[HTML][HTML] Computational pathology identifies immune-mediated collagen disruption to predict clinical outcomes in gynecologic malignancies
Communications Medicine, 2024•nature.com
Background The role of immune cells in collagen degradation within the tumor
microenvironment (TME) is unclear. Immune cells, particularly tumor-infiltrating lymphocytes
(TILs), are known to alter the extracellular matrix, affecting cancer progression and patient
survival. However, the quantitative evaluation of the immune modulatory impact on collagen
architecture within the TME remains limited. Methods We introduce CollaTIL, a
computational pathology method that quantitatively characterizes the immune-collagen …
microenvironment (TME) is unclear. Immune cells, particularly tumor-infiltrating lymphocytes
(TILs), are known to alter the extracellular matrix, affecting cancer progression and patient
survival. However, the quantitative evaluation of the immune modulatory impact on collagen
architecture within the TME remains limited. Methods We introduce CollaTIL, a
computational pathology method that quantitatively characterizes the immune-collagen …
Background
The role of immune cells in collagen degradation within the tumor microenvironment (TME) is unclear. Immune cells, particularly tumor-infiltrating lymphocytes (TILs), are known to alter the extracellular matrix, affecting cancer progression and patient survival. However, the quantitative evaluation of the immune modulatory impact on collagen architecture within the TME remains limited.
Methods
We introduce CollaTIL, a computational pathology method that quantitatively characterizes the immune-collagen relationship within the TME of gynecologic cancers, including high-grade serous ovarian (HGSOC), cervical squamous cell carcinoma (CSCC), and endometrial carcinomas. CollaTIL aims to investigate immune modulatory impact on collagen architecture within the TME, aiming to uncover the interplay between the immune system and tumor progression.
Results
We observe that an increased immune infiltrate is associated with chaotic collagen architecture and higher entropy, while immune sparse TME exhibits ordered collagen and lower entropy. Importantly, CollaTIL-associated features that stratify disease risk are linked with gene signatures corresponding to TCA-Cycle in CSCC, and amino acid metabolism, and macrophages in HGSOC.
Conclusions
CollaTIL uncovers a relationship between immune infiltration and collagen structure in the TME of gynecologic cancers. Integrating CollaTIL with genomic analysis offers promising opportunities for future therapeutic strategies and enhanced prognostic assessments in gynecologic oncology.
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