Researchers from the University of Michigan Rogel Cancer Center have uncovered clues as to why kidney cancers respond so differently to treatment, opening up new tailored treatment options.
Not all kidney cancers behave the same, and some have wildly differing responses to immunotherapy or other treatments – resulting in wildly different outcomes for patients.
By sequencing the RNA of individual cells within multiple benign and cancerous kidney tumors, the researchers have identified the cells from which different subtypes of kidney cancer originate, the pathways involved and how the tumor microenvironment impacts cancer development and response to treatment.
The findings, published in PNAS, could help researchers better understand renal cell carcinoma development and guide oncologists in optimising therapies for each patient.
“Single cell RNA sequencing was key to allowing us to monitor gene expression patterns in each individual cell, revealing the mechanisms at play within the tumour microenvironment that can predict overall survival,” says study author Arul Chinnaiyan, MD, PhD, director of the Michigan Center for Translational Pathology and SP Hicks Professor of Pathology at Michigan Medicine.
Researchers produced gene expression atlases for normal kidney and renal cell carcinoma samples. They predicted the putative cell of origin for more than 10 subtypes of renal cell cancer. Their analysis also uncovered pathways and interactions within the tumour microenvironment that predicted if the tumour would respond to immunotherapy. These findings could help develop biomarkers to guide kidney cancer treatment.
“By understanding the cell type where a cancer originates, it may allow us to target more precise treatments for that cancer type as well as better understand response to therapy,” Dr Chinnaiyan said.
Source: University of Michigan
Journal information: “Single-cell analyses of renal cell cancers reveal insights into tumor microenvironment, cell of origin, and therapy response,” PNAS. DOI: 10.1073/pnas.2103240118
