/efeitos dos fármacos , Neoplasias da Mama/tratamento farmacológico , Neoplasias da Mama/sangue , Ado-Trastuzumab Emtansina/uso terapêutico , Pessoa de Meia-Idade , Trastuzumab/uso terapêutico , Antineoplásicos Imunológicos/uso terapêutico , Adulto , Idoso , Maitansina/uso terapêutico , Maitansina/análogos & derivadosRESUMO
Breast cancer, as a highly prevalent cancer among women, is one of the main causes of female mortality due to cancer. There is a need for more treatment options to improve the survival time of breast cancer patients. Metastasis to distant organs is a standard indicator of advanced breast cancer and a primary cause of breast cancer mortality, making the control of breast cancer metastasis crucial. Targeted therapy, with its advantages of precision, high effectiveness, and minimal side effects, has garnered significant attention as a hot research topic in breast cancer treatment. Among these therapies, anti-angiogenic therapy aim to inhibit tumor angiogenesis, control tumor growth, and reduce metastasis. Additionally, anti-angiogenic therapy can restructure the tumor vasculature, enhancing the effectiveness of other anti-cancer drugs. Lenvatinib, an orally available small molecule multi-targeted tyrosine kinase inhibitor, exerts its anti-tumor effects mainly by inhibiting tumor angiogenesis and tumor cell proliferation. It has been approved for the treatment of thyroid cancer, renal cell carcinoma, and hepatocellular carcinoma. Due to its multi-targeted nature, lenvatinib not only has direct anti-tumor effects but also possesses immunomodulatory activity, which can enhance the tumor immune response. This makes it a promising candidate for a broad range of cancers. Recent studies have explored the role of lenvatinib in breast cancer, including its various mechanisms of action and its use as a monotherapy or in combination to control breast cancer progression. This review will summarize the molecular mechanisms and research progress of lenvatinib in breast cancer treatment, discussing its potential applications and therapeutic prospects in managing breast cancer.
Assuntos
Antineoplásicos , Neoplasias da Mama , Compostos de Fenilureia , Quinolinas , Humanos , Quinolinas/uso terapêutico , Compostos de Fenilureia/uso terapêutico , Neoplasias da Mama/tratamento farmacológico , Neoplasias da Mama/patologia , Feminino , Antineoplásicos/uso terapêutico , Inibidores de Proteínas Quinases/uso terapêutico , Neovascularização Patológica/tratamento farmacológico , Inibidores da Angiogênese/uso terapêuticoRESUMO
Background: Breast cancer is the most widespread malignant tumor worldwide. Single-cell sequencing technology offers novel insights and methods to understand the onset, progression, and treatment of tumors. Nevertheless, there is currently an absence of a thorough and unbiased report on the comprehensive research status of single-cell sequencing in breast cancer. This study seeks to summarize and quantify the dynamics and trends of research on breast cancer single-cell sequencing by bibliometric analysis. Methods: Research articles and reviews related to breast cancer single-cell sequencing were selected from the WoSCC database. Visualization of data regarding countries, institutions, authors, references, and keywords was performed by CiteSpace and VOSviewer software. Results: 583 articles and reviews were analyzed in this study. The quantity of publications related to breast cancer single-cell sequencing has been increasing annually. These studies originate from 302 institutions in 46 countries, with YMAX S WICHA producing the most publications and WANG Y being the most cited author. Nature Communications is the most researched journal, while Nature holds the highest number of citations. These journals predominantly cover topics in the molecular/biological/immunological fields. Moreover, an analysis of reference and keyword bursts revealed that current research trends in this area are primarily centered on "clonal evolution," "tumor microenvironment," and "immunotherapy." Conclusion: Breast cancer single-cell sequencing is a rapidly growing area of scientific interest. Future research requires more frequent and in-depth collaborations among countries, institutions, and authors. Furthermore, "clonal evolution," "tumor microenvironment," and "immunotherapy" are likely to become major focal points in upcoming research on breast cancer single-cell sequencing.
RESUMO
Triple-negative breast cancer (TNBC) still one of the most challenging sub-type in breast cancer clinical. Caffeic acid (CA) derived from effective components of traditional Chinese herbal medicine has been show potential against TNBCs. Our research has found that CA can inhibit the proliferation of TNBC cells while also suppressing the size of cancer stem cell spheres. Additionally, it reduces reactive oxygen species (ROS) levels and disruption of mitochondrial membrane potential. Simultaneously, CA influences the stemness of TNBC cells by reducing the expression of the stem cell marker protein CD44. Furthermore, we have observed that CA can modulate the FOXO1/FIS signaling pathway, disrupting mitochondrial function, inducing mitochondrial autophagy, and exerting anti-tumor activity. Additionally, changes in the immune microenvironment were detected using a mass cytometer, we found that CA can induce M1 polarization of macrophages, enhancing anti-tumor immune responses to exert anti-tumor activity. In summary, CA can be considered as a lead compound for further research in targeting TNBC.