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PD-L1 Overexpression in Solid Tumours Forecast in 18 Major Markets 2017-2027 - Research and Markets
[July 12, 2017]

PD-L1 Overexpression in Solid Tumours Forecast in 18 Major Markets 2017-2027 - Research and Markets

The "PD-L1 Overexpression in Solid Tumours Forecast in 18 Major Markets 2017-2027" report has been added to Research and Markets' offering.

PD-1 is a T-cell immune checkpoint that is involved in the dampening of autoimmunity in the peripheral effector phase of T-cell activation. This leads to a tolerance' of cells expressing PD-L1 (programmed death ligand-1). PD-L1 is expressed normally on a number of different cell types including; placenta, vascular endothelium, pancreatic islet cells, muscle cells, hepatocytes, epithelium, mesenchymal stem cells, B-cells, T-cells, dendritic cells, macrophages and mast cells.

This report provides the current prevalent population for PDL-1 over-expression in cancer populations across 18 Major Markets (USA, Canada, France, Germany, Italy, Spain, UK, Russia, Turkey, audi Arabia, Japan, China, Argentina, Brazil, Mexico, India, South Africa and Australia) split by gender and 5-year age cohort. Along with the current prevalence, the report also contains a disease overview of the risk factors, disease diagnosis and prognosis along with specific variations by geography and ethnicity.

Providing a value-added level of insight from the analysis team, several of the main cancers with PDL-1 over-expression have been quantified and presented alongside the overall prevalence figures.

Key Topics Covered:

1. Introduction

2. Cause of the Disease

3. Diagnosis of the Disease

4. Variation by Geography/Ethnicity

5. Disease Prognosis (News - Alert) & Clinical Course

6. Key Cancers associated with the condition

7. Methodology for quantification of patient numbers

8. Top-line Prevalence for PD-L1 over-expression in Cancer populations

9. PD-L1 over-expression by type of cancer

10. Abbreviations used in the report

11. Patient-Based Offering

12. Online Pricing Data and Platforms

13. References

14. Appendix

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