Going for a “KDIP” in colorectal cancer treatment
[...]they showed that despite a short half-life of 30.9 min in serum, intravenous administration of KDIP resulted in a significant, dose-dependent reduction of tumour growth in a syngeneic subcutaneous mouse model of KITENIN-overexpressing CT26 cells, but had little effect on non-overexpressing CT26...
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Published in | Clinical and translational discovery Vol. 2; no. 3 |
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Main Authors | , |
Format | Journal Article |
Language | English |
Published |
Birtinya
John Wiley & Sons, Inc
01.09.2022
Wiley |
Subjects | |
Online Access | Get full text |
ISSN | 2768-0622 2768-0622 |
DOI | 10.1002/ctd2.108 |
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Abstract | [...]they showed that despite a short half-life of 30.9 min in serum, intravenous administration of KDIP resulted in a significant, dose-dependent reduction of tumour growth in a syngeneic subcutaneous mouse model of KITENIN-overexpressing CT26 cells, but had little effect on non-overexpressing CT26 tumours. Furthermore, intravenous KDIP treatment also reduced liver colonisation by KITENIN-overexpressing CT26 cells in a hepatic metastasis model. [...]while shedding light on a novel aspect of KITENIN's biology and how homodimerization regulates its stability, the authors have shown this feature to be a novel actionable target for cancer intervention and designed a first tool, KDIP, to modulate it. First and foremost, in this study, the authors have shown the efficacy of KDIP in syngeneic mouse models alone, leaving the question of whether the same effect also applies to human tumours unanswered. |
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AbstractList | [...]they showed that despite a short half-life of 30.9 min in serum, intravenous administration of KDIP resulted in a significant, dose-dependent reduction of tumour growth in a syngeneic subcutaneous mouse model of KITENIN-overexpressing CT26 cells, but had little effect on non-overexpressing CT26 tumours. Furthermore, intravenous KDIP treatment also reduced liver colonisation by KITENIN-overexpressing CT26 cells in a hepatic metastasis model. [...]while shedding light on a novel aspect of KITENIN's biology and how homodimerization regulates its stability, the authors have shown this feature to be a novel actionable target for cancer intervention and designed a first tool, KDIP, to modulate it. First and foremost, in this study, the authors have shown the efficacy of KDIP in syngeneic mouse models alone, leaving the question of whether the same effect also applies to human tumours unanswered. |
Author | Kaur, Jastrinjan Soucek, Laura |
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Cites_doi | 10.3389/fchem.2021.682675 10.1158/0008-5472.CAN-04-0275 10.18632/oncotarget.3087 10.1186/s12943-021-01368-w 10.1166/jnn.2019.15899 10.1158/0008-5472.CAN-05-0590 10.1002/mc.22572 10.1038/mt.2014.105 |
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Copyright | 2022 The Authors. published by John Wiley & Sons Australia, Ltd on behalf of Shanghai Institute of Clinical Bioinformatics. 2022. This work is published under http://creativecommons.org/licenses/by/4.0/ (the "License"). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. |
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SubjectTerms | Cancer therapies Colorectal cancer Conflicts of interest Design Glioma Liver Metastasis Peptides Proteins Signal transduction Tumors |
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Title | Going for a “KDIP” in colorectal cancer treatment |
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