On the basis of these findings, we evaluated two therapeutic strategies: the p75NTR modulator LM11A-31 and a compound we have developed, CN016. The BDNF Met66 variant shows about 49% prevalence in East Asian populations and 1 to 20% in other ethnic groups, suggesting population-specific susceptibility to CIPN. These findings establish BDNF genetic variation as a crucial determinant of CIPN risk and validate two promising therapeutic approaches, providing a foundation for personalized neuroprotective strategies in cancer treatment.
NCAM-positive NCLCs derived from hiPSCs enhance peripheral nerve regeneration through vascularization and Schwann cell-mediated remyelination, resulting in structural and functional recovery equivalent to autografts. This strategy offers a safe, scalable alternative to donor nerve harvest, and integration with bioengineered conduits could further expand clinical applicability in peripheral nerve reconstruction.
SCENIC analysis revealed HAND2, IKZF2 and SOX10 as transcriptional regulators of human NGFR+ antigen-presenting TAS cells, and they frequently expressed enteric glial cell markers SOX10, PLP1, CDH19 and NCAM1. In summary, our study demonstrates that the frequency and spatial distribution of TAS subpopulations, particularly NGFR+ TAS organization within TLS, varies between CRC patients and correlates with DFS and distinct changes in the TME.
In addition, we further discussed the potential mechanisms by which neurotrophin and adrenergic pathways regulate the balance between microenvironmental immunosuppression and lasting anti-tumor immunity. The purpose of this article is to define NGF/BDNF as shapers of the osteosarcoma immune microenvironment and to delineate biomarker-guided therapeutic opportunities for clinical testing.
Rescue experiments with siRNA against NGFR and an ERK1/2 inhibitor further established that PHOX1 drove malignant phenotypes via NGFR and downstream ERK1/2 signaling. In conclusion, our study defines PHOX1 as a methylation-sensitive oncogene in GC, orchestrating tumor progression through transcriptional activation of NGFR, and the PHOX1-NGFR-ERK1/2 axis may serve as a therapeutic target for metastatic GC.
The p75NTR knockdown mitigates diabetic periodontitis by inhibiting the recruitment of inflammatory macrophages and the secretion of inflammatory factors.
Overexpression of TCF-1 confers resistance to apoptosis, limits excessive activation, and promotes a less differentiated phenotype, collectively enhancing CAR-T cell persistence and long-term efficacy. These findings suggest that TCF-1 modulation represents a promising strategy to improve durability and safety of CAR-T cell therapy in relapsed or refractory hematologic malignancies.
The expression of p75NTR has not been described in this tumour entity before and its significance with regard to tumour promoting or tumour suppressing function or indication of a neurogenic differentiation remains undetermined. After a 3-year follow-up the dog was clinically healthy, indicating a successful surgical treatment.
3 months ago
Journal
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VIM (Vimentin) • NGFR (Nerve Growth Factor Receptor)
Here, we show that several stem cell subpopulations with distinct phenotypes co-exist in a tumor, each having impact on different clinical parameters. The cell subpopulations identified by the use of different CSC markers were found to be dynamic populations, able to switch between phenotypes. In addition, our data suggest that the stem cell heterogeneity is acquired and evolves parallel with carcinoma progression.
3 months ago
Journal
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ALDH1A1 (Aldehyde Dehydrogenase 1 Family Member A1) • BMI1 (BMI1 proto-oncogene, polycomb ring finger) • NGFR (Nerve Growth Factor Receptor)
TrkA inhibition significantly reduced tumor growth and invasion, with efficacy comparable to standard chemotherapeutics (5-FU, cisplatin)...In zebrafish, Trk-targeted interventions reduced metastatic dissemination. These findings highlight TrkA as a key regulator of cSCC survival and metastasis, suggesting its potential as a therapeutic target either alone or in combination with existing treatments.
The efficacy of CD271-targeted NIR-PIT was comparable to that of EGFR-targeted NIR-PIT in mouse models, even though the cell-surface expression of CD271 was lower than that of EGFR. This is the first study to demonstrate the efficacy of CD271-targeted NIR-PIT, which we believe will have a significant impact on the future development of cancer stem cell-targeted therapy.