@article{MTMT:36193581,
	title = {Re-epithelialization of cancer cells increases autophagy and DNA damage: Implications for breast cancer dormancy and relapse},
	url = {https://m2.mtmt.hu/api/publication/36193581},
	author = {Drago-Garcia, D. and Giri, S. and Chatterjee, R. and Simoni-Nieves, A. and Abedrabbo, M. and Genna, A. and Uribe, Rios M.L. and Lindzen, M. and Sekar, A. and Gupta, N. and Aharoni, N. and Bhandari, T. and Mayalagu, A. and Schwarzmüller, L. and Tarade, N. and Zhu, R. and Mohan-Raju, H.-R. and Karatekin, F. and Roncato, F. and Eyal-Lubling, Y. and Keidar, T. and Nof, Y. and Nataraj, N.B. and Bernshtein, K.S. and Wagner, B. and Nair, N.U. and Sanghvi, N. and Alon, R. and Seger, R. and Pikarsky, E. and Donzelli, S. and Blandino, G. and Wiemann, S. and Lev, S. and Prywes, R. and Barkan, D. and Rueda, O.M. and Caldas, C. and Ruppin, E. and Shiloh, Y. and Dahlhoff, M. and Yarden, Y.},
	doi = {10.1126/scisignal.ado3},
	journal-iso = {SCI SIGNAL},
	journal = {SCIENCE SIGNALING},
	volume = {18},
	unique-id = {36193581},
	issn = {1945-0877},
	abstract = {Cellular plasticity mediates tissue development as well as cancer growth and progression. In breast cancer, a shift to a more epithelial phenotype (epithelialization) underlies a state of reversible cell growth arrest called tumor dormancy, which enables drug resistance, tumor recurrence, and metastasis. Here, we explored the mechanisms driving epithelialization and dormancy in aggressive mesenchymal-like breast cancer cells in three-dimensional cultures. Overexpressing either of the epithelial lineage-associated transcription factors OVOL1 or OVOL2 suppressed cell proliferation and migration and promoted transition to an epithelial morphology. The expression of OVOL1 (and of OVOL2 to a lesser extent) was regulated by steroid hormones and growth factors and was more abundant in tumors than in normal mammary cells. An uncharacterized and indirect target of OVOL1/2, C1ORF116, exhibited genetic and epigenetic aberrations in breast tumors, and its expression correlated with poor prognosis in patients. We further found that C1ORF116 was an autophagy receptor that directed the degradation of antioxidant proteins, including thioredoxin. Through C1ORF116 and unidentified mediators, OVOL1 expression dysregulated both redox homeostasis (in association with increased ROS, decreased glutathione, and redistribution of the transcription factor NRF2) and DNA damage and repair (in association with increased DNA oxidation and double-strand breaks and an altered interplay among the kinases p38-MAPK, ATM, and others). Because these effects, as they accumulate in cells, can promote metastasis and dormancy escape, the findings suggest that OVOLs not only promote dormancy entry and maintenance in breast cancer but also may ultimately drive dormancy exit and tumor recurrence. Copyright © 2025 The Authors, some rights reserved.},
	keywords = {Female; Female; Humans; metabolism; PHENOTYPE; GENETICS; TRANSCRIPTION FACTOR; TRANSCRIPTION FACTOR; transcription factors; ARTICLE; RNA; METASTASIS; human; MORPHOLOGY; Prognosis; gene expression regulation; immunoblotting; controlled study; GLUTATHIONE; epithelium; cell proliferation; cell proliferation; pathology; Cell Line, Tumor; Breast Neoplasms; Mass spectrometry; Gene Expression; DNA Repair; Gene Expression Regulation, Neoplastic; Cell Movement; Homeostasis; human cell; unclassified drug; protein expression; cell migration; reactive oxygen metabolite; breast tumor; cancer recurrence; immunofluorescence; breast cancer; Neoplasm Recurrence, Local; DNA Damage; DNA Damage; Cell viability; oxidation reduction reaction; promoter region; down regulation; tumor recurrence; real time polymerase chain reaction; genetic conservation; growth factor; Autophagy; cancer cell; steroid hormone; cell motion; RNA isolation; tumor cell line; epigenetics; colony formation; transcription factor Nrf2; double stranded DNA break; autophagy related protein; epithelization; RNA sequencing; ATM protein; three dimensional cell culture; autophagy (cellular); chromosome 1 open reading frame; protein OVOL1; protein OVOL2},
	year = {2025},
	eissn = {1937-9145}
}

@article{MTMT:36299400,
	title = {Autophagy in the regulation of cancer dormancy},
	url = {https://m2.mtmt.hu/api/publication/36299400},
	author = {Gunes, D. and Ustal, A. and Ertem, Y.E. and Akkoc, Y. and Gozuacik, D.},
	doi = {10.1002/1873-3468.70139},
	journal-iso = {FEBS LETT},
	journal = {FEBS LETTERS},
	volume = {&},
	unique-id = {36299400},
	issn = {0014-5793},
	abstract = {Relapse and metastasis continue to be major factors in cancer patient morbidity and death. Cancer dormancy is one of the reasons why cancer recurs after months or years of treatment. With the ability to reactivate, dormant tumors are transitioning into a growth latency stage that shields them from immune surveillance and traditional chemotherapy medications. Over the past decade, research efforts have concentrated on understanding processes governing the dormant state better. The ultimate goal of these efforts is to improve cancer diagnosis, treatment of metastatic illness, and prevention of relapse. Cancer tolerance to stress may depend on autophagy, a cellular stress and recycling system that promotes cancer growth and survival. Recent studies indicated that autophagy may help cancer cells to survive in primary and metastatic environments, to withstand treatment, to develop a dormant state, and to transition from the dormancy to a proliferative state. In this Review, we will discuss the autophagy–dormancy connection in primary and metastatic cancer. © 2025 Federation of European Biochemical Societies.},
	keywords = {Recurrence; CANCER; METASTASIS; METASTASIS; review; human; nonhuman; PREVENTION; phase 2 clinical trial; recurrent disease; cancer patient; cancer diagnosis; cancer growth; cell stress; cellular stress; Autophagy; immunosurveillance; cancer cell; immunological monitoring; dormancy; malignant neoplasm; autophagy (cellular)},
	year = {2025},
	eissn = {1873-3468},
	pages = {&}
}

@article{MTMT:35774835,
	title = {hsa-mir-483-3p modulates delayed breast cancer recurrence},
	url = {https://m2.mtmt.hu/api/publication/35774835},
	author = {Kim, O.-H. and Jeon, T.J. and Kang, H. and Chang, E.S. and Hong, S.A. and Kim, M.K. and Lee, H.J.},
	doi = {10.1038/s41598-024-84437-6},
	journal-iso = {SCI REP},
	journal = {SCIENTIFIC REPORTS},
	volume = {15},
	unique-id = {35774835},
	abstract = {Patients with estrogen receptor-positive breast cancer undergoing continuous adjuvant hormone therapy often experience delayed recurrence with tamoxifen use, potentially causing adverse effects. However, the lack of biomarkers hampers patient selection for extended endocrine therapy. This study aimed to elucidate the molecular mechanisms underlying delayed recurrence and identify biomarkers. When miRNA expression was assessed in luminal breast cancer tissues with and without delayed recurrence using NanoString, a significant increase in the expression of miR483-3p was observed in samples from patients with delayed recurrence compared with those without. miR483-3p expression was elevated in tamoxifen resistant (TAMR) EFM19 cells than in non-resistant EFM19 cells. Notably, genes associated with cancer metastasis (AMOTL2, ANKRD1, CTGF, and VEGF) were upregulated in TAMR EFM19 cells, although cell motility and proliferation were reduced. Transfection of miR483-3p mimics into both non-resistant EFM19 and MCF7 cells resulted in increased expression of cancer metastasis-related genes, but decreased proliferation and migration. Given that miR483-3p can bind to the 3’UTR region of O-GlcNAc transferase (OGT) and potentially affect its protein expression, we examined OGT protein levels and found that transfection with miR483-3p mimics selectively reduced OGT expression. Overall, breast cancer cells subjected to long-term hormone therapy displayed elevated miR483-3p expression, reducing motility and dormancy induction via decreased OGT expression. These findings suggest that miR483-3p is a potential biomarker for long-term endocrine therapy. © The Author(s) 2024.},
	keywords = {Adult; Female; ARTICLE; human; controlled study; clinical article; human cell; protein expression; human tissue; breast cancer; breast cancer; tamoxifen; vasculotropin; cancer tissue; genetic transfection; 3' untranslated region; cell motility; dormancy; connective tissue growth factor; MCF-7 cell line; Estrogen receptor positive breast cancer; Breast cancer recurrence; EFM-19 cell line; delayed recurrence; miR483-3p},
	year = {2025},
	eissn = {2045-2322}
}

@article{MTMT:35774834,
	title = {Secreted LGALS3BP facilitates distant metastasis of breast cancer},
	url = {https://m2.mtmt.hu/api/publication/35774834},
	author = {Kim, S.-S. and Park, I. and Kim, J. and Ka, N.-L. and Lim, G.Y. and Park, M.-Y. and Hwang, S. and Kim, J.-E. and Park, S.Y. and Kim, J.-S. and Rhee, H.-W. and Lee, M.-O.},
	doi = {10.1186/s13058-024-01958-8},
	journal-iso = {BREAST CANCER RES},
	journal = {BREAST CANCER RESEARCH},
	volume = {27},
	unique-id = {35774834},
	issn = {1465-5411},
	abstract = {Background: Patients with estrogen receptor (ER)-positive breast cancer (BC) can be treated with endocrine therapy targeting ER, however, metastatic recurrence occurs in 25% of the patients who have initially been treated. Secreted proteins from tumors play important roles in cancer metastasis but previous methods for isolating secretory proteins had limitations in identifying novel targets. Methods: We applied an in situ secretory protein labeling technique using TurboID to analyze secretome from tamoxifen-resistant (TAMR) BC. The increased expression of LGALS3BP was validated using western blotting, qPCR, ELISA, and IF. Chromatin immunoprecipitation was applied to analyze estrogen-dependent regulation of LGALS3BP transcription. The adhesive and angiogenic functions of LGALS3BP were evaluated by abrogating LGALS3BP expression using either shRNA-mediated knockdown or a neutralizing antibody. Xenograft mouse experiments were employed to assess the in vivo metastatic potential of TAMR cells and the LGALS3BP protein. Clinical evaluation of LGALS3BP risk was carried out with refractory clinical specimens from tamoxifen-treated ER-positive BC patients and publicly available databases. Results: TAMR secretome analysis revealed that 176 proteins were secreted at least 2-fold more from MCF7/TAMR cells than from sensitive cells, and biological processes such as cell adhesion and angiogenesis were associated with the TAMR secretome. Galectin-3 binding protein (LGALS3BP) was one of the top 10 most highly secreted proteins in the TAMR secretome. The expression level of LGALS3BP was suppressed by estrogen signaling, which involves direct ERα binding to its promoter region. Secreted LGALS3BP in the TAMR secretome helped BC cells adhere to the extracellular matrix and promoted the tube formation of human umbilical vein endothelial cells. Compared with sensitive cells, xenograft animal experiments with MCF7/TAMR cells showed increased pulmonary metastasis, which completely disappeared in LGALS3BP-knockdown TAMR cells. Finally, higher levels of LGALS3BP were associated with poor prognosis in ER-positive BC patients treated with adjuvant tamoxifen in the clinic. Conclusion: TAMR secretome analysis identified secretory proteins, such as LGALS3BP, that are involved in biological processes closely related to metastasis. Secreted LGALS3BP from the TAMR cells promoted adhesion of the cells to the extracellular matrix and vasculature formation, which may support metastasis of TAMR cells. © The Author(s) 2024.},
	keywords = {Animals; Female; Female; Humans; metabolism; MICE; GENETICS; CHROMATIN IMMUNOPRECIPITATION; ARTICLE; MOUSE; METASTASIS; METASTASIS; MCF-7 CELLS; human; animal; Neoplasm Metastasis; Cell Adhesion; Cell Adhesion; polymerase chain reaction; gene expression regulation; controlled study; PROTEIN SECRETION; nonhuman; animal tissue; animal model; animal experiment; enzyme linked immunosorbent assay; pathology; clinical article; Cell Line, Tumor; Western blotting; Drug Resistance; Breast Neoplasms; Estrogen Receptor alpha; Gene Expression Regulation, Neoplastic; human cell; unclassified drug; protein expression; neutralizing antibody; in vivo study; Xenograft Model Antitumor Assays; ADJUVANT THERAPY; breast tumor; tumor volume; cancer recurrence; breast cancer; drug screening; extracellular matrix; tumor marker; Neovascularization, Pathologic; Drug Resistance, Neoplasm; tamoxifen; tamoxifen; tamoxifen; carrier protein; Carrier Proteins; Bagg albino mouse; Receptors, Estrogen; Drug therapy; distant metastasis; Estrogen receptor; Antigens, Neoplasm; tumor antigen; lung metastasis; SHORT HAIRPIN RNA; neovascularization (pathology); tumor cell line; tumor xenograft; cancer prognosis; secretome; secretome; Biomarkers, Tumor; estrogen signaling; Secretory protein; MCF-7 cell line; umbilical vein endothelial cell; galectin 3 binding protein; Tamoxifen-resistant breast cancer; Lgals3bp; LGALS3BP protein, human},
	year = {2025},
	eissn = {1465-542X}
}

@article{MTMT:35774838,
	title = {Epigenomic heterogeneity as a source of tumour evolution},
	url = {https://m2.mtmt.hu/api/publication/35774838},
	author = {Laisné, M. and Lupien, M. and Vallot, C.},
	doi = {10.1038/s41568-024-00757-9},
	journal-iso = {NAT REV CANCER},
	journal = {NATURE REVIEWS CANCER},
	volume = {25},
	unique-id = {35774838},
	issn = {1474-175X},
	abstract = {In the past decade, remarkable progress in cancer medicine has been achieved by the development of treatments that target DNA sequence variants. However, a purely genetic approach to treatment selection is hampered by the fact that diverse cell states can emerge from the same genotype. In multicellular organisms, cell-state heterogeneity is driven by epigenetic processes that regulate DNA-based functions such as transcription; disruption of these processes is a hallmark of cancer that enables the emergence of defective cell states. Advances in single-cell technologies have unlocked our ability to quantify the epigenomic heterogeneity of tumours and understand its mechanisms, thereby transforming our appreciation of how epigenomic changes drive cancer evolution. This Review explores the idea that epigenomic heterogeneity and plasticity act as a reservoir of cell states and therefore as a source of tumour evolution. Best practices to quantify epigenomic heterogeneity and explore its various causes and consequences are discussed, including epigenomic reprogramming, stochastic changes and lasting memory. The design of new therapeutic approaches to restrict epigenomic heterogeneity, with the long-term objective of limiting cancer development and progression, is also addressed. © Springer Nature Limited 2024.},
	keywords = {Animals; Humans; DNA; GENETICS; EVOLUTION; review; human; animal; Genotype; Therapy; nonhuman; DNA sequence; pathology; Gene Expression; ETIOLOGY; Neoplasms; neoplasm; Epigenesis, Genetic; Genetic Heterogeneity; Genetic Heterogeneity; genetic epigenesis; genetic epigenesis; epigenetics; Epigenomics; CELL DYSFUNCTION; neoplastic cell transformation},
	year = {2025},
	eissn = {1474-1768},
	pages = {7-26}
}

@article{MTMT:35774837,
	title = {The complex landscape of luminal breast cancer},
	url = {https://m2.mtmt.hu/api/publication/35774837},
	author = {Lutz, C. and Messal, H.A. and Vareslija, D. and Prekovic, S.},
	doi = {10.1530/ERC-24-0201},
	journal-iso = {ENDOCR-RELAT CANCER},
	journal = {ENDOCRINE-RELATED CANCER},
	volume = {32},
	unique-id = {35774837},
	issn = {1351-0088},
	abstract = {The breast epithelium, vital for mammary gland function, is influenced by oestrogen through the oestrogen receptor (ER) signalling pathway. Luminal breast cancer (BC), characterised by ER expression, comprises the majority of all BCs and presents significant clinical challenges due to therapy resistance and recurrence. Despite advancements in understanding luminal disease, improving long-term survival and reducing relapse of BC patients by predicting therapy efficacy and understanding resistance mechanisms remain critical challenges. This review discusses luminal BC biology, focusing on the molecular classification of primary disease, metastatic spread, and experimental models. © 2024 the author(s).},
	keywords = {Animals; Adult; Female; Female; Humans; metabolism; signal transduction; METASTASIS; METASTASIS; review; human; animal; pathology; Breast Neoplasms; drug combination; endocrine system; breast tumor; breast cancer; breast cancer; Receptors, Estrogen; Estrogen receptor; Estrogen receptor; breast epithelium; Long term survival; steroid receptor; Steroid hormone receptors; Disease modelling; endocrine cancer; endocrine cancer},
	year = {2025},
	eissn = {1479-6821}
}

@article{MTMT:36299399,
	title = {Bridging the Gap in Breast Cancer Dormancy: Models, Mechanisms, and Translational Challenges},
	url = {https://m2.mtmt.hu/api/publication/36299399},
	author = {Sabit, H. and Abdel-Ghany, S. and Albrahim, Y. and Wadan, A.-H.S. and Rashwan, S. and Arneth, R. and Arneth, B.},
	doi = {10.3390/ph18070961},
	journal-iso = {PHARMACEUTICALS-BASE},
	journal = {PHARMACEUTICALS},
	volume = {18},
	unique-id = {36299399},
	abstract = {Breast cancer (BC) poses a significant clinical challenge due to late metastatic recurrence, driven by dormant disseminated tumor cells (DTCs). This review emphasizes the urgency of addressing tumor dormancy to reduce metastatic relapse, a major contributor to BC mortality. DTCs evade conventional therapies and immune surveillance, reactivating unpredictably, thus necessitating targeted strategies. Current research is fragmented, with conflicting data, inadequate models, and a lack of biomarkers hindering progress. This review synthesizes these gaps and proposes actionable priorities, advocating for integrated, standardized approaches. It highlights the roles of single-cell multi-omics, spatial transcriptomics, and humanized long-term models in unraveling dormancy mechanisms. The review also emphasizes macrophage-targeted therapies, dormancy-specific trials, and biomarker validation, offering paths to clinical translation. Ultimately, this work emphasizes the urgent need for integrated multi-omics approaches, including single-cell and spatial transcriptomics, combined with advanced computational analysis. Moreover, this review critically analyzes the existing research landscape, meticulously identifying key gaps, and proposing concrete, forward-looking directions for both fundamental research and clinical translation in the challenging field of BC dormancy. © 2025 by the authors.},
	keywords = {Female; FIBRONECTIN; METASTASIS; review; human; Survival Analysis; MACROPHAGE; computer analysis; neutrophil; cell proliferation; Gene Expression; COLLAGEN; immunotherapy; interleukin 6; interleukin 2; Immunogenicity; breast cancer; Molecular Biology; transcriptomics; DNA methylation; DNA Damage; clinical assessment; HYPOXIA; microenvironment; Laminin; Translational research; Translational research; epithelial mesenchymal transition; single cell analysis; Pi3K/Akt signaling; MAPK signaling; Neutrophil extracellular trap; mTOR signaling; BC; multiomics; Tumor dormancy; autophagy (cellular); single cell RNA seq; biosurveillance; Metastatic recurrence},
	year = {2025},
	eissn = {1424-8247}
}

@article{MTMT:35774836,
	title = {Cancer evolution: from Darwin to the Extended Evolutionary Synthesis},
	url = {https://m2.mtmt.hu/api/publication/35774836},
	author = {Savy, T. and Flanders, L. and Karpanasamy, T. and Sun, M. and Gerlinger, M.},
	doi = {10.1016/j.trecan.2025.01.001},
	journal-iso = {TRENDS CANCER},
	journal = {TRENDS IN CANCER},
	volume = {11},
	unique-id = {35774836},
	issn = {2405-8025},
	abstract = {The fundamental evolutionary nature of cancer has been recognized for decades. Increasingly powerful genetic and single cell sequencing technologies, as well as preclinical models, continue to unravel the evolution of premalignant cells, and progression to metastatic stages and to drug-resistant end-stage disease. Here, we summarize recent advances and distil evolutionary principles and their relevance for the clinic. We reveal how cancer cell and microenvironmental plasticity are intertwined with Darwinian evolution and demonstrate the need for a conceptual framework that integrates these processes. This warrants the adoption of the recently developed Extended Evolutionary Synthesis (EES). © 2025 The Authors},
	keywords = {METASTASIS; METASTASIS; MUTAGENESIS; MUTAGENESIS; review; human; Biomarkers; nonhuman; biological marker; Drug Resistance; Drug Resistance; synthesis; cancer cell; conceptual framework; CELLULAR PLASTICITY; cancer evolution; macroevolution; malignant neoplasm; cell plasticity},
	year = {2025},
	eissn = {2405-8033},
	pages = {204-215}
}

@article{MTMT:35959793,
	title = {Tumor dormancy and relapse: understanding the molecular mechanisms of cancer recurrence},
	url = {https://m2.mtmt.hu/api/publication/35959793},
	author = {Tufail, Muhammad and Jiang, Can-Hua and Li, Ning},
	doi = {10.1186/s40779-025-00595-2},
	journal-iso = {MILITARY MED RES},
	journal = {MILITARY MEDICAL RESEARCH},
	volume = {12},
	unique-id = {35959793},
	issn = {2095-7467},
	abstract = {Cancer recurrence, driven by the phenomenon of tumor dormancy, presents a formidable challenge in oncology. Dormant cancer cells have the ability to evade detection and treatment, leading to relapse. This review emphasizes the urgent need to comprehend tumor dormancy and its implications for cancer recurrence. Despite notable advancements, significant gaps remain in our understanding of the mechanisms underlying dormancy and the lack of reliable biomarkers for predicting relapse. This review provides a comprehensive analysis of the cellular, angiogenic, and immunological aspects of dormancy. It highlights the current therapeutic strategies targeting dormant cells, particularly combination therapies and immunotherapies, which hold promise in preventing relapse. By elucidating these mechanisms and proposing innovative research methodologies, this review aims to deepen our understanding of tumor dormancy, ultimately facilitating the development of more effective strategies for preventing cancer recurrence and improving patient outcomes.},
	keywords = {metabolism; SIGNALING PATHWAYS; BREAST-CANCER; ANGIOGENESIS; EXTRACELLULAR-MATRIX; Biomarkers; Therapy; cancer recurrence; PROMOTES; CELL-CYCLE PROGRESSION; Wnt signaling pathway; epigenetic alterations; Tumor dormancy},
	year = {2025},
	eissn = {2054-9369},
	orcid-numbers = {Tufail, Muhammad/0000-0003-3442-7216}
}

@article{MTMT:35897804,
	title = {Towards understanding cancer dormancy over strategic hitching up mechanisms to technologies},
	url = {https://m2.mtmt.hu/api/publication/35897804},
	author = {Yang, Sumin and Seo, Jieun and Choi, Jeonghyeon and Kim, Sung-Hyun and Kuk, Yunmin and Park, Kyung Chan and Kang, Mingon and Byun, Sangwon and Joo, Jae-Yeol},
	doi = {10.1186/s12943-025-02250-9},
	journal-iso = {MOL CANCER},
	journal = {MOLECULAR CANCER},
	volume = {24},
	unique-id = {35897804},
	issn = {1476-4598},
	keywords = {CANCER; Artificial intelligence; cancer recurrence; Cancer dormancy; cancer transcriptomics},
	year = {2025},
	eissn = {1476-4598}
}

@article{MTMT:36193580,
	title = {Targeting Cancer Drug-Tolerant Persister Cells in Minimal Residual Disease},
	url = {https://m2.mtmt.hu/api/publication/36193580},
	author = {Zhang, W. and Chattrakarn, S. and Chen, F. and Chai, H. and Maranga, M. and Zhang, J.},
	doi = {10.53941/ijddp.2025.100011},
	journal-iso = {INT J DRUG DISCOV PHARM},
	journal = {INTERNATIONAL JOURNAL OF DRUG DISCOVERY AND PHARMACOLOGY},
	volume = {4},
	unique-id = {36193580},
	abstract = {Cancer cells that survive therapeutic drug pressure are a significant cause of disease relapse and progression, impeding curative cancer treatment. Drug-triggered Darwinian selection and the emergence of subclones harbouring specific mutations that confer resistance have been well documented and extensively studied. However, these genetic alterations, while important, do not fully explain clinical observations where some patients, after a drug holiday, regain sensitivity to the same treatment despite previous disease progression. This phenomenon highlights the possibility that drug resistance may not solely rely on genetic mutations but could also involve reversible, non-genetic mechanisms. Recent studies have highlighted the existence of drug-tolerant persister cells (DTPs), a subpopulation of cancer cells that can survive short-term therapeutic pressure without acquiring resistance-associated genetic alterations. These cells exhibit a temporary yet reversible tolerance to the initial treatment while also acquiring cross-tolerance to other anticancer therapies. The presence of DTPs underscores a dynamic and complex plasticity in tumours, wherein cancer cells can utilise epigenetic rewiring, metabolic reprogramming, and specific signalling pathways to transit between drug-tolerant and drug-sensitive states to adapt to environmental pressures. Furthermore, this adaptive resilience enables DTPs to act as a reservoir for the development of genetically stable resistance, resulting in cancer therapy failure and eventual relapse. In this mini-review, we examine recent evidence on DTPs to provide an overview of their characteristics, development, and survival mechanisms. © 2025 by the authors.},
	keywords = {MINIMAL RESIDUAL DISEASE; Drug Resistance; drug tolerance; Ferroptosis; drug‐tolerant persister cells},
	year = {2025},
	eissn = {2653-6234}
}

@article{MTMT:36000844,
	title = {Molecular mechanisms altering cell identity in cancer},
	url = {https://m2.mtmt.hu/api/publication/36000844},
	author = {Zippo, Alessio and Beyes, Sven},
	doi = {10.1038/s41388-025-03314-2},
	journal-iso = {ONCOGENE},
	journal = {ONCOGENE},
	unique-id = {36000844},
	issn = {0950-9232},
	year = {2025},
	eissn = {1476-5594}
}

@article{MTMT:35335008,
	title = {Advancements in Understanding the Hide-and-Seek Strategy of Hibernating Breast Cancer Cells and Their Implications in Oncology from a Broader Perspective: A Comprehensive Overview},
	url = {https://m2.mtmt.hu/api/publication/35335008},
	author = {Al-Ruwishan, A. and Amer, B. and Salem, A. and Abdi, A. and Chimpandu, N. and Esa, A. and Melemenis, A. and Saleem, M.Z. and Mathew, R. and Gamallat, Y.},
	doi = {10.3390/cimb46080492},
	journal-iso = {CURR ISSUES MOL BIOL},
	journal = {CURRENT ISSUES IN MOLECULAR BIOLOGY},
	volume = {46},
	unique-id = {35335008},
	issn = {1467-3037},
	year = {2024},
	eissn = {1467-3045},
	pages = {8340-8367}
}

@article{MTMT:35309371,
	title = {A Functional Survey of the Regulatory Landscape of Estrogen Receptor-Positive Breast Cancer Evolution},
	url = {https://m2.mtmt.hu/api/publication/35309371},
	author = {Barozzi, I. and Slaven, N. and Canale, E. and Lopes, R. and Amorim, Monteiro Barbosa I. and Bleu, M. and Ivanoiu, D. and Pacini, C. and Mensa', E. and Chambers, A. and Bravaccini, S. and Ravaioli, S. and Győrffy, Balázs and Dieci, M.V. and Pruneri, G. and Galli, G.G. and Magnani, L.},
	doi = {10.1158/2159-8290.CD-23-1157},
	journal-iso = {CANCER DISCOV},
	journal = {CANCER DISCOVERY},
	volume = {14},
	unique-id = {35309371},
	issn = {2159-8274},
	year = {2024},
	eissn = {2159-8290},
	pages = {1612-1630},
	orcid-numbers = {Győrffy, Balázs/0000-0002-5772-3766}
}

@article{MTMT:35323251,
	title = {The evolutionary theory of cancer: challenges and potential solutions},
	url = {https://m2.mtmt.hu/api/publication/35323251},
	author = {Laplane, Lucie and Maley, Carlo C.},
	doi = {10.1038/s41568-024-00734-2},
	journal-iso = {NAT REV CANCER},
	journal = {NATURE REVIEWS CANCER},
	volume = {24},
	unique-id = {35323251},
	issn = {1474-175X},
	year = {2024},
	eissn = {1474-1768},
	pages = {718-733}
}

@article{MTMT:34934284,
	title = {Epigenetic Control of Cancer Cell Dormancy and Awakening in Endocrine Therapy Resistance},
	url = {https://m2.mtmt.hu/api/publication/34934284},
	author = {Llinas-Bertran, Arnau and Bellet-Ezquerra, Meritxell and Seoane, Jose A.},
	doi = {10.1158/2159-8290.CD-24-0282},
	journal-iso = {CANCER DISCOV},
	journal = {CANCER DISCOVERY},
	volume = {14},
	unique-id = {34934284},
	issn = {2159-8274},
	year = {2024},
	eissn = {2159-8290},
	pages = {704-706}
}

@article{MTMT:35335009,
	title = {Unveiling the Complex Ecosystem of Breast Cancer: Crucial Insights for Patients and Doctors},
	url = {https://m2.mtmt.hu/api/publication/35335009},
	author = {Mokbel, K.},
	doi = {10.21873/anticanres.17150},
	journal-iso = {ANTICANCER RES},
	journal = {ANTICANCER RESEARCH},
	volume = {44},
	unique-id = {35335009},
	issn = {0250-7005},
	year = {2024},
	eissn = {1791-7530},
	pages = {3317-3319}
}

@article{MTMT:35335010,
	title = {Cancer drug-tolerant persister cells: from biological questions to clinical opportunities},
	url = {https://m2.mtmt.hu/api/publication/35335010},
	author = {Russo, M. and Chen, M. and Mariella, E. and Peng, H. and Rehman, S.K. and Sancho, E. and Sogari, A. and Toh, T.S. and Balaban, N.Q. and Batlle, E. and Bernards, R. and Garnett, M.J. and Hangauer, M. and Leucci, E. and Marine, J.-C. and O’Brien, C.A. and Oren, Y. and Patton, E.E. and Robert, C. and Rosenberg, S.M. and Shen, S. and Bardelli, A.},
	doi = {10.1038/s41568-024-00737-z},
	journal-iso = {NAT REV CANCER},
	journal = {NATURE REVIEWS CANCER},
	volume = {24},
	unique-id = {35335010},
	issn = {1474-175X},
	year = {2024},
	eissn = {1474-1768},
	pages = {694-717}
}