For a long time plasticity has been mainly restricted to the brain but evidence has now paved the way to link this term to tumors. Indeed, from the very first steps of initiation to the latest stages of metastasis development, including therapeutic resistance, tumor cells have to adapt and this is termed tumor plasticity.
Within this research topic we want to tackle mechanisms involved in tumor plasticity by using in vitro models (organoids, tumor-on-chip) or in vivo models (PDXs, GEMMs) and validation on patient samples. The tumor plasticity field has rapidly evolved thanks to cutting edge technologies including scRNAseq, intravital microscopy and more recently spatial proteomic and transcriptomic methods. Improving our knowledge on methods used by tumor cells to escape therapies and to disseminate is urgently needed, not only for cancer biology understanding but also to identify innovative targets for further therapeutic strategies. We are specifically interested in colorectal and breast cancers as well as glioblastoma and melanoma.
By focusing on these specific cancer types and using in vitro or in vivo models we aim to address the following areas of research:
• Phenotypic heterogeneity and plasticity
The use of widespread scRNAseq analysis to explore tumor heterogeneity has shed light on tumor complexity and the existence of a variety of non-genetic cell states. The transition dynamic between these cell-states, the so-called cell plasticity, seems to fuel tumor adaptation to various environmental stresses, including therapeutic resistance. The recent development of spatial transcriptomics and proteomics technologies should improve our understanding of the tumor ecosystem. We encourage manuscripts relating to the major contribution of scRNAseq technology in deciphering tumor heterogeneity and highlighting the emergence of spatial omic technologies that promise to comprehensively characterize tumor architecture.
• Therapeutic escape: Tumor plasticity likely plays a major role in tumor adaptability and avoidance of therapeutic interventions. We welcome submissions which investigate and discuss the function of therapeutic escape resulting from tumor plasticity to further understanding of this interplay.
• Tumor dissemination: The metastatic abilities of tumors contribute to cancer complications and the danger of the condition: understanding how tumor plasticity, including plastic regulation of genes and cellular functions, contributes to tumor metastasis may further improve our ability to target and treat cancer in the future. We welcome papers that develop our understanding of tumor metastasis may also allow us to target cancer to limit or prevent metastasis.
For a long time plasticity has been mainly restricted to the brain but evidence has now paved the way to link this term to tumors. Indeed, from the very first steps of initiation to the latest stages of metastasis development, including therapeutic resistance, tumor cells have to adapt and this is termed tumor plasticity.
Within this research topic we want to tackle mechanisms involved in tumor plasticity by using in vitro models (organoids, tumor-on-chip) or in vivo models (PDXs, GEMMs) and validation on patient samples. The tumor plasticity field has rapidly evolved thanks to cutting edge technologies including scRNAseq, intravital microscopy and more recently spatial proteomic and transcriptomic methods. Improving our knowledge on methods used by tumor cells to escape therapies and to disseminate is urgently needed, not only for cancer biology understanding but also to identify innovative targets for further therapeutic strategies. We are specifically interested in colorectal and breast cancers as well as glioblastoma and melanoma.
By focusing on these specific cancer types and using in vitro or in vivo models we aim to address the following areas of research:
• Phenotypic heterogeneity and plasticity
The use of widespread scRNAseq analysis to explore tumor heterogeneity has shed light on tumor complexity and the existence of a variety of non-genetic cell states. The transition dynamic between these cell-states, the so-called cell plasticity, seems to fuel tumor adaptation to various environmental stresses, including therapeutic resistance. The recent development of spatial transcriptomics and proteomics technologies should improve our understanding of the tumor ecosystem. We encourage manuscripts relating to the major contribution of scRNAseq technology in deciphering tumor heterogeneity and highlighting the emergence of spatial omic technologies that promise to comprehensively characterize tumor architecture.
• Therapeutic escape: Tumor plasticity likely plays a major role in tumor adaptability and avoidance of therapeutic interventions. We welcome submissions which investigate and discuss the function of therapeutic escape resulting from tumor plasticity to further understanding of this interplay.
• Tumor dissemination: The metastatic abilities of tumors contribute to cancer complications and the danger of the condition: understanding how tumor plasticity, including plastic regulation of genes and cellular functions, contributes to tumor metastasis may further improve our ability to target and treat cancer in the future. We welcome papers that develop our understanding of tumor metastasis may also allow us to target cancer to limit or prevent metastasis.
