4.6 Review

Tumoral stem cell reprogramming as a driver of cancer: Theory, biological models, implications in cancer therapy

期刊

SEMINARS IN CANCER BIOLOGY
卷 32, 期 -, 页码 3-9

出版社

ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
DOI: 10.1016/j.semcancer.2014.02.001

关键词

Oncogenes; Tumoral reprogramming; Stem cells; Cancer stem cell; Mouse model

类别

资金

  1. FEDER
  2. MICINN [SAF2012-32810]
  3. MEC OncoBIO Consolider-Ingenio [CSD2007-0017]
  4. NIH grant [R01 CA109335-04A1]
  5. ARIMMORA Project (FP7-ENV, European Union Seventh Framework Program)
  6. Junta de Castilla y Leon [BIO/SA06/13]
  7. proyecto en red de investigacion en celulas madre tumorales - Obra Social Kutxa y Conserjeria de Sanidad de la Junta de Castilla y Leon
  8. FSE-Conserjeria de Educacion de la Junta de Castilla y Leon [CSI020-12]

向作者/读者索取更多资源

Cancer is a clonal malignant disease originated in a single cell and characterized by the accumulation of partially differentiated cells that are phenotypically reminiscent of normal stages of differentiation. According to current models, therapeutic strategies that block oncogene activity are likely to selectively target tumor cells. However, recent evidences have revealed that cancer stem cells could arise through a tumor stem cell reprogramming mechanism, suggesting that genetic lesions that initiate the cancer process might be dispensable for tumor progression and maintenance. This review addresses the impact of these results toward a better understanding of cancer development and proposes new approaches to treat cancer in the future. (C) 2014 Elsevier Ltd. All rights reserved.

作者

我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。

评论

主要评分

4.6
评分不足

次要评分

新颖性
-
重要性
-
科学严谨性
-
评价这篇论文

推荐

Article Hematology

Conditional expression of HGAL leads to the development of diffuse large B-cell lymphoma in mice

Javier Raboso-Gallego, Ana Casado-Garcia, Xiaoyu Jiang, Marta Isidro-Hernandez, Andrew J. Gentles, Shuchun Zhao, Yaso Natkunam, Oscar Blanco, Veronica Dominguez, Belen Pintado, Diego Alonso-Lopez, Javier De las Rivas, Carolina Vicente-Duenas, Izidore S. Lossos, Isidro Sanchez-Garcia

Summary: The study shows that constitutive enforced expression of HGAL leads to DLBCL development, and this protein is mainly present in germinal center B lymphocytes.
Article Immunology

Heterogeneous disease-propagating stem cells in juvenile myelomonocytic leukemia

Eleni Louka, Benjamin Povinelli, Alba Rodriguez-Meira, Gemma Buck, Wei Xiong, Guanlin Wang, Nikolaos Sousos, Neil Ashley, Angela Hamblin, Christopher A. G. Booth, Anindita Roy, Natalina Elliott, Deena Iskander, Josu de la Fuente, Nicholas Fordham, Sorcha O'Byrne, Sarah Inglott, Ruggiero Norfo, Mariolina Salio, Supat Thongjuea, Anupama Rao, Irene Roberts, Adam J. Mead

Summary: Juvenile myelomonocytic leukemia (JMML) is a childhood leukemia with poor prognosis caused by RAS-pathway mutations. The cellular hierarchy of JMML is complex, with LSCs present in HSPCs, providing new avenues for monitoring and treating the disease.

JOURNAL OF EXPERIMENTAL MEDICINE (2021)

Article Cell Biology

Transitions in lineage specification and gene regulatory networks in hematopoietic stem/progenitor cells over human development

Anindita Roy, Guanlin Wang, Deena Iskander, Sorcha O'Byrne, Natalina Elliott, Jennifer O'Sullivan, Gemma Buck, Elisabeth F. Heuston, Wei Xiong Wen, Alba Rodriguez Meira, Peng Hua, Anastasios Karadimitris, Adam J. Mead, David M. Bodine, Irene Roberts, Bethan Psaila, Supat Thongjuea

Summary: Human hematopoiesis is a dynamic process that starts in utero 18-21 days post-conception, and understanding the site- and stage-specific variations is crucial for unraveling the origin of hematological disorders. The comparison of 57,489 HSPCs from 5 different tissues revealed significant transitions in cellular architecture and gene regulatory networks at different locations and developmental stages, with hematopoietic stem cells showing progression from cycling to quiescence during ontogeny. The dataset was also useful for understanding aberrant hematopoiesis in comparison to two cancers that present at distinct time points in postnatal life.

CELL REPORTS (2021)

Article Oncology

Transient Inhibition of the JAK/STAT Pathway Prevents B-ALL Development in Genetically Predisposed Mice

Ana Casado-Garcia, Marta Isidro-Hernandez, Ninad Oak, Andrea Mayado, Christine Mann-Ran, Javier Raboso-Gallego, Silvia Aleman-Arteaga, Alexandra Buhles, Dario Sterker, Elena G. Sanchez, Jorge Martinez-Cano, Oscar Blanco, Alberto Orfao, Diego Alonso-Lopez, Javier De Las Rivas, Susana Riesco, Pablo Prieto-Matos, Africa Gonzalez-Murillo, Francisco Javier Garcia Criado, Maria Begona Garcia Cenador, Thomas Radimerski, Manuel Ramirez-Orellana, Cesar Cobaleda, Jun J. Yang, Carolina Vicente-Duenas, Andreas Weiss, Kim E. Nichols, Isidro Sanchez-Garcia

Summary: This study demonstrates that early-life administration of the JAK1/2 inhibitor ruxolitinib significantly reduces the risk of B-ALL in mice. This finding presents a potential strategy for preventing the development of B-ALL.

CANCER RESEARCH (2022)

Article Multidisciplinary Sciences

Ezh2 is essential for the generation of functional yolk sac derived erythro-myeloid progenitors

Wen Hao Neo, Yiran Meng, Alba Rodriguez-Meira, Muhammad Z. H. Fadlullah, Christopher A. G. Booth, Emanuele Azzoni, Supat Thongjuea, Marella F. T. R. de Bruijn, Sten Eirik W. Jacobsen, Adam J. Mead, Georges Lacaud

Summary: The study reveals the crucial role of Ezh2 in modulating Wnt signaling during the generation of EMPs from YS HE. Loss of EZH2 activity in HE leads to the generation of non-functional EMPs due to a lack of Wnt signaling downregulation, while the generation of primitive erythroid cells is not affected. EZH2 is essential for the generation of functional EMPs at the onset of the endothelial-to-hematopoietic transition but becomes dispensable later on.

NATURE COMMUNICATIONS (2021)

Letter Oncology

Potential role of STAG1 mutations in genetic predisposition to childhood hematological malignancies

Claudia Saitta, Stefano Rebellato, Laura Rachele Bettini, Giovanni Giudici, Nicolo Panini, Eugenio Erba, Valentina Massa, Franziska Auer, Ulrike Friedrich, Julia Hauer, Andrea Biondi, Grazia Fazio, Giovanni Cazzaniga

BLOOD CANCER JOURNAL (2022)

Review Biochemistry & Molecular Biology

Childhood B-Cell Preleukemia Mouse Modeling

Marta Isidro-Hernandez, Silvia Aleman-Arteaga, Ana Casado-Garcia, Belen Ruiz-Corzo, Susana Riesco, Pablo Prieto-Matos, Jorge Martinez-Cano, Lucia Sanchez, Cesar Cobaleda, Isidro Sanchez-Garcia, Carolina Vicente-Duenas

Summary: Leukemia is the most common cancer in children, with B-cell acute lymphoblastic leukemia (B-ALL) being the most prevalent form. The development of pediatric leukemia is believed to occur through a multi-step or multi-hit mechanism, including prenatal and postnatal steps. Although many initiating events for childhood leukemia occur in utero at a higher frequency than the actual incidence of the disease, the reason why only a small percentage of children with these preleukemic hits develop full-blown leukemia remains unknown. Mouse models that replicate the multi-step process of childhood B-ALL will be crucial in identifying environmental or other factors associated with an increased risk of the disease.

INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES (2022)

Letter Oncology

Clinical and immunophenotypic characteristics of familial leukemia predisposition caused by PAX5 germline variants

Adela Escudero, Masatoshi Takagi, Franziska Auer, Ulrike Anne Friedrich, Satoshi Miyamoto, Atsushi Ogawa, Kohsuke Imai, Barbara Pascual, Maria Vela, Polina Stepensky, Layal Yasin, Sarah Elitzur, Arndt Borkhardt, Antonio Perez-Martinez, Julia Hauer

LEUKEMIA (2022)

Article Oncology

The CHK2 kinase is recurrently mutated and functionally impaired in the germline of pediatric cancer patients

Rabea Wagener, Carolin Walter, Franziska Auer, Deya Alzoubi, Julia Hauer, Ute Fischer, Julian Varghese, Martin Dugas, Arndt Borkhardt, Triantafyllia Brozou

Summary: Through whole-exome sequencing, we identified CHEK2 germline variants in 32/418 (7.7%) pediatric cancer patients, with 46.8% of them having leukemia. Functional analysis revealed that 5 pathogenic variants impaired CHK2 protein function. In conclusion, CHEK2 variants increase the risk for not only adult-onset but also pediatric cancer.

INTERNATIONAL JOURNAL OF CANCER (2023)

Review Oncology

Viewing AML through a New Lens: Technological Advances in the Study of Epigenetic Regulation

Laura C. C. Godfrey, Alba Rodriguez-Meira

Summary: This review outlines the recent advances in technology that enable the study of epigenetic mechanisms in blood cells with greater precision and resolution. The study of these mechanisms is crucial for understanding normal blood cell function and disease development. The new technologies allow for specific epigenetic changes to be introduced and the study of individual cells, providing a new lens for exploring epigenetic regulation.

CANCERS (2022)

Article Hematology

Cytokine Hyperresponsiveness in Children With ETV6::RUNX1-positive Acute Lymphoblastic Leukemia After Challenge With Common Pathogens

Nadine Ruechel, Marina Oldenburg, Stefan Janssen, Aleksandra A. Pandyra, Wei Liu, Eleni Vasileiou, Daniel Hein, Vera Helena Jepsen, Ute Fischer, Daniel Picard, Gesine Koegler, Julia Hauer, Franziska Auer, Angelina Beer, Ortwin Adams, Colin MacKenzie, Martin Jaeger, Mihai G. Netea, Arndt Borkhardt, Katharina L. Gossling

HEMASPHERE (2023)

Article Genetics & Heredity

A clinical screening tool to detect genetic cancer predisposition in pediatric oncology shows high sensitivity but can miss a substantial percentage of affected children

Ulrike A. Friedrich, Marc Bienias, Claudia Zinke, Maria Prazenicova, Judith Lohse, Arne Jahn, Maria Menzel, Jonas Langanke, Carolin Walter, Rabea Wagener, Triantafyllia Brozou, Julian Varghese, Martin Dugas, Miriam Erlacher, Evelin Schrock, Meinolf Suttorp, Arndt Borkhardt, Julia Hauer, Franziska Auer

Summary: This study assessed the efficacy of clinical checklists in detecting genetic cancer predisposition in children with cancer, and found that the clinical checklist showed high sensitivity in identifying cancer predisposition, but there were still limitations.

GENETICS IN MEDICINE (2023)

Article Genetics & Heredity

Single-cell multi-omics identifies chronic inflammation as a driver of TP53-mutant leukemic evolution

Alba Rodriguez-Meira, Ruggiero Norfo, Sean Wen, Agathe L. Chedeville, Haseeb Rahman, Jennifer O'Sullivan, Guanlin Wang, Eleni Louka, Warren W. Kretzschmar, Aimee Paterson, Charlotte Brierley, Jean-Edouard Martin, Caroline Demeule, Matthew Bashton, Nikolaos Sousos, Daniela Moralli, Lamia Subha Meem, Joana Carrelha, Bishan Wu, Angela Hamblin, Helene Guermouche, Florence Pasquier, Christophe Marzac, Francois Girodon, William Vainchenker, Mark Drummond, Claire Harrison, J. Ross Chapman, Isabelle Plo, Sten Eirik W. Jacobsen, Bethan Psaila, Supat Thongjuea, Ileana Antony-Debre, Adam J. Mead

Summary: This study analyzes hematopoietic stem/progenitor cells from patients with secondary acute myeloid leukemia (sAML) transforming from myeloproliferative neoplasm. They find that chronic inflammation suppresses TP53 wild-type cells while enhancing the fitness advantage of TP53-mutant cells, promoting genetic evolution. These findings will aid in the development of risk-stratification, early detection, and treatment strategies for TP53-mutant leukemia.

NATURE GENETICS (2023)

Review Immunology

Infectious triggers and novel therapeutic opportunities in childhood B cell leukaemia

Cesar Cobaleda, Carolina Vicente-Duenas, Isidro Sanchez-Garcia

Summary: B cell acute lymphoblastic leukaemia (B-ALL) is the most common form of childhood cancer, but treatment still fails in a significant percentage of patients. Studies have shown that a small percentage of healthy newborns carry preleukaemic clones, but only a small proportion of them will progress to overt leukemia.

NATURE REVIEWS IMMUNOLOGY (2021)

暂无数据