Abstract 62P
Background
Sintilimab (Sin) helps the body to restore the anti-tumor response of T lymphocytes. However, in clinical use, the treatment process is more complicated due to adverse effects and different dosing regimens. It is not clear whether prebiotics (PREB) have a potentiating effect on Sin for lung adenocarcinoma, and this study intends to investigate the inhibitory effect, safety and possible mechanism of Sin combined with PREB on lung adenocarcinoma from animal experiments.
Methods
Lewis lung adenocarcinoma cells were inoculated into the right axilla of mice subcutaneously to prepare the Lewis lung cancer mouse model and treated in groups. The volume of transplanted tumors was measured, the histopathology of the liver and kidney of mice was observed by H&E staining, the levels of ALT, AST, UREA, CREA, WBC, RBC, and HGB in blood were analyzed biochemically; the ratio of T-cell subpopulations in blood, spleen, and bone marrow was detected by flow cytometry, the expression of PD-L1 in tumor tissue was detected by immunofluorescence staining, and 16S rRNA to analyze the diversity of fecal flora.
Results
Sin inhibited tumor growth and regulated immune cell homeostasis in lung adenocarcinoma mice, but liver and kidney histopathology showed different degrees of damage after Sin treatment, while the addition of PREB reduced liver and kidney damage in lung adenocarcinoma mice and promoted Sin's regulation of immune cells. In addition, the beneficial effects of Sin were associated with changes in intestinal flora diversity.
Conclusions
The mechanism by which Sintilimab combined with prebiotics inhibits tumor volume and regulates immune cell subpopulation balance in lung adenocarcinoma mice may be related to gut microbes.
Clinical trial identification
Editorial acknowledgement
Legal entity responsible for the study
Chengdu Fifth People's Hospital.
Funding
Has not received any funding.
Disclosure
All authors have declared no conflicts of interest.
Resources from the same session
4P - Spatially resolved transcriptome elucidates bidirectional tertiary lymphoid structure interacts with tumor microenvironment of non-small cell lung cancer
Presenter: Xin Zhao
Session: Poster session 09
5P - Tertiary lymphoid structures (TLS) presence and stromal blood vessels heterogeneity differentially influence recurrence, lymphovascular, and perineural invasion in breast cancer molecular subtypes
Presenter: Andrei Cosma
Session: Poster session 09
6P - Combined single-cell and spatially resolved mapping of the human lymph node ecosystem reveals fundamental principles of lymphoma tissue organization
Presenter: Daniel Hübschmann
Session: Poster session 09
7P - Engineered salmonella blocks cancer metastasis by activating NK cells in an IFN-γ-dependent manner
Presenter: JIANDONG HUANG
Session: Poster session 09
8P - Modulating tumor microenvironment using a VEGF active immunotherapeutic approach in gastrointestinal tumors: Beyond angiogenesis modulation
Presenter: Mónica Bequet-Romero
Session: Poster session 09
9P - Identification of a μCT-based radiomic signature of CD8+ tumour infiltrating lymphocytes in an orthotopic murine model
Presenter: Giulia Mazzaschi
Session: Poster session 09
10P - Cancer cells induce intracellular gap formation in sinusoidal endothelial cells to produce liver metastasis through pro-inflammatory paracrine mechanisms
Presenter: Hoang Truong
Session: Poster session 09
11P - Targeting stromal cells to reverse immune suppression in triple-negative breast cancer
Presenter: Julia Chen
Session: Poster session 09
12P - Immuno-suppressive role of tumour-derived GDF-15 on myeloid cells
Presenter: Christine Schuberth-Wagner
Session: Poster session 09
13P - Disrupting the immunosuppressive tumor microenvironment using genetically engineered macrophages for triple-negative breast cancer therapy
Presenter: Sabrina Traxel
Session: Poster session 09