# Inflammation drives tumor growth in an immunocompetent implantable metastasis model

**Authors:** Connor Giles, Jungwoo Lee

PMC · DOI: 10.21203/rs.3.rs-4719290/v1 · Research Square · 2024-08-11

## TL;DR

This study introduces a new model to study cancer metastasis after tumor cell spread, showing that inflammation can promote tumor growth.

## Contribution

A novel serially transplantable metastasis model is developed to study post-dissemination tumor growth and therapy effects.

## Key findings

- 69% of scaffolds developed post-dissemination cancer growth after transplantation.
- Surgical resection via biopsy punch increased tumor burden and inflammation markers.
- Chemotherapy initially reduced DTC growth but did not prevent long-term progression.

## Abstract

Nearly 90% of cancer deaths are due to metastasis. Conventional cancer therapeutics including chemotherapy, surgery, and radiotherapy, are effective in treating primary tumors, but may aggravate disseminated tumor cells (DTCs) into regaining a proliferative state. Models isolating the post dissemination environment are needed to address the potential risks of these therapies, however modeling post dissemination environments is challenging. Often, host organisms become moribund due to primary tumor mass before native metastatic niches can evolve. Implantable tissue engineered niches have been used to attract circulating tumor cells independent of the primary tumor. Here, we serially transplant such tissue engineered niches with recruited DTCs in order to isolate the post dissemination environment. After transplantaion, 69% of scaffolds developed overt post-dissemination cancer growth, however 100% of scaffolds did not grow to a life-threatening critical size within twelve weeks. Adjuvant chemotherapy, while initially effective, did not prevent long-term DTC growth in scaffolds. Subjecting these transplanted niches to surgical resection via biopsy punch enhanced CD31, MMP9, Ly6G, and tumor burden compared to control scaffolds. Biopsy punching was able to rescue tumor incidence from prior chemotherapy. This model of serial transplantation of engineered DTC niches is a highly controllable and flexible method of establishing and systematically investigating the post-dissemination niche.

## Linked entities

- **Genes:** PECAM1 (platelet and endothelial cell adhesion molecule 1) [NCBI Gene 5175], MMP9 (matrix metallopeptidase 9) [NCBI Gene 4318], Ly6g (lymphocyte antigen 6 family member G) [NCBI Gene 546644]
- **Diseases:** cancer (MONDO:0004992)

## Full-text entities

- **Genes:** PECAM1 (platelet and endothelial cell adhesion molecule 1) [NCBI Gene 5175] {aka CD31, CD31/EndoCAM, GPIIA', PECA1, PECAM-1, endoCAM}, MMP9 (matrix metallopeptidase 9) [NCBI Gene 4318] {aka CLG4B, GELB, MANDP2, MMP-9}
- **Diseases:** cancer (MESH:D009369), Inflammation (MESH:D007249), metastasis (MESH:D009362)

## Full text

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## Figures

3 figures with captions in the complete paper: https://tomesphere.com/paper/PMC11326373/full.md

## References

58 references — full list in the complete paper: https://tomesphere.com/paper/PMC11326373/full.md

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Source: https://tomesphere.com/paper/PMC11326373