ReviewFrontiers in oncology2021
Senescence-Induced Chemoresistance in Triple Negative Breast Cancer and Evolution-Based Treatment Strategies.
Review in Frontiers in oncology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 49 citations in OpenAlex.
- Postbiotics as Emerging Strategy Targeting Obesity- and Aging-Related Breast Cancer-Prospects in Prophylaxis and Therapy.Life (Basel, Switzerland) · 2026Review
- Therapy-induced senescence in breast cancer and cardiovascular disease: a double-edged biological process.Frontiers in cardiovascular medicine · 2026Review
- The Novel ROCK Inhibitor Fasudil Derivative Fasudil-D-6h Prevents Tumour Progression by Regulating the Adherens Junction Signalling Pathway in Triple-Negative Breast Cancer.Breast cancer (Dove Medical Press) · 2026Article
- The double-edged sword of SASP in breast cancer: from tumor suppression to progression and therapy resistance.Frontiers in oncology · 2026Review
- Mapping the Progression of Therapy-Induced Senescence to Therapy Tolerance: An Evolutionarily Conserved Mechanism for Optimizing Cancer Treatment with Senotherapeutics.ACS pharmacology & translational science · 2025Article
- Article
- Loss of Predicted Cell Adhesion Molecule MPZL3 Promotes EMT in Ovarian Cancer.Cancer research communications · 2025Article
- The interplay of cellular senescence and reprogramming shapes the biological landscape of aging and cancer revealing novel therapeutic avenues.Frontiers in cell and developmental biology · 2025Review
- Potentiating doxorubicin activity through BCL-2 inhibition in p53 wild-type and mutated triple-negative breast cancer.Frontiers in oncology · 2025Article
- Interplay between epigenetics, senescence and cellular redox metabolism in cancer and its therapeutic implications.Redox biology · 2024Review
- Marizomib Promotes Senescence or Long-Term Apoptosis in Melanoma Cancer Cells.Molecules (Basel, Switzerland) · 2024Article
- Review
- Unveiling innovative therapeutic strategies and future trajectories on stimuli-responsive drug delivery systems for targeted treatment of breast carcinoma.Naunyn-Schmiedeberg's archives of pharmacology · 2024Review
- Article
- Senescence Promotes the Recovery of Stemness among Cancer Cells via Reprograming.Biomolecules · 2024Review
- Article
- Fractionation and phytochemical composition of an ethanolic extract ofFrontiers in pharmacology · 2024Article
- Defining melanoma combination therapies that provide senolytic sensitivity in human melanoma cells.Frontiers in cell and developmental biology · 2024Article
- Green Tea Leaves and Rosemary Extracts Selectively Induce Cell Death in Triple-Negative Breast Cancer Cells and Cancer Stem Cells and Enhance the Efficacy of Common Chemotherapeutics.Evidence-based complementary and alternative medicine : eCAM · 2024Article
- Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Triple negative breast cancer (TNBC) is classically treated with combination chemotherapies. Although, initially responsive to chemotherapies, TNBC patients frequently develop drug-resistant, metastatic disease. Chemotherapy resistance can develop through many mechanisms, including induction of a transient growth-arrested state, known as the therapy-induced senescence (TIS). In this paper, we will focus on chemoresistance in TNBC due to TIS. One of the key characteristics of senescent cells is a complex secretory phenotype, known as the senescence-associated secretory proteome (SASP), which by prompting immune-mediated clearance of senescent cells maintains tissue homeostasis and suppresses tumorigenesis. However, in cancer, particularly with TIS, senescent cells themselves as well as SASP promote cellular reprograming into a stem-like state responsible for the emergence of drug-resistant, aggressive clones. In addition to chemotherapies, outcomes of recently approved immune and DNA damage-response (DDR)-directed therapies are also affected by TIS, implying that this a common strategy used by cancer cells for evading treatment. Although there has been an explosion of scientific research for manipulating TIS for prevention of drug resistance, much of it is still at the pre-clinical stage. From an evolutionary perspective, cancer is driven by natural selection, wherein the fittest tumor cells survive and proliferate while the tumor microenvironment influences tumor cell fitness. As TIS seems to be preferred for increasing the fitness of drug-challenged cancer cells, we will propose a few tactics to control it by using the principles of evolutionary biology. We hope that with appropriate therapeutic intervention, this detrimental cellular fate could be diverted in favor of TNBC patients.
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