Loss of inhibition over master pathways of bone mass regulation results in osteosclerotic bone metastases in prostate cancer

Prostate cancer is the most common cancer among men in industrialised countries. Most patients with prostate cancer, however, will not die of it. As a result, many of them will experience symptomatic metastasis during the course of the disease. Prostate cancer has a high propensity to metastasize to bone. Unlike many other cancers prostate cancer cells induce a rather osteosclerotic than osteolytic reaction in the bone marrow by interfering with physiological bone remodelling. A proper understanding of the mechanisms of tumour cell-induced bone alterations and exaggerated bone deposition in prostate cancer may open new and urgently needed therapeutic approaches in the field of palliative care for affected patients. In this review we focus on the central role of two major regulators of bone mass, the wingless type integration site family members (WNTs) and the bone morphogenetic proteins (BMPs), in the development of osteosclerotic bone metastases.

Thermal 2-loop master spectral function at finite momentum

When considering NLO corrections to thermal particle production in the “relativistic” regime, in which the invariant mass squared of the produced particle is K2 ~ (πT)2, then the production rate can be expressed as a sum of a few universal “master” spectral functions. Taking the most complicated 2-loop master as an example, a general strategy for obtaining a convergent 2-dimensional integral representation is suggested. The analysis applies both to bosonic and fermionic statistics, and shows that for this master the non-relativistic approximation is only accurate for K2 ~(8πT)2, whereas the zero-momentum approximation works surprisingly well. Once the simpler masters have been similarly resolved, NLO results for quantities such as the right-handed neutrino production rate from a Standard Model plasma or the dilepton production rate from a QCD plasma can be assembled for K2 ~ (πT)2.