CORRESPONDENCE

Tumour cells produce receptor activator of NF-B ligand (RANKL) in skeletal metastases

L Huang¹, Y Y Cheng¹, L T C Chow², M H Zheng³ and S M Kumta⁴

¹ Department of Orthopaedics and Traumatology, Chinese University of Hong Kong, Shatin, NT, Hong Kong SAR
² Department of Anatomical and Cellular Pathology, Chinese University of Hong Kong
³ Department of Orthopaedic Surgery, University of Western Australia
⁴ Department of Orthopaedics and Traumatology, Chinese University of Hong Kong; sm-kumta@cuhk.edu.hk

Keywords: necropsy; view and grant system; death certification; coroner

The first 150 words of the full text of this article appear below.

Osteolytic bone destruction is a common complication of tumours that metastasise to bone. Several solid tumours, most notably breast carcinoma, lung carcinoma, and prostate carcinoma, commonly metastasise to bone in patients with advanced disease, where they cause osteolysis and associated pain, hypercalcemia, and fracture. It is generally accepted that osteoclasts are the only cells capable of resorbing mineralised bone. In osteolytic metastases, it has been shown that tumour cells direct osteoclastic bone resorption through a vicious cycle^1,2: in particular, tumour cell produced parathyroid hormone related protein (PTH-rP) facilitates bone resorption and, as a consequence, transforming growth factor ß is released from the bone matrix and promotes the progression of bone metastases by further inducing PTH-rP production by tumour cells. Other tumour cell products, such as macrophage colony stimulating factor, interleukin 6 (IL-6), IL-11, and tumour necrosis factor , have also been reported to be associated with tumour induced osteolysis.

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