@article{MTMT:34202172,
	title = {Principles of metabolome conservation in animals},
	url = {https://m2.mtmt.hu/api/publication/34202172},
	author = {Liska, Orsolya and Boross, Gábor and Rocabert, Charles and Szappanos, Balázs and Tengölics, Roland and Papp, Balázs},
	doi = {10.1073/pnas.2302147120},
	journal-iso = {P NATL ACAD SCI USA},
	journal = {PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA},
	volume = {120},
	unique-id = {34202172},
	issn = {0027-8424},
	abstract = {Metabolite levels shape cellular physiology and disease susceptibility, yet the general principles governing metabolome evolution are largely unknown. Here, we introduce a measure of conservation of individual metabolite levels among related species. By analyzing multispecies tissue metabolome datasets in phylogenetically diverse mammals and fruit flies, we show that conservation varies extensively across metabolites. Three major functional properties, metabolite abundance, essentiality, and association with human diseases predict conservation, highlighting a striking parallel between the evolutionary forces driving metabolome and protein sequence conservation. Metabolic network simulations recapitulated these general patterns and revealed that abundant metabolites are highly conserved due to their strong coupling to key metabolic fluxes in the network. Finally, we show that biomarkers of metabolic diseases can be distinguished from other metabolites simply based on evolutionary conservation, without requiring any prior clinical knowledge. Overall, this study uncovers simple rules that govern metabolic evolution in animals and implies that most tissue metabolome differences between species are permitted, rather than favored by natural selection. More broadly, our work paves the way toward using evolutionary information to identify biomarkers, as well as to detect pathogenic metabolome alterations in individual patients.},
	keywords = {PROTEIN; MODELS; Systems biology; RESOURCE; molecular evolution; Optimality; METABOLIC NETWORKS; Phylogenetic comparative method},
	year = {2023},
	eissn = {1091-6490},
	orcid-numbers = {Boross, Gábor/0000-0002-7208-5678; Szappanos, Balázs/0000-0002-5075-1799}
}

@article{MTMT:34146082,
	title = {Fully accessible fitness landscape of oncogene-negative lung adenocarcinoma},
	url = {https://m2.mtmt.hu/api/publication/34146082},
	author = {Yousefi, Maryam and Andrejka, Laura and Szamecz, Márton and Winslow, Monte M. and Petrov, Dmitri A. and Boross, Gábor},
	doi = {10.1073/pnas.2303224120},
	journal-iso = {P NATL ACAD SCI USA},
	journal = {PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA},
	volume = {120},
	unique-id = {34146082},
	issn = {0027-8424},
	abstract = {Cancer genomes are almost invariably complex with genomic alterations cooperating during each step of carcinogenesis. In cancers that lack a single dominant oncogene mutation, cooperation between the inactivation of multiple tumor suppressor genes can drive tumor initiation and growth. Here, we shed light on how the sequential acquisition of genomic alterations generates oncogene-negative lung tumors. We couple tumor barcoding with combinatorial and multiplexed somatic genome editing to characterize the fitness landscapes of three tumor suppressor genes NF1, RASA1, and PTEN, the inactivation of which jointly drives oncogene-negative lung adenocarcinoma initiation and growth. The fitness landscape was surprisingly accessible, with each additional mutation leading to growth advantage. Furthermore, the fitness landscapes remained fully accessible across backgrounds with the inactivation of additional tumor suppressor genes. These results suggest that while predicting cancer evolution will be challenging, acquiring the multiple alterations that drive the growth of oncogene-negative tumors can be facilitated by the lack of constraints on mutational order.},
	year = {2023},
	eissn = {1091-6490},
	orcid-numbers = {Szamecz, Márton/0009-0008-5711-3061; Boross, Gábor/0000-0002-7208-5678}
}

@misc{MTMT:33780517,
	title = {Fully accessible fitness landscape of oncogene-negative lung adenocarcinoma.},
	url = {https://m2.mtmt.hu/api/publication/33780517},
	author = {Yousefi, Maryam and Andrejka, Laura and Winslow, Monte M and Petrov, Dmitri A and Boross, Gábor},
	unique-id = {33780517},
	abstract = {Cancer genomes are almost invariably complex with genomic alterations cooperating during each step of carcinogenesis. In cancers that lack a single dominant oncogene mutation, cooperation between the inactivation of multiple tumor suppressor genes can drive tumor initiation and growth. Here, we shed light on how the sequential acquisition of genomic alterations generates oncogene-negative lung tumors. We couple tumor barcoding with combinatorial and multiplexed somatic genome editing to characterize the fitness landscapes of three tumor suppressor genes NF1, RASA1, and PTEN, the inactivation of which jointly drives oncogene-negative lung adenocarcinoma initiation and growth. The fitness landscape was surprisingly accessible, with each additional mutation leading to growth advantage. Furthermore, the fitness landscapes remained fully accessible across backgrounds with additional tumor suppressor mutations. These results suggest that while predicting cancer evolution will be challenging, acquiring the multiple alterations required for the growth of oncogene-negative tumors can be facilitated by the lack of constraints on mutational order.},
	year = {2023},
	orcid-numbers = {Boross, Gábor/0000-0002-7208-5678}
}

@article{MTMT:33597875,
	title = {Combinatorial Inactivation of Tumor Suppressors Efficiently Initiates Lung Adenocarcinoma with Therapeutic Vulnerabilities},
	url = {https://m2.mtmt.hu/api/publication/33597875},
	author = {Yousefi, Maryam and Boross, Gábor and Weiss, Carly and Murray, Christopher W. and Hebert, Jess D. and Cai, Hongchen and Ashkin, Emily L. and Karmakar, Saswati and Andrejka, Laura and Chen, Leo and Wang, Minwei and Tsai, Min K. and Lin, Wen-Yang and Li, Chuan and Yakhchalian, Pegah and Colón, Caterina I. and Chew, Su-Kit and Chu, Pauline and Swanton, Charles and Kunder, Christian A. and Petrov, Dmitri A. and Winslow, Monte M.},
	doi = {10.1158/0008-5472.CAN-22-0059},
	journal-iso = {CANCER RES},
	journal = {CANCER RESEARCH},
	volume = {82},
	unique-id = {33597875},
	issn = {0008-5472},
	year = {2022},
	eissn = {1538-7445},
	pages = {1589-1602},
	orcid-numbers = {Boross, Gábor/0000-0002-7208-5678; Hebert, Jess D./0000-0002-8778-5941; Cai, Hongchen/0000-0002-5921-5773; Karmakar, Saswati/0000-0003-0315-5924; Andrejka, Laura/0000-0002-2202-5626; Tsai, Min K./0000-0003-4732-4259; Li, Chuan/0000-0002-4381-3891; Yakhchalian, Pegah/0000-0003-4646-2430; Colón, Caterina I./0000-0001-6073-8793; Swanton, Charles/0000-0002-4299-3018; Kunder, Christian A./0000-0003-1514-7550; Petrov, Dmitri A./0000-0002-3664-9130}
}

@article{MTMT:32106320,
	title = {Limited evolutionary conservation of multidrug resistance and collateral sensitivity (vol 36, pg 1601, 2019)},
	url = {https://m2.mtmt.hu/api/publication/32106320},
	author = {Apjok, Gábor and Boross, Gábor and Nyerges, Ákos and Fekete, Gergely and Lázár, Viktória and Papp, Balázs and Pál, Csaba and Csörgő, Bálint},
	doi = {10.1093/molbev/msab116},
	journal-iso = {MOL BIOL EVOL},
	journal = {MOLECULAR BIOLOGY AND EVOLUTION},
	volume = {38},
	unique-id = {32106320},
	issn = {0737-4038},
	keywords = {evolutionary biology; Biochemistry & Molecular Biology},
	year = {2021},
	eissn = {1537-1719},
	pages = {3029-3029},
	orcid-numbers = {Boross, Gábor/0000-0002-7208-5678; Nyerges, Ákos/0000-0002-1581-490X; Csörgő, Bálint/0000-0003-0397-6845}
}

@article{MTMT:30776198,
	title = {Rapid decline of bacterial drug-resistance in an antibiotic-free environment through phenotypic reversion.},
	url = {https://m2.mtmt.hu/api/publication/30776198},
	author = {Dunai, Anett and Spohn, Réka and Farkas, Zoltán and Lázár, Viktória and Györkei, Ádám and Apjok, Gábor and Boross, Gábor and Szappanos, Balázs and Grézal, Gábor and Faragó, Anikó and Bodai, László and Papp, Balázs and Pál, Csaba},
	doi = {10.7554/eLife.47088},
	journal-iso = {ELIFE},
	journal = {ELIFE},
	volume = {8},
	unique-id = {30776198},
	issn = {2050-084X},
	abstract = {Antibiotic resistance typically induces a fitness cost that shapes the fate of antibiotic-resistant bacterial populations. However, the cost of resistance can be mitigated by compensatory mutations elsewhere in the genome, and therefore the loss of resistance may proceed too slowly to be of practical importance. We present our study on the efficacy and phenotypic impact of compensatory evolution in Escherichia coli strains carrying multiple resistance mutations. We have demonstrated that drug-resistance frequently declines within 480 generations during exposure to an antibiotic-free environment. The extent of resistance loss was found to be generally antibiotic-specific, driven by mutations that reduce both resistance level and fitness costs of antibiotic-resistance mutations. We conclude that phenotypic reversion to the antibiotic-sensitive state can be mediated by the acquisition of additional mutations, while maintaining the original resistance mutations. Our study indicates that restricting antimicrobial usage could be a useful policy, but for certain antibiotics only.},
	keywords = {EVOLUTION; Antibiotic resistance; E. coli; evolutionary biology; compensatory mutations},
	year = {2019},
	eissn = {2050-084X},
	orcid-numbers = {Boross, Gábor/0000-0002-7208-5678; Szappanos, Balázs/0000-0002-5075-1799; Grézal, Gábor/0000-0003-1685-4791; Bodai, László/0000-0001-8411-626X}
}

@article{MTMT:30703953,
	title = {Limited evolutionary conservation of the phenotypic effects of antibiotic resistance mutations},
	url = {https://m2.mtmt.hu/api/publication/30703953},
	author = {Apjok, Gábor and Boross, Gábor and Nyerges, Ákos and Fekete, Gergely and Lázár, Viktória and Papp, Balázs and Pál, Csaba and Csörgő, Bálint},
	doi = {10.1093/molbev/msz109},
	journal-iso = {MOL BIOL EVOL},
	journal = {MOLECULAR BIOLOGY AND EVOLUTION},
	volume = {36},
	unique-id = {30703953},
	issn = {0737-4038},
	year = {2019},
	eissn = {1537-1719},
	pages = {1601-1611},
	orcid-numbers = {Boross, Gábor/0000-0002-7208-5678; Nyerges, Ákos/0000-0002-1581-490X; Csörgő, Bálint/0000-0003-0397-6845}
}

@article{MTMT:30420930,
	title = {Pathogen diversity drives the evolution of generalist MHC-II alleles in human populations},
	url = {https://m2.mtmt.hu/api/publication/30420930},
	author = {Manczinger, Máté and Boross, Gábor and Kemény, Lajos and Müller, Viktor and Lenz, Tobias L. and Papp, Balázs and Pál, Csaba},
	doi = {10.1371/journal.pbio.3000131},
	journal-iso = {PLOS BIOL},
	journal = {PLOS BIOLOGY},
	volume = {17},
	unique-id = {30420930},
	issn = {1544-9173},
	abstract = {Whereas specialist major histocompatibility complex (MHC) molecules initiate immune response against only relatively few pathogens, generalists provide protection against a broad range. Accordingly, this study shows that the geographical distribution of generalist MHC alleles in human populations reflects exposure to diverse infectious diseases.},
	year = {2019},
	eissn = {1545-7885},
	orcid-numbers = {Manczinger, Máté/0000-0003-0831-9617; Boross, Gábor/0000-0002-7208-5678; Kemény, Lajos/0000-0002-2119-9501; Müller, Viktor/0000-0001-8212-4880}
}

@article{MTMT:34146093,
	title = {Káros és kompenzáló mutációk: lehet-e szerepük a biológiai sokféleség evolúciójában?},
	url = {https://m2.mtmt.hu/api/publication/34146093},
	author = {Boross, Gábor Zoltán and Boross, Gábor},
	doi = {10.1556/2065.179.2018.5.2},
	journal-iso = {MAGYAR TUDOMÁNY},
	journal = {MAGYAR TUDOMÁNY},
	volume = {179},
	unique-id = {34146093},
	issn = {0025-0325},
	year = {2018},
	eissn = {1588-1245},
	orcid-numbers = {Boross, Gábor/0000-0002-7208-5678}
}

@article{MTMT:30338873,
	title = {Pathogen diversity drives the evolution of generalist antigen presentation in human populations},
	url = {https://m2.mtmt.hu/api/publication/30338873},
	author = {Manczinger, Máté and Boross, Gábor and Kemény, Lajos and Müller, Viktor and Tobias, L. Lenz and Papp, Balázs and Pál, Csaba},
	journal-iso = {IMMUNOLÓGIAI SZEMLE},
	journal = {IMMUNOLÓGIAI SZEMLE},
	volume = {10},
	unique-id = {30338873},
	issn = {2061-0203},
	year = {2018},
	pages = {18-18},
	orcid-numbers = {Boross, Gábor/0000-0002-7208-5678; Kemény, Lajos/0000-0002-2119-9501; Müller, Viktor/0000-0001-8212-4880}
}