Di Maio M.,Italian National Cancer Institute |
Bria E.,Medical Oncology du |
Banna G.L.,Medical Oncology Unit |
Puglisi F.,University of Udine |
And 3 more authors.
Anti-Cancer Drugs | Year: 2013
A significant proportion of cancer patients experience nausea or vomiting during the course of their disease, either because of the cancer itself or because of the treatment received. Highly or moderately emetogenic drugs are part of the standard chemotherapy regimens frequently used in patients with lung cancer, breast cancer, ovarian cancer, and several other common solid tumors. In this review, we describe the impact of nausea and vomiting in patients receiving chemotherapy, and the main progress achieved in the prophylaxis of chemotherapy-induced nausea and vomiting with the introduction of neurokinin 1 inhibitors. The adherence to existing guidelines is particularly important to avoid suboptimal prophylaxis and maximize patients' outcome. This review is focused on lung, breast, ovarian, and colorectal cancer, which are among the solid tumors characterized by a numeric and clinical relevance of the chemotherapy-induced nausea and vomiting issue because of the wide use of highly and/or moderately emetogenic chemotherapy regimens. © 2013 Wolters Kluwer Health Lippincott Williams & Wilkins.
Brunello E.,University of Verona |
Brunelli M.,University of Verona |
Bogina G.,Ospedale Sacro Cuore |
Calio A.,University of Verona |
And 14 more authors.
Journal of Experimental and Clinical Cancer Research | Year: 2012
Background: Lobular breast carcinoma usually shows poor responsiveness to chemotherapies and often lacks targeted therapies. Since FGFR1 expression has been shown to play pivotal roles in primary breast cancer tumorigenesis, we sought to analyze the status of FGFR1 gene in a metastatic setting of lobular breast carcinoma, since promising FGFR1 inhibitors has been recently developed. Methods. Fifteen tissue metastases from lobular breast carcinomas with matched primary infiltrative lobular breast carcinoma were recruited. Eleven cases showed loco-regional lymph-nodal and four haematogenous metastases. FGFR-1 gene (8p12) amplification was evaluated by chromogenic in situ hybridization (CISH) analysis. Her-2/neu and topoisomerase-IIα gene status was assessed. E-cadherin and Hercept Test were also performed. We distinguished amplification (>6 or cluster of signals) versus gains (3-6 signals) of the locus specific FGFR-1 gene. Results: Three (20%) primary lobular breast carcinomas showed >6 or cluster of FGFR1 signals (amplification), six cases (40%) had a mean of three (range 3-6) chromogenic signals (gains) whereas in 6 (40%) was not observed any abnormality. Three of 15 metastasis (20%) were amplified, 2/15 (13,4%) did not. The ten remaining cases (66,6%) showed three chromogenic signals. The three cases with FGFR-1 amplification matched with those primary breast carcinomas showing FGFR-1 amplification. The six cases showing FGFR-1 gains in the primary tumour again showed FGFR-1 gains in the metastases. Four cases showed gains of FGFR-1 gene signals in the metastases and not in the primary tumours. Her-2/neu gene amplification was not observed in all cases but one (6%) case. Topoisomerase-IIα was not amplified in all cases. Conclusions: 1) a subset of metastatic lobular breast carcinoma harbors FGFR-1 gene amplification or gains of chromogenic signals; 2) a minor heterogeneity has been observed after matching primary and metastatic carcinomas; 3) in the era of tailored therapies, patients affected by the lobular subtype of breast carcinoma with FGFR1 amplification could be approached to the new target biological therapy such as emerging FGFR-1 inhibitors. © 2012 Brunello et al.; licensee BioMed Central Ltd.