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Article ; Online: Epigenetic Control of Cancer Cell Dormancy and Awakening in Endocrine Therapy Resistance.

Llinas-Bertran, Arnau / Bellet-Ezquerra, Meritxell / Seoane, Jose A

2024 Volume 14, Issue 5, Page(s) 704–706

Abstract: Summary: Rosano, Sofyali, Dhiman, and colleagues show that epigenetic-related changes occur in endocrine therapy (ET)-induced dormancy in estrogen receptor positive (ER+) breast cancer, as well as in its reawakening. Targeting these epigenetic changes ... ...

Abstract	Summary: Rosano, Sofyali, Dhiman, and colleagues show that epigenetic-related changes occur in endocrine therapy (ET)-induced dormancy in estrogen receptor positive (ER+) breast cancer, as well as in its reawakening. Targeting these epigenetic changes blocks the entrance to dormancy and reduces the persister cancer cell population, enhancing the cytotoxic effects of ET in vitro. See related article by Rosano et al., p. 866 (9).
MeSH term(s)	Humans ; Epigenesis, Genetic/drug effects ; Drug Resistance, Neoplasm/genetics ; Breast Neoplasms/drug therapy ; Breast Neoplasms/genetics ; Breast Neoplasms/pathology ; Antineoplastic Agents, Hormonal/pharmacology ; Antineoplastic Agents, Hormonal/therapeutic use ; Female ; Receptors, Estrogen/metabolism ; Gene Expression Regulation, Neoplastic/drug effects
Chemical Substances	Antineoplastic Agents, Hormonal ; Receptors, Estrogen
Language	English
Publishing date	2024-05-08
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2625242-9
ISSN	2159-8290 ; 2159-8274
ISSN (online)	2159-8290
ISSN	2159-8274
DOI	10.1158/2159-8290.CD-24-0282
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Epigenetic Control of Cancer Cell Dormancy and Awakening in Endocrine Therapy Resistance.

Llinas-Bertran, Arnau / Bellet-Ezquerra, Meritxell / Seoane, Jose A

Cancer discovery

2024 , Page(s) OF1–OF3

Abstract	Summary: Rosano, Sofyali, Dhiman, and colleagues show that epigenetic-related changes occur in endocrine therapy (ET)-induced dormancy in estrogen receptor positive (ER+) breast cancer, as well as in its reawakening. Targeting these epigenetic changes blocks the entrance to dormancy and reduces the persister cancer cell population, enhancing the cytotoxic effects of ET in vitro. See related article by Rosano et al. (9).
Language	English
Publishing date	2024-04-10
Publishing country	United States
Document type	Journal Article
ZDB-ID	2625242-9
ISSN	2159-8290 ; 2159-8274
ISSN (online)	2159-8290
ISSN	2159-8274
DOI	10.1158/2159-8290.CD-24-0282
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: Machine Learning Based Microbiome Signature to Predict Inflammatory Bowel Disease Subtypes.

Liñares-Blanco, Jose / Fernandez-Lozano, Carlos / Seoane, Jose A / López-Campos, Guillermo

Frontiers in microbiology

2022 Volume 13, Page(s) 872671

Abstract: Inflammatory bowel disease (IBD) is a chronic disease with unknown pathophysiological mechanisms. There is evidence of the role of microorganims in this disease development. Thanks to the open access to multiple omics data, it is possible to develop ... ...

Abstract	Inflammatory bowel disease (IBD) is a chronic disease with unknown pathophysiological mechanisms. There is evidence of the role of microorganims in this disease development. Thanks to the open access to multiple omics data, it is possible to develop predictive models that are able to prognosticate the course and development of the disease. The interpretability of these models, and the study of the variables used, allows the identification of biological aspects of great importance in the development of the disease. In this work we generated a metagenomic signature with predictive capacity to identify IBD from fecal samples. Different Machine Learning models were trained, obtaining high performance measures. The predictive capacity of the identified signature was validated in two external cohorts. More precisely a cohort containing samples from patients suffering Ulcerative Colitis and another from patients suffering Crohn's Disease, the two major subtypes of IBD. The results obtained in this validation (AUC 0.74 and AUC = 0.76, respectively) show that our signature presents a generalization capacity in both subtypes. The study of the variables within the model, and a correlation study based on text mining, identified different genera that play an important and common role in the development of these two subtypes.
Language	English
Publishing date	2022-05-17
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2587354-4
ISSN	1664-302X
ISSN	1664-302X
DOI	10.3389/fmicb.2022.872671
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Article ; Online: Machine Learning Algorithms Reveals Country-Specific Metagenomic Taxa from American Gut Project Data.

Liñares-Blanco, Jose / Fernandez-Lozano, Carlos / Seoane, Jose A / Lopez-Campos, Guillermo

Studies in health technology and informatics

2021 Volume 281, Page(s) 382–386

Abstract: In recent years, microbiota has become an increasingly relevant factor for the understanding and potential treatment of diseases. In this work, based on the data reported by the largest study of microbioma in the world, a classification model has been ... ...

Abstract	In recent years, microbiota has become an increasingly relevant factor for the understanding and potential treatment of diseases. In this work, based on the data reported by the largest study of microbioma in the world, a classification model has been developed based on Machine Learning (ML) capable of predicting the country of origin (United Kingdom vs United States) according to metagenomic data. The data were used for the training of a glmnet algorithm and a Random Forest algorithm. Both algorithms obtained similar results (0.698 and 0.672 in AUC, respectively). Furthermore, thanks to the application of a multivariate feature selection algorithm, eleven metagenomic genres highly correlated with the country of origin were obtained. An in-depth study of the variables used in each model is shown in the present work.
MeSH term(s)	Algorithms ; Machine Learning ; Metagenomics ; United Kingdom ; United States
Language	English
Publishing date	2021-05-27
Publishing country	Netherlands
Document type	Journal Article
ISSN	1879-8365
ISSN (online)	1879-8365
DOI	10.3233/SHTI210185
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Article ; Online: Chromatin regulators mediate anthracycline sensitivity in breast cancer.

Seoane, Jose A / Kirkland, Jacob G / Caswell-Jin, Jennifer L / Crabtree, Gerald R / Curtis, Christina

Nature medicine

2019 Volume 25, Issue 11, Page(s) 1721–1727

Abstract: Anthracyclines are a highly effective component of curative breast cancer chemotherapy but are associated with substantial ... ...

Abstract	Anthracyclines are a highly effective component of curative breast cancer chemotherapy but are associated with substantial morbidity
MeSH term(s)	Adult ; Aged ; Anthracyclines/administration & dosage ; Breast Neoplasms/drug therapy ; Breast Neoplasms/genetics ; Breast Neoplasms/pathology ; Cell Line, Tumor ; Chromatin/drug effects ; Chromatin/genetics ; Chromatin Assembly and Disassembly/drug effects ; Chromatin Assembly and Disassembly/genetics ; DNA Topoisomerases, Type II/genetics ; Drug Resistance, Neoplasm/genetics ; Female ; Gene Expression Regulation, Neoplastic/drug effects ; Histone-Lysine N-Methyltransferase/genetics ; Humans ; Jumonji Domain-Containing Histone Demethylases/genetics ; Middle Aged ; Myeloid-Lymphoid Leukemia Protein/genetics ; Poly-ADP-Ribose Binding Proteins/antagonists & inhibitors ; Poly-ADP-Ribose Binding Proteins/genetics ; Polycomb-Group Proteins/genetics ; Topoisomerase II Inhibitors/administration & dosage
Chemical Substances	Anthracyclines ; Chromatin ; KMT2A protein, human ; Poly-ADP-Ribose Binding Proteins ; Polycomb-Group Proteins ; Topoisomerase II Inhibitors ; Myeloid-Lymphoid Leukemia Protein (149025-06-9) ; Jumonji Domain-Containing Histone Demethylases (EC 1.14.11.-) ; KDM4B protein, human (EC 1.14.11.-) ; Histone-Lysine N-Methyltransferase (EC 2.1.1.43) ; DNA Topoisomerases, Type II (EC 5.99.1.3) ; TOP2A protein, human (EC 5.99.1.3)
Language	English
Publishing date	2019-11-07
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	1220066-9
ISSN	1546-170X ; 1078-8956
ISSN (online)	1546-170X
ISSN	1078-8956
DOI	10.1038/s41591-019-0638-5
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Zs.A 4212: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MG 39: Show issues

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Article ; Online: ZFP281 drives a mesenchymal-like dormancy program in early disseminated breast cancer cells that prevents metastatic outgrowth in the lung.

Nobre, Ana Rita / Dalla, Erica / Yang, Jihong / Huang, Xin / Wullkopf, Lena / Risson, Emma / Razghandi, Pedram / Anton, Melisa Lopez / Zheng, Wei / Seoane, Jose A / Curtis, Christina / Kenigsberg, Ephraim / Wang, Jianlong / Aguirre-Ghiso, Julio A

Nature cancer

2022 Volume 3, Issue 10, Page(s) 1165–1180

Abstract: Increasing evidence shows that cancer cells can disseminate from early evolved primary lesions much earlier than the classical metastasis models predicted. Here, we reveal at a single-cell resolution that mesenchymal-like (M-like) and pluripotency-like ... ...

Abstract	Increasing evidence shows that cancer cells can disseminate from early evolved primary lesions much earlier than the classical metastasis models predicted. Here, we reveal at a single-cell resolution that mesenchymal-like (M-like) and pluripotency-like programs coordinate dissemination and a long-lived dormancy program of early disseminated cancer cells (DCCs). The transcription factor ZFP281 induces a permissive state for heterogeneous M-like transcriptional programs, which associate with a dormancy signature and phenotype in vivo. Downregulation of ZFP281 leads to a loss of an invasive, M-like dormancy phenotype and a switch to lung metastatic outgrowth. We also show that FGF2 and TWIST1 induce ZFP281 expression to induce the M-like state, which is linked to CDH1 downregulation and upregulation of CDH11. We found that ZFP281 not only controls the early dissemination of cancer cells but also locks early DCCs in a dormant state by preventing the acquisition of an epithelial-like proliferative program and consequent metastases outgrowth.
MeSH term(s)	Humans ; Fibroblast Growth Factor 2 ; Neoplasms ; Transcription Factors/genetics ; Lung
Chemical Substances	Fibroblast Growth Factor 2 (103107-01-3) ; Transcription Factors
Language	English
Publishing date	2022-09-01
Publishing country	England
Document type	Journal Article ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ISSN	2662-1347
ISSN (online)	2662-1347
DOI	10.1038/s43018-022-00424-8
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Cell of Origin Influences Pancreatic Cancer Subtype.

Flowers, Brittany M / Xu, Hang / Mulligan, Abigail S / Hanson, Kathryn J / Seoane, Jose A / Vogel, Hannes / Curtis, Christina / Wood, Laura D / Attardi, Laura D

Cancer discovery

2021 Volume 11, Issue 3, Page(s) 660–677

Abstract: Pancreatic ductal adenocarcinoma (PDAC) is a deadly disease with a 5-year survival rate of approximately 9%. An improved understanding of PDAC initiation and progression is paramount for discovering strategies to better detect and combat this disease. ... ...

Abstract	Pancreatic ductal adenocarcinoma (PDAC) is a deadly disease with a 5-year survival rate of approximately 9%. An improved understanding of PDAC initiation and progression is paramount for discovering strategies to better detect and combat this disease. Although transcriptomic analyses have uncovered distinct molecular subtypes of human PDAC, the factors that influence subtype development remain unclear. Here, we interrogate the impact of cell of origin and different
MeSH term(s)	Acinar Cells/metabolism ; Acinar Cells/pathology ; Alleles ; Animals ; Biomarkers, Tumor ; Carcinoma, Pancreatic Ductal/diagnosis ; Carcinoma, Pancreatic Ductal/etiology ; Carcinoma, Pancreatic Ductal/metabolism ; Cell Transformation, Neoplastic/genetics ; Cell Transformation, Neoplastic/metabolism ; Computational Biology/methods ; Disease Models, Animal ; Disease Susceptibility ; Gene Expression Profiling ; Gene Expression Regulation, Neoplastic ; Humans ; Immunohistochemistry ; Kaplan-Meier Estimate ; Mice ; Mutation ; Oncogenes ; Pancreatic Neoplasms/diagnosis ; Pancreatic Neoplasms/etiology ; Pancreatic Neoplasms/metabolism ; Pancreatic Neoplasms/mortality ; Prognosis ; Proto-Oncogene Proteins p21(ras)/genetics ; Transcriptome
Chemical Substances	Biomarkers, Tumor ; KRAS protein, human ; Proto-Oncogene Proteins p21(ras) (EC 3.6.5.2)
Language	English
Publishing date	2021-05-19
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2625242-9
ISSN	2159-8290 ; 2159-8274
ISSN (online)	2159-8290
ISSN	2159-8274
DOI	10.1158/2159-8290.CD-20-0633
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Article ; Online: The Mettl3 epitranscriptomic writer amplifies p53 stress responses.

Raj, Nitin / Wang, Mengxiong / Seoane, Jose A / Zhao, Richard L / Kaiser, Alyssa M / Moonie, Nancie A / Demeter, Janos / Boutelle, Anthony M / Kerr, Craig H / Mulligan, Abigail S / Moffatt, Clare / Zeng, Shelya X / Lu, Hua / Barna, Maria / Curtis, Christina / Chang, Howard Y / Jackson, Peter K / Attardi, Laura D

Molecular cell

2022 Volume 82, Issue 13, Page(s) 2370–2384.e10

Abstract: The p53 transcription factor drives anti-proliferative gene expression programs in response to diverse stressors, including DNA damage and oncogenic signaling. Here, we seek to uncover new mechanisms through which p53 regulates gene expression using ... ...

Abstract	The p53 transcription factor drives anti-proliferative gene expression programs in response to diverse stressors, including DNA damage and oncogenic signaling. Here, we seek to uncover new mechanisms through which p53 regulates gene expression using tandem affinity purification/mass spectrometry to identify p53-interacting proteins. This approach identified METTL3, an m
MeSH term(s)	Animals ; Carcinogenesis ; Methyltransferases/metabolism ; Mice ; RNA ; Transcription Factors/metabolism ; Tumor Suppressor Protein p53/genetics
Chemical Substances	Transcription Factors ; Tumor Suppressor Protein p53 ; RNA (63231-63-0) ; Methyltransferases (EC 2.1.1.-) ; Mettl3 protein, mouse (EC 2.1.1.-)
Language	English
Publishing date	2022-05-04
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1415236-8
ISSN	1097-4164 ; 1097-2765
ISSN (online)	1097-4164
ISSN	1097-2765
DOI	10.1016/j.molcel.2022.04.010
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Zs.A 5055: Show issues

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Article ; Online: Functional screening of amplification outlier oncogenes in organoid models of early tumorigenesis.

Cell reports

2023 Volume 42, Issue 11, Page(s) 113355

Abstract: Somatic copy number gains are pervasive across cancer types, yet their roles in oncogenesis are insufficiently evaluated. This inadequacy is partly due to copy gains spanning large chromosomal regions, obscuring causal loci. Here, we employed organoid ... ...

Abstract	Somatic copy number gains are pervasive across cancer types, yet their roles in oncogenesis are insufficiently evaluated. This inadequacy is partly due to copy gains spanning large chromosomal regions, obscuring causal loci. Here, we employed organoid modeling to evaluate candidate oncogenic loci identified via integrative computational analysis of extreme copy gains overlapping with extreme expression dysregulation in The Cancer Genome Atlas. Subsets of "outlier" candidates were contextually screened as tissue-specific cDNA lentiviral libraries within cognate esophagus, oral cavity, colon, stomach, pancreas, and lung organoids bearing initial oncogenic mutations. Iterative analysis nominated the kinase DYRK2 at 12q15 as an amplified head and neck squamous carcinoma oncogene in p53
MeSH term(s)	Humans ; Tumor Suppressor Protein p53/genetics ; Oncogenes ; Cell Transformation, Neoplastic/genetics ; Neoplasms/genetics ; Carcinogenesis/genetics ; Gene Amplification
Chemical Substances	Tumor Suppressor Protein p53
Language	English
Publishing date	2023-11-01
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2649101-1
ISSN	2211-1247 ; 2211-1247
ISSN (online)	2211-1247
ISSN	2211-1247
DOI	10.1016/j.celrep.2023.113355
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Article ; Online: p53 governs an AT1 differentiation programme in lung cancer suppression.

Kaiser, Alyssa M / Gatto, Alberto / Hanson, Kathryn J / Zhao, Richard L / Raj, Nitin / Ozawa, Michael G / Seoane, José A / Bieging-Rolett, Kathryn T / Wang, Mengxiong / Li, Irene / Trope, Winston L / Liou, Douglas Z / Shrager, Joseph B / Plevritis, Sylvia K / Newman, Aaron M / Van Rechem, Capucine / Attardi, Laura D

Nature

2023 Volume 619, Issue 7971, Page(s) 851–859

Abstract: Lung cancer is the leading cause of cancer deaths ... ...

Abstract	Lung cancer is the leading cause of cancer deaths worldwide
MeSH term(s)	Animals ; Mice ; Alveolar Epithelial Cells/cytology ; Alveolar Epithelial Cells/metabolism ; Alveolar Epithelial Cells/pathology ; Cell Differentiation ; Lung/cytology ; Lung/metabolism ; Lung/pathology ; Lung Neoplasms/genetics ; Lung Neoplasms/metabolism ; Lung Neoplasms/pathology ; Lung Neoplasms/prevention & control ; Mice, Knockout ; Tumor Suppressor Protein p53/deficiency ; Tumor Suppressor Protein p53/genetics ; Tumor Suppressor Protein p53/metabolism ; Alleles ; Gene Expression Profiling ; Chromatin Assembly and Disassembly ; DNA/metabolism ; Lung Injury/genetics ; Lung Injury/metabolism ; Lung Injury/pathology ; Disease Progression ; Cell Lineage ; Regeneration ; Cell Self Renewal
Chemical Substances	Tumor Suppressor Protein p53 ; Trp53 protein, mouse ; Hras protein, mouse (EC 3.6.5.2) ; DNA (9007-49-2)
Language	English
Publishing date	2023-07-19
Publishing country	England
Document type	Journal Article
ZDB-ID	120714-3
ISSN	1476-4687 ; 0028-0836
ISSN (online)	1476-4687
ISSN	0028-0836
DOI	10.1038/s41586-023-06253-8
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Zs.A 26: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MG 9: Show issues
Zs.MO 244: Show issues

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