their report G?tte and coworkers [1] analyzed the manifestation of c-Met in 200 individuals with ductal carcinoma in situ. 91 lobular carcinomas). We constructed ten cells microarrays with three replicates per sample. Pearson’s chi-squared and Fisher’s precise test were used to analyze the results. None of the 155 breast tumors analyzed by FISH offered amplification of MET and 35 instances (22%) had a low grade of polysomy (three to five copies) of chromosome 7. Polysomy was more frequently observed in DIC (25%; P = 0.001). We tried to correlate polysomy of MET in the DIC group with Org 27569 grade tumor size lymph node status medical stage and manifestation of HER2 P53 estrogen receptor (ER) and progesterone receptor (PR). We observed that the absence of manifestation of PR was the unique statistically significant variable (P = 0.001). Moreover the ER+/PR- samples presented the highest rate of polysomy (38%) compared to ER+/PR+ tumors (15%) (Table ?(Table11). Table 1 Results of IHC of c-Met and FISH of LSI D7S486/CEP7 applied to lobular and ductal carcinomas Out of 168 tumors analyzed by immunohistochemistry 65 (38.7%) presented manifestation of c-Met. When histological types were compared the DIC group also showed the highest quantity of c-Met-positive samples (48%; P = 0.001). From your analysis with the clinico-pathological variables the negativity for PR was Org 27569 again statistically significant (P = 0.001). The ER+/PR- tumors offered more frequent manifestation of c-Met (68%) compared to ER+/PR+ tumors (32%) and were correlated with polysomy (P = 0.020) (Table ?(Table22). Table 2 IHC and FISH results of MET relating to the status of PR receptor in DIC carcinomas We can conclude that amplification of MET in breast cancer is not a common event as opposed to other malignancy Org 27569 subtypes (renal gastric and lung carcinomas). Although found in breast tumors it seems that overexpression of c-Met is not mainly due to increassed gene copy quantity of MET/polysomy7. However polysomy in the ER+/PR- group could be an important mechanism – although not the only one – responsible for the differential manifestation observed in this type of DIC. This c-Met overexpression and the presence of polysomy 7 could be important events to be considered with regard to the known poor response to endocrine therapies of ER+/PR- breast tumors. Lack of PR manifestation in ER+ tumors may be a surrogate marker of aberrant growth element signaling [3] that may be associated with their more aggressive end result as has already been Org 27569 explained [4]. Our study suggests that it would be interesting to investigate new Rabbit polyclonal to HAtag. therapeutic options for ER+/PR- DIC which may include c-Met inhibitors. Abbreviations DIC: ductal infiltrating carcinoma; ER: estrogen receptor; FISH: fluorescent in situ hybridization; PR: progesterone receptor. Competing interests The authors declare that they have no competing interests. Acknowledgements Grants PI05/0961 and PI06/1513 from Ministerio de Sanidad y Consumo ISCIII and RTICC 06/0020/19. Tumoral samples belong to the Org 27569 ‘Xarxa de Banc de Tumors de Catalunya’ (XBTC). Notes See related study article by G?tte et al..