Management of patients with advanced prostate cancer could be greatly improved by more sensitive, non-invasive techniques that allow more accurate staging and localisation of sites of metastases and low-volume recurrent disease.
The anatomical detail provided by CT allows better localisation of sites of physiologic activity and pathology identified by PET, thereby improving image interpretation and also providing rapid, low-noise transmission CT data for attenuation correction of PET emission data, essential for quantitative measurements.
In our preliminary experience PET-CT fusion imaging appears to be able to significantly improve the localisation of the site of primary tumours.
With respect to the high resolution EEG technique, the MEG technique allowed a more precise localisation of the sites of neural activity buried into the cortical sulci, but was unable to detect the response of the crown of the cortical giri and of the frontal-mesial cortex (including the supplementary motor area), because of its poor sensitivity to radially oriented dipoles.
Six peptides containing internal citrulline residues were sequenced, which enabled the localisation of nine sites of modification (Table 1).
An even better correlation is observed if we consider the localisation of the sites in the 3D structure of the LRRs.
Other parameters, such as performance status, interval between primary tumour and metastatic disease, sex, age, hepatic function, pretherapeutic serum concentration of S100, or number and localisation of metastatic sites had no significant impact on overall survival.
Routine use of single-photon emission computed tomography (SPECT) and particularly of hybrid SPECT/computed tomography (CT) has significantly improved localisation of tumour sites and evaluation of somatostatin receptor (SSTR) expression, which is important for predicting the likelihood of response to somatostatin analogues (SSA).
In RA this approach has demonstrated improved localisation to sites of inflammation by measuring increased levels of fluorescence in inflamed paws with a fluorescently labelled PEGylated anti-TNFα agent compared to a non-PEGylated TNFα inhibitor [ 53].
These experiments confirmed that the H-2Kd-E-cad mutant expressed in NHU cells was functional, as it efficiently incapacitated endogenous E-cadherin by blocking localisation to sites of cell-cell contact and preventing recruitment of α- and β-catenin.
