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The human body contains around 40 trillion cells made up from over 200 different cell types. This combination of different cells enables metazoan tissues to achieve complex phenotypes that no one cell type can achieve alone. For example, in the intestine, epithelial cells control nutrient uptake, whereas stromal fibroblasts support epithelial renewal, and tissue-resident leukocytes patrol against infection. No one cell type can perform all these jobs, but together they can collaborate to form a complex tissue epithelium with adaptive immunosurveillance. Such multicellular collaboration requires different cell types to communicate with one another.
Just like healthy intestinal tissue, colorectal cancer (CRC) tumours also contain epithelial, stromal, lymphoid, and myeloid cells. And like healthy tissues, CRC tumours use these different cells to achieve complex phenotypes. The difference with cancer is that these phenotypes (such as immune evasion and metastasis) can kill, rather than aid, the host organism. Unfortunately, we know very little about how the different cell types in cancer communicate with one another to drive tumours.
The human body contains around 40 trillion cells made up from over 200 different cell types. This combination of different cells enables metazoan tissues to achieve complex phenotypes that no one cell type can achieve alone. For example, in the intestine, epithelial cells control nutrient uptake, whereas stromal fibroblasts support epithelial renewal, and tissue-resident leukocytes patrol against infection. No one cell type can perform all these jobs, but together they can collaborate to form a complex tissue epithelium with adaptive immunosurveillance. Such multicellular collaboration requires different cell types to communicate with one another.
Just like healthy intestinal tissue, colorectal cancer (CRC) tumours also contain epithelial, stromal, lymphoid, and myeloid cells. And like healthy tissues, CRC tumours use these different cells to achieve complex phenotypes. The difference with cancer is that these phenotypes (such as immune evasion and metastasis) can kill, rather than aid, the host organism. Unfortunately, we know very little about how the different cell types in cancer communicate with one another to drive tumours.
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论文共 65 篇作者统计合作学者相似作者
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Gregory Sebepos-Rogers,Jahangir Sufi,Xiao Qin,Petra Vlckova, David Sanders, Charles Murray,Farooq Rahman,Christopher Tape,Andrew M. Smith
Gastroenterologyno. 5 (2024): S-160-S-161
Trends in Cell Biology (2024)
Brendan C Jones, Giada Benedetti,Giuseppe Calà,Lucinda Tullie,Ian C Simcock, Roberto Lutman, Monika Balys, Ramin Amiri,Jahangir Sufi, Owen Arthurs,Simon Eaton,Glenn Anderson,
biorxiv(2024)
Jinhai Deng,Teng Pan, Dan Wang, Yourae Hong,Zaoqu Liu,Xingang Zhou,Zhengwen An, Lifeng Li,Giovanna Alfano,Gang Li,Luigi Dolcetti,Rachel Evans,
EMBO molecular medicine (2024)
James W. Opzoomer, Rhianna O’Sullivan,Jahangir Sufi,Ralitsa Madsen,Xiao Qin, Ewa Basiarz,Christopher J. Tape
biorxiv(2024)
TRENDS IN CANCERno. 3 (2024): 185-195
Callum Baird Nattress,Daniel Fowler,Petra Vlckova, Colin Hutton,Maria Ramos Zapatero,Jahangir Sufi,Ferran Cardoso Rodriguez, Ashley Campbell, Angeliki Kanouta,Magdalena Buschhaus,Kerry Chester,John Anderson,
Daniel Fowler,Marta Barisa, Alba Southern,Callum Nattress,Elizabeth Hawkins, Eleni Vassalou, Angeliki Kanouta,John Counsell, Enrique Rota,Petra Vlckova,Benjamin Draper, Tessa De Mooij,
Science translational medicineno. 749 (2024): eadg9814-eadg9814
biorxiv(2023)
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作者统计
#Papers: 61
#Citation: 1801
H-Index: 20
G-Index: 28
Sociability: 6
Diversity: 2
Activity: 54
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