@article{MTMT:35938772,
	title = {Genomic and fragmentomic landscapes of cell-free DNA for early cancer detection},
	url = {https://m2.mtmt.hu/api/publication/35938772},
	author = {Bruhm, Daniel C. and Vulpescu, Nicholas A. and Foda, Zachariah H. and Phallen, Jillian and Scharpf, Robert B. and Velculescu, Victor E.},
	doi = {10.1038/s41568-025-00795-x},
	journal-iso = {NAT REV CANCER},
	journal = {NATURE REVIEWS CANCER},
	unique-id = {35938772},
	issn = {1474-175X},
	year = {2025},
	eissn = {1474-1768}
}

@article{MTMT:36000056,
	title = {ALK in cancer: from function to therapeutic targeting},
	url = {https://m2.mtmt.hu/api/publication/36000056},
	author = {Voena, Claudia and Ambrogio, Chiara and Iannelli, Fabio and Chiarle, Roberto},
	doi = {10.1038/s41568-025-00797-9},
	journal-iso = {NAT REV CANCER},
	journal = {NATURE REVIEWS CANCER},
	unique-id = {36000056},
	issn = {1474-175X},
	year = {2025},
	eissn = {1474-1768}
}

@article{MTMT:36001149,
	title = {Translating premalignant biology to accelerate non-small-cell lung cancer interception},
	url = {https://m2.mtmt.hu/api/publication/36001149},
	author = {Mazzilli, Sarah A. and Rahal, Zahraa and Rouhani, Maral J. and Janes, Sam M. and Kadara, Humam and Dubinett, Steven M. and Spira, Avrum E.},
	doi = {10.1038/s41568-025-00791-1},
	journal-iso = {NAT REV CANCER},
	journal = {NATURE REVIEWS CANCER},
	unique-id = {36001149},
	issn = {1474-175X},
	year = {2025},
	eissn = {1474-1768}
}

@article{MTMT:36013937,
	title = {Using mathematical modelling and AI to improve delivery and efficacy of therapies in cancer},
	url = {https://m2.mtmt.hu/api/publication/36013937},
	author = {Harkos, Constantinos and Hadjigeorgiou, Andreas G. and Voutouri, Chrysovalantis and Kumar, Ashwin S. and Stylianopoulos, Triantafyllos and Jain, Rakesh K.},
	doi = {10.1038/s41568-025-00796-w},
	journal-iso = {NAT REV CANCER},
	journal = {NATURE REVIEWS CANCER},
	unique-id = {36013937},
	issn = {1474-175X},
	year = {2025},
	eissn = {1474-1768},
	orcid-numbers = {Voutouri, Chrysovalantis/0000-0003-3172-9489}
}

@article{MTMT:36118987,
	title = {Targeted protein degradation for cancer therapy},
	url = {https://m2.mtmt.hu/api/publication/36118987},
	author = {Hinterndorfer, M. and Spiteri, V.A. and Ciulli, A. and Winter, G.E.},
	doi = {10.1038/s41568-025-00817-8},
	journal-iso = {NAT REV CANCER},
	journal = {NATURE REVIEWS CANCER},
	unique-id = {36118987},
	issn = {1474-175X},
	abstract = {Targeted protein degradation (TPD) aims at reprogramming the target specificity of the ubiquitin–proteasome system, the major cellular protein disposal machinery, to induce selective ubiquitination and degradation of therapeutically relevant proteins. Since its conception over 20 years ago, TPD has gained a lot of attention mainly due to improvements in the design of bifunctional proteolysis targeting chimeras (PROTACs) and understanding the mechanisms underlying molecular glue degraders. Today, PROTACs are on the verge of a first clinical approval and recent structural and mechanistic insights combined with technological leaps promise to unlock the rational design of protein degraders, following the lead of lenalidomide and related clinically approved analogues. At the same time, the TPD universe is expanding at a record speed with the discovery of novel modalities beyond molecular glue degraders and PROTACs. Here we review the recent progress in the field, focusing on newly discovered degrader modalities, the current state of clinical degrader candidates for cancer therapy and upcoming design approaches. © Springer Nature Limited 2025.},
	year = {2025},
	eissn = {1474-1768}
}

@article{MTMT:36231517,
	title = {Regulatory T cells in the tumour microenvironment},
	url = {https://m2.mtmt.hu/api/publication/36231517},
	author = {Imianowski, C.J. and Chen, Q. and Workman, C.J. and Vignali, D.A.A.},
	doi = {10.1038/s41568-025-00832-9},
	journal-iso = {NAT REV CANCER},
	journal = {NATURE REVIEWS CANCER},
	unique-id = {36231517},
	issn = {1474-175X},
	abstract = {The powerful suppressive capabilities of regulatory T (Treg) cells and their appreciable contribution to tumour progression make them attractive immunotherapeutic targets. However, their role in systemic immune homeostasis makes it important to find ways to specifically target tumour-infiltrating Treg cells while leaving the wider system unperturbed. It is also unknown whether therapies depleting or disrupting the function of tumour-infiltrating Treg cells will provide the greatest efficacy while limiting immune-related adverse events. In addition, Treg cells share much of their biology with conventional CD4+ T cells, introducing challenges when designing targeted immunotherapies. In this Review, we discuss recent advances in differentiating tumour-infiltrating Treg cells from their systemic and tissue-resident counterparts and understanding how the biology of tumour-infiltrating Treg cells differs from conventional CD4+ T cells. We also discuss how recent technological advances may enable the study of tumour-infiltrating Treg cells in even greater detail, helping to identify new targets for next-generation immunotherapeutic drugs. © Springer Nature Limited 2025.},
	keywords = {review; human; Therapy; Homeostasis; regulatory T lymphocyte; tumor growth; CD4+ T lymphocyte; Drug therapy; Tumor microenvironment; neoplastic cell transformation},
	year = {2025},
	eissn = {1474-1768}
}

@article{MTMT:36145654,
	title = {Challenges of small cell lung cancer heterogeneity and phenotypic plasticity},
	url = {https://m2.mtmt.hu/api/publication/36145654},
	author = {Simpson, Kathryn L. and Rothwell, Dominic G. and Blackhall, Fiona and Dive, Caroline},
	doi = {10.1038/s41568-025-00803-0},
	journal-iso = {NAT REV CANCER},
	journal = {NATURE REVIEWS CANCER},
	volume = {25},
	unique-id = {36145654},
	issn = {1474-175X},
	abstract = {Small cell lung cancer (SCLC) is an aggressive neuroendocrine malignancy with similar to 7% 5-year overall survival reflecting early metastasis and rapid acquired chemoresistance. Immunotherapy briefly extends overall survival in similar to 15% cases, yet predictive biomarkers are lacking. Targeted therapies are beginning to show promise, with a recently approved delta-like ligand 3 (DLL3)-targeted therapy impacting the treatment landscape. The increased availability of patient-faithful models, accumulating human tumour biobanks and numerous comprehensive molecular profiling studies have collectively facilitated the mapping and understanding of substantial intertumoural and intratumoural heterogeneity. Beyond the almost ubiquitous loss of wild-type p53 and RB1, SCLC is characterized by heterogeneously mis-regulated expression of MYC family members, yes-associated protein 1 (YAP1), NOTCH pathway signalling, anti-apoptotic BCL2 and epigenetic regulators. Molecular subtypes are based on the neurogenic transcription factors achaete-scute homologue 1 (ASCL1) and neurogenic differentiation factor 1 (NEUROD1), the rarer non-neuroendocrine transcription factor POU class 2 homeobox 3 (POU2F3), and immune- and inflammation-related signatures. Furthermore, SCLC shows phenotypic plasticity, including neuroendocrine-to-non-neuroendocrine transition driven by NOTCH signalling, which is associated with disease progression, chemoresistance and immune modulation and, in mouse models, with metastasis. Although these features pose substantial challenges, understanding the molecular vulnerabilities of transcription factor subtypes, the functional relevance of plasticity and cell cooperation offer opportunities for personalized therapies informed by liquid and tissue biomarkers.},
	keywords = {STEM-CELLS; MHC CLASS-I; MOUSE MODELS; SCLC; CIRCULATING TUMOR-CELLS; vasculogenic mimicry; PULMONARY NEUROENDOCRINE CELLS; rovalpituzumab tesirine; EXTRACHROMOSOMAL DNA AMPLIFICATION},
	year = {2025},
	eissn = {1474-1768},
	pages = {447-462},
	orcid-numbers = {Dive, Caroline/0000-0002-1726-8850}
}

@article{MTMT:36224591,
	title = {Phosphoinositide kinases in cancer: from molecular mechanisms to therapeutic opportunities},
	url = {https://m2.mtmt.hu/api/publication/36224591},
	author = {Llorente, A. and Arora, G.K. and Murad, R. and Emerling, B.M.},
	doi = {10.1038/s41568-025-00810-1},
	journal-iso = {NAT REV CANCER},
	journal = {NATURE REVIEWS CANCER},
	volume = {25},
	unique-id = {36224591},
	issn = {1474-175X},
	abstract = {Phosphoinositide kinases, extending beyond the well-known phosphoinositide 3-kinase (PI3K), are key players in the dynamic and site-specific phosphorylation of lipid phosphoinositides. Unlike PI3Ks, phosphatidylinositol 4-kinases (PI4Ks) and phosphatidylinositol phosphate kinases (PIPKs) do not usually exhibit mutational alterations, but mostly show altered expression in tumours, orchestrating a broad spectrum of signalling, metabolic and immune processes, all of which are crucial in the pathogenesis of cancer. Dysregulation of PI4Ks and PIPKs has been associated with various malignancies, which has sparked considerable interest towards their therapeutic targeting. In this Review we summarize the current understanding of the lesser-studied phosphoinositide kinase families, PI4K and PIPK, focusing on their functions and relevance in cancer. In addition, we provide an overview of ongoing efforts driving the preclinical and clinical development of phosphoinositide kinase-targeting molecules. © Springer Nature Limited 2025.},
	keywords = {Animals; Humans; metabolism; GENETICS; signal transduction; signal transduction; review; human; animal; Therapy; nonhuman; enzymology; ETIOLOGY; Neoplasms; neoplasm; phosphatidylinositol 3 kinase; phosphatidylinositol 3 kinase; Drug therapy; adverse drug reaction; Phosphotransferases (Alcohol Group Acceptor); phosphotransferase; phosphatidylinositide; phosphatidylinositol kinase; phosphatidylinositol kinase; Molecular targeted therapy; molecularly targeted therapy; malignant neoplasm; phosphatidylinositol 4 phosphate kinase; Phosphatidylinositol 3-Kinases; 1-Phosphatidylinositol 4-Kinase; neoplastic cell transformation},
	year = {2025},
	eissn = {1474-1768},
	pages = {463-487}
}

@article{MTMT:35839407,
	title = {Decoding the functional impact of the cancer genome through protein-protein interactions},
	url = {https://m2.mtmt.hu/api/publication/35839407},
	author = {Fu, Haian and Mo, Xiulei and Ivanov, Andrey A.},
	doi = {10.1038/s41568-024-00784-6},
	journal-iso = {NAT REV CANCER},
	journal = {NATURE REVIEWS CANCER},
	volume = {25},
	unique-id = {35839407},
	issn = {1474-175X},
	year = {2025},
	eissn = {1474-1768},
	pages = {189-208},
	orcid-numbers = {Fu, Haian/0000-0002-2362-7979}
}

@article{MTMT:35896516,
	title = {Tumour hypoxia in driving genomic instability and tumour evolution},
	url = {https://m2.mtmt.hu/api/publication/35896516},
	author = {Suvac, Alexandru and Ashton, Jack and Bristow, Robert G.},
	doi = {10.1038/s41568-024-00781-9},
	journal-iso = {NAT REV CANCER},
	journal = {NATURE REVIEWS CANCER},
	volume = {25},
	unique-id = {35896516},
	issn = {1474-175X},
	year = {2025},
	eissn = {1474-1768},
	pages = {167-188}
}