ORCID Profile
0000-0002-7797-9822
Current Organisations
Third Affiliated Hospital of Sun Yat-Sen University
,
Saint John Fisher College
,
Sun Yat-Sen University
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Publisher: American Association for Cancer Research (AACR)
Date: 08-2023
DOI: 10.1158/0008-5472.23814807.V1
Abstract: Original picture
Publisher: American Association for Cancer Research (AACR)
Date: 08-2023
DOI: 10.1158/0008-5472.23814804.V1
Abstract: Original picture
Publisher: American Association for Cancer Research (AACR)
Date: 08-2023
DOI: 10.1158/0008-5472.23814810.V1
Abstract: Original picture
Publisher: American Association for Cancer Research (AACR)
Date: 08-2023
DOI: 10.1158/0008-5472.23814795.V1
Abstract: Original picture
Publisher: American Association for Cancer Research (AACR)
Date: 08-2023
DOI: 10.1158/0008-5472.23814792.V1
Abstract: supp. figure legends S1-S7
Publisher: American Association for Cancer Research (AACR)
Date: 08-2023
DOI: 10.1158/0008-5472.23814789.V1
Abstract: All supplementary tables in one excel file
Publisher: American Association for Cancer Research (AACR)
Date: 08-2023
DOI: 10.1158/0008-5472.23814807
Abstract: Original picture
Publisher: American Association for Cancer Research (AACR)
Date: 08-2023
DOI: 10.1158/0008-5472.23814819
Abstract: Original picture
Publisher: American Association for Cancer Research (AACR)
Date: 08-2023
DOI: 10.1158/0008-5472.23814810
Abstract: Original picture
Publisher: American Association for Cancer Research (AACR)
Date: 08-2023
DOI: 10.1158/0008-5472.23814789
Abstract: All supplementary tables in one excel file
Publisher: American Association for Cancer Research (AACR)
Date: 08-2023
DOI: 10.1158/0008-5472.23814813
Abstract: Original picture
Publisher: American Association for Cancer Research (AACR)
Date: 08-2023
DOI: 10.1158/0008-5472.23814804
Abstract: Original picture
Publisher: American Association for Cancer Research (AACR)
Date: 25-05-2023
DOI: 10.1158/0008-5472.CAN-22-3398
Abstract: BRCA1 deficiency generates an acidic microenvironment to promote cancer metastasis and immunotherapy resistance that can be reversed using a sialyltransferase inhibitor.
Publisher: American Association for Cancer Research (AACR)
Date: 08-2023
DOI: 10.1158/0008-5472.23814816
Abstract: Original picture
Publisher: American Society of Hematology
Date: 11-08-2011
DOI: 10.1182/BLOOD-2010-08-303800
Abstract: A large body of evidence suggests hemopoietic stem cells (HSCs) exist in an endosteal niche close to bone, whereas others suggest that the HSC niche is intimately associated with vasculature. In this study, we show that transplanted hemopoietic stem and progenitor cells (HSPCs) home preferentially to the trabecular-rich metaphysis of the femurs in nonablated mice at all time points from 15 minutes to 15 hours after transplantation. Within this region, they exist in an endosteal niche in close association with blood vessels. The preferential homing of HSPCs to the metaphysis occurs rapidly after transplantation, suggesting that blood vessels within this region may express a unique repertoire of endothelial adhesive molecules. One candidate is hyaluronan (HA), which is highly expressed on the blood vessel endothelium in the metaphysis. Analysis of the early stages of homing and the spatial dis-tribution of transplanted HSPCs at the single-cell level in mice devoid of Has3-synthesized HA, provides evidence for a previously undescribed role for HA expressed on endothelial cells in directing the homing of HSPCs to the metaphysis.
Publisher: American Association for Cancer Research (AACR)
Date: 08-2023
DOI: 10.1158/0008-5472.23814792
Abstract: supp. figure legends S1-S7
Publisher: American Association for Cancer Research (AACR)
Date: 08-2023
DOI: 10.1158/0008-5472.23814813.V1
Abstract: Original picture
Publisher: American Association for Cancer Research (AACR)
Date: 08-2023
DOI: 10.1158/0008-5472.C.6769338
Abstract: Abstract Cancer metastasis is an extremely complex process affected by many factors. An acidic microenvironment can drive cancer cell migration toward blood vessels while also h ering immune cell activity. Here, we identified a mechanism mediated by sialyltransferases that induces an acidic tumor-permissive microenvironment (ATPME) in BRCA1-mutant and most BRCA1-low breast cancers. Hypersialylation mediated by ST8SIA4 perturbed the mammary epithelial bilayer structure and generated an ATPME and immunosuppressive microenvironment with increased PD-L1 and PD1 expressions. Mechanistically, BRCA1 deficiency increased expression of VEGFA and IL6 to activate TGFβ–ST8SIA4 signaling. High levels of ST8SIA4 led to accumulation of polysialic acid (PSA) on mammary epithelial membranes that facilitated escape of cancer cells from immunosurveillance, promoting metastasis and resistance to αPD1 treatment. The sialyltransferase inhibitor 3Fax-Peracetyl Neu5Ac neutralized the ATPME, sensitized cancers to immune checkpoint blockade by activating CD8 T cells, and inhibited tumor growth and metastasis. Together, these findings identify a potential therapeutic option for cancers with a high level of PSA. Significance: BRCA1 deficiency generates an acidic microenvironment to promote cancer metastasis and immunotherapy resistance that can be reversed using a sialyltransferase inhibitor. /
Publisher: American Association for Cancer Research (AACR)
Date: 08-2023
DOI: 10.1158/0008-5472.C.6769338.V1
Abstract: Abstract Cancer metastasis is an extremely complex process affected by many factors. An acidic microenvironment can drive cancer cell migration toward blood vessels while also h ering immune cell activity. Here, we identified a mechanism mediated by sialyltransferases that induces an acidic tumor-permissive microenvironment (ATPME) in BRCA1-mutant and most BRCA1-low breast cancers. Hypersialylation mediated by ST8SIA4 perturbed the mammary epithelial bilayer structure and generated an ATPME and immunosuppressive microenvironment with increased PD-L1 and PD1 expressions. Mechanistically, BRCA1 deficiency increased expression of VEGFA and IL6 to activate TGFβ–ST8SIA4 signaling. High levels of ST8SIA4 led to accumulation of polysialic acid (PSA) on mammary epithelial membranes that facilitated escape of cancer cells from immunosurveillance, promoting metastasis and resistance to αPD1 treatment. The sialyltransferase inhibitor 3Fax-Peracetyl Neu5Ac neutralized the ATPME, sensitized cancers to immune checkpoint blockade by activating CD8 T cells, and inhibited tumor growth and metastasis. Together, these findings identify a potential therapeutic option for cancers with a high level of PSA. Significance: BRCA1 deficiency generates an acidic microenvironment to promote cancer metastasis and immunotherapy resistance that can be reversed using a sialyltransferase inhibitor. /
Publisher: American Association for Cancer Research (AACR)
Date: 08-2023
DOI: 10.1158/0008-5472.23814816.V1
Abstract: Original picture
Publisher: American Association for Cancer Research (AACR)
Date: 08-2023
DOI: 10.1158/0008-5472.23814795
Abstract: Original picture
Publisher: American Association for Cancer Research (AACR)
Date: 08-2023
DOI: 10.1158/0008-5472.23814819.V1
Abstract: Original picture
No related grants have been discovered for Todd Camenisch.