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Articles by Simona Colla
Author Correction: Synthetic vulnerabilities of mesenchymal subpopulations in pancreatic cancer
Correction to: Nature https://doi.org/10.1038/nature21064 Published online 8 February 2017 In the version of this article initially published, in Extended Data Fig. 10d, the image showing CC3 staining/EPI tumors treated with AUY922 (d10) was duplicated from the image showing CC3 staining/EPI tumors vehicle treated (d10). Due to the age of the article, the figure cannot be updated directly. We provide the corrected figure and the raw data as Supplementary Information accompanying this amendment.
Author Correction: Oncogene ablation-resistant pancreatic cancer cells depend on mitochondrial function
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Correction to: Nature https://doi.org/10.1038/nature13611 Published online 10 August 2014 Since the version of the article initially published, a sample mislabeling issue has been brought to the authors’ attention concerning the immunoblots shown in Figs. 4a and 2b. The samples in Fig. 4a should have been labeled as “No. 3” and “No. 4”, rather than “No. 1” and “No. 2” as originally indicated. An updated version of Fig. 4a with the corrected sample identifiers is shown below as Fig. 1.
By Andrea Viale, Piergiorgio Pettazzoni, Costas A. Lyssiotis, Haoqiang Ying, Nora Sánchez, Matteo Marchesini, Alessandro Carugo, Tessa Green, Sahil Seth, Virginia Giuliani, Maria Kost-Alimova, Florian Muller Verified, Florian Muller Verified, Simona Colla, Luigi Nezi, Giannicola Genovese, Angela Deem, Avnish Kapoor, Wantong Yao, Emanuela Brunetto, Ya’an Kang, Min Yuan, John M. Asara, Y. Alan Wang, Timothy Heffernan, Alec C. Kimmelman, Huamin Wang, Jason Fleming, Lewis C. Cantley, Ronald DePinho, Giulio F. Draetta
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Nature
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A STAT3 degrader demonstrates efficacy in venetoclax resistant acute myeloid leukemia - Leukemia
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Abstract Acute myeloid leukemia (AML) is an aggressive myeloid malignancy with a poor prognosis. Venetoclax (Ven), a BCL2 inhibitor, has shown promising results but often leads to relapse due to mitochondrial dysregulation, particularly due to upregulation of the anti-apoptotic protein MCL1. Overexpression of the transcription factor STAT3 has been linked to poor survival in AML patients.
By Samarpana Chakraborty, Claudia Morganti, Kimberly Zaldana, Bianca Pena, Bianca Peña, Divij Verma, Nadege Gitego, Feiyang Ma, Srinivas Aluri, Kith Pradhan, Shanisha Gordon-Mitchell, Ioannis Mantzaris, Mendel Goldfinger, Eric Feldman Verified, Kira Gritsman, Stefan E. Hubner, Yi Qiu, Brandon Brown, Abdullah Khasawneh, Anna Skwarska, Marina Konopleva, Yoko Tabe, Evripidis Gavathiotis, Simona Colla, Jared Gollob, Joyoti Dey, Steven Kornblau, Sergei B Koralov, Keisuke Ito, Aditi Shastri
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Nature
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Author Correction: Clonal evolution of hematopoietic stem cells after autologous stem cell transplantation - Nature Genetics
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Correction to: Nature Genetics https://doi.org/10.1038/s41588-025-02235-w, published online 1 July 2025. In the version of this article originally published, Linda Zhang and Jennifer Padilla (both at the Department of Molecular and Cellular Biology, Baylor College of Medicine, Houston, TX, USA) did not appear in the author list or author contributions. The error has been corrected in the HTML and PDF versions of the article.
By Koichi Saeki, Hiroshi Haeno, Chiraag Kapadia, Ken Furudate, Jyoti Nangalia, Michael Chapman, Satoko Ogata, Courtney DiNardo, Nitin Jain, Farhad Ravandi, Jianhua Zhang, Robert Orlowski, Kapil Bhalla, Simona Colla, Hagop Kantarjian, Rashmi Kanagal-Shamanna, Carlos Bueso-Ramos, Daisuke Nakada, Gheath Al-Atrash, P. Andrew Futreal, Margaret A. Goodell, Guillermo Garcia-Manero
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Nature
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Clonal evolution of hematopoietic stem cells after autologous stem cell transplantation - Nature Genetics
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Abstract The impact of exogenous stressors, such as cancer chemotherapies, on the genomic integrity and clonal dynamics of normal hematopoiesis is not well defined. We conducted whole-genome sequencing on 1,276 single-cell-derived hematopoietic stem and progenitor cell (HSPC) colonies from ten patients with multiple myeloma treated with chemotherapies and six normal donors.
By Koichi Saeki, Hiroshi Haeno, Chiraag Kapadia, Ken Furudate, Jyoti Nangalia, Michael Chapman, Courtney DiNardo, Nitin Jain, Farhad Ravandi, Jianhua Zhang, Robert Orlowski, Kapil Bhalla, Simona Colla, Hagop Kantarjian, Rashmi Kanagal-Shamanna, Carlos Bueso-Ramos, Daisuke Nakada, Gheath Al-Atrash, P. Andrew Futreal, Margaret A. Goodell, Guillermo Garcia-Manero, Satoko Ogata
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Nature
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A Machine Learning-Based Method for Automatically Identifying Novel Cells in Annotating Single-Cell RNA-Seq Data
MOTIVATION: Single-cell RNA sequencing (scRNA-seq) has been widely used to decompose complex tissues into functionally distinct cell types. The first and usually the most important step of scRNA-seq data analysis is to accurately annotate the cell labels. In recent years, many supervised annotation methods have been developed and shown to be more convenient and accurate than unsupervised cell clustering.
"Isolation, Culture, and Immunophenotypic Analysis of Bone Marrow HSPCs" by Irene Ganan-Gomez, Karen Clise-Dwyer et al.
Drug testing assays in hematopoietic stem and progenitor cells (HSPCs) are fundamental in biological studies of myelodysplastic syndromes (MDS) but have historically entailed a technical challenge. This protocol allows the efficient isolation of MDS HSPCs from bone marrow mononuclear cell fractions and their culturing with the support of stromal cells for improved maintenance during drug testing.
Emerging Treatments for Myelodysplastic Syndromes: Biological Rationales and Clinical Translation
Home > UTHealth > GSBS > Journal Articles > 518 Cell Reports Medicine myelodysplastic syndromes, hypomethylating agents, secondary acute myeloid leukemia, novel therapeutic agents DOWNLOADS Included in Bioinformatics Commons, Biological Phenomena, Cell Phenomena, and Immunity Commons, Biomedical Informatics Commons, Medical Cell Biology Commons, Oncology Commons COinS
Orthogonal proteogenomic analysis identifies the druggable PA2G4-MYC axis in 3q26 AML - Nature Communications
Abstract The overexpression of the ecotropic viral integration site-1 gene (EVI1/MECOM) marks the most lethal acute myeloid leukemia (AML) subgroup carrying chromosome 3q26 abnormalities. By taking advantage of the intersectionality of high-throughput cell-based and gene expression screens selective and pan-histone deacetylase inhibitors (HDACis) emerge as potent repressors of EVI1.
STAT3 protects hematopoietic stem cells by preventing activation of a deleterious autocrine type-I interferon response - Leukemia
Abstract Hematopoietic stem and progenitor cells (HSPCs) maintain blood-forming and immune activity, yet intrinsic regulators of HSPCs remain elusive. STAT3 function in HSPCs has been difficult to dissect as Stat3-deficiency in the hematopoietic compartment induces systemic inflammation, which can impact HSPC activity. Here, we developed mixed bone marrow (BM) chimeric mice with inducible Stat3 deletion in 20% of the hematopoietic compartment to avoid systemic inflammation.
Emerging treatments for myelodysplastic syndromes: Biological rationales and clinical translation
Shastri A. Will B. Steidl U. Verma A. Stem and progenitor cell alterations in myelodysplastic syndromes. Blood. 2017; 129: 1586-1594https://doi.org/10.1182/blood-2016-10-696062 Treatment of MDS. Blood. Blood. 2019; 133: 1096-1107 Garcia-Manero G. Chien K.S. Montalban-Bravo G. Myelodysplastic syndromes: 2021 update on diagnosis, risk stratification and management. Am. J. Hematol. 2020; 95: 1399-1420https://doi.org/10.1002/ajh.25950 Fenaux P. Mufti G.J. Hellstrom-Lindberg E. Santini V. Finelli C. Giagounidis A.
Myelodysplastic syndrome (MDS) researcher: Leaps of faith led to my career at MD Anderson
Growing up in Italy, I found my happy place with science. Even when dealing with a challenging home life, science offered an escape. But I didn’t get my start in research until later in life. Now, as a principal investigator with my own lab at MD Anderson, I work with a talented group of researchers focused on myelodysplastic syndrome, specifically how it develops and becomes resistant to treatment. My lab is my life.
Myelodysplastic syndrome (MDS) researcher: Leaps of faith led to my career at MD Anderson
Growing up in Italy, I found my happy place with science. Even when dealing with a challenging home life, science offered an escape. But I didn’t get my start in research until later in life. Now, as a principal investigator with my own lab at MD Anderson, I work with a talented group of researchers focused on myelodysplastic syndrome, specifically how it develops and becomes resistant to treatment. My lab is my life.
Author Correction: Stem cell architecture drives myelodysplastic syndrome progression and predicts response to venetoclax-based therapy - Nature Medicine
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Correction to: Nature Medicine https://doi.org/10.1038/s41591-022-01696-4, published online 3 March 2022. In the version of this article initially published, the name of the Edward P. Evans Foundation was shown incorrectly in the first sentence of the Acknowledgements. The name has been corrected in the HTML and PDF versions of the paper.
By Irene Ganan-Gomez, Feiyang Ma, Kelly S. Chien, Ganiraju Manyam, Caleb A. Class, Rashmi Kanagal-Shamanna, Sanam Loghavi, Sarah Schneider, Vera Adema, Michael McLellan, Nicola Giuliani, Matteo Pellegrini, Jing L. Wang, Jason Renard Walker, Ziyi Li, Koichi Takahashi, Michael Andreeff, Simona Colla, Muharrem Muftuoglu
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Nature
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EZH2 Inhibitors: The Unpacking Revolution
Cancer Research Highlights Vera Adema and Simona Colla DOI: 10.1158/0008-5472.CAN-21-4311 Published February 2022 This article requires a subscription to view the full text. You may purchase access to this article or login to access your subscription using the links below. Abstract The methylation of lysine 27 on histone H3 (H3K27me3) is a chromatin mark associated with nucleosome condensation and gene expression silencing. EZH2 is a lysine methyltransferase that catalyzes H3K27me3.
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