
A novel immunotherapeutic strategy was developed to treat mouse cutaneous squamous cell carcinoma (mCSCC) by generating homologous neutralizing antibodies against tumor cells.


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Current cancer therapeutic strategies still face great challenges especially due to tumor relapse, drug resistance, and low treatment efficiency. The reason is that some tumor cells are able to outsmart the host immune mechanisms and evade the immune system. In this study, using the mouse cutaneous squamous cell carcinoma (mCSCC) as an example, a new cancer immunotherapeutic strategy with homologous neutralizing-antibodies was established. The experiment is divided into three stages. In the first stage, mCSCC cells were isolated and cultured from DMBA/TPA-induced mCSCC. In the second stage, the expanded tumor cells were then injected into healthy mice in order to produce anti-tumor homologous neutralizing-antibodies. In the final stage, therapeutic serum was extracted from healthy mice and injected back into tumor mice. ELISA assay was used to analyze the levels of p53, Bcl-xL, NF-κB, and Bax. The findings demonstrated that the serum treatment reduced tumor volume while also reversing changes in p53, Bcl-xL, NF-κB, and Bax. In conclusion, a novel immunotherapeutic strategy was developed to treat mCSCC, although more study is required to fully understand the mechanism of this serum treatment.

### Competing Interest Statement

The authors have declared no competing interest.

Generating specific homologous neutralizing-antibodies: a novel therapeutic strategy in cancer treatment

generating-homologous-neutralizing-antibodies-as-a-novel-immunotherapeutic-strategy-for-treating-mouse-cutaneous-squamous-cell-carcinoma


Generating Homologous Neutralizing Antibodies as a Novel Immunotherapeutic Strategy for Treating Mouse Cutaneous Squamous Cell Carcinoma


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The author highlights the critical role of PD-1 glycosylation in modulating the activity of immune checkpoint inhibitors, emphasizing the importance of fucosylated glycans in antibody binding.


Monoclonal antibodies targeting the immune checkpoint PD-1 have provided significant clinical benefit across a number of solid tumors, with differences in efficacy and toxicity profiles possibly related to their intrinsic molecular properties. Here, we report that camrelizumab and cemiplimab engage PD-1 through interactions with its fucosylated glycan. Using a combination of protein and cell glycoengineering, we demonstrate that the two antibodies bind preferentially to PD-1 with a core fucose at the asparagine N58 residue. We then provide evidence that the concentration of fucosylated PD-1 in the blood of non-small cell lung cancer patients varies across different stages of disease. This study illustrates how glycoprofiling of surface receptors and related circulating forms can inform the development of differentiated antibodies that discriminate glycosylation variants and achieve enhanced selectivity and paves the way towards the implementation of personalized therapeutic approaches.

### Competing Interest Statement

CC, TC, FAS, AT, CG, GC, FS are or were employees of InterVenn Biosciences, a company that identifies biomarkers and commercializes diagnostic tests. HL is a consultant of InterVenn Biosciences and received travel grants and consultant fees from Bristol-Myers Squibb, Alector, and MSD. HL received research support from Bristol-Myers Squibb, Novartis, GlycoEra and Palleon Pharmaceuticals.

Variable PD-1 glycosylation modulates the activity of immune checkpoint inhibitors

Impact-of-PD-1-Glycosylation-on-Immune-Checkpoint-Inhibitors


Impact of PD-1 Glycosylation on Immune Checkpoint Inhibitors



The author argues that the combination of tiragolumab and atezolizumab improves outcomes by activating macrophages and regulatory T cells, leading to a more favorable response in patients.


A high baseline of intratumoural macrophages and regulatory T cells is associated with better outcomes in patients with non-small cell lung cancer treated with atezolizumab plus tiragolumab, but not with atezolizumab alone.

Anti-TIGIT antibody improves PD-L1 blockade through myeloid and Treg cells - Nature

Impact-of-Anti-TIGIT-Antibody-on-PD-L1-Blockade-Outcomes


Impact of Anti-TIGIT Antibody on PD-L1 Blockade Outcomes
