Shivakumar Keerthikumar

1 Introduction Prostate cancer is one of the most common malignancies worldwide, with ≈1.4 million new cases each year.[1] Most patients in high-income countries present with localized disease. Patients with intermediate to high-risk disease receive curative treatments, such as radiotherapy or radical prostatectomy, to ablate or remove the tumor.[2] Unfortunately, some patients subsequently develop disease recurrence and progress to advanced prostate cancer.

Abstract Tumour development and progression reshape the physical properties of the surrounding tumour microenvironment (TME) including its biomechanical traits. This is driven by a prominent cell type in the TME, cancer associated fibroblasts (CAFs), which increases tissue stiffness via extracellular matrix deposition and remodelling. Currently, it is unclear whether there are also physical changes to CAFs at the cellular level and, if so, how they relate to patient outcome.

Introduction Neuroendocrine prostate cancer (NEPC) is difficult to treat. As the androgen receptor (AR) is not expressed in these tumours, they are inherently resistant to androgen deprivation therapy and AR signalling inhibitors. NEPC is also heterogeneous, arising at different clinical stages and with varying histopathologies [1]. In rare cases, patients are diagnosed with NEPC [2].