Michele Basso

Catholic University of the Sacred Heart , Milano, Lombardy, Italy

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Publications (32)140.89 Total impact

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    ABSTRACT: Estrogen receptor (ER), progesterone receptor (PR), and HER2/neu are the most important tissue markers in the management of breast cancer, in the adjuvant setting and in the setting of metastatic disease. Many studies have demonstrated a discordance of expression between primary breast cancer, synchronous axillary metastases, and metastatic sites. The aim of this article is to review studies on discordance of expression of these predictive parameters to better understand the importance of a reassessment of biomolecular status to modify treatment strategies. We performed a literature review to identify studies that assessed ER, PR, and HER2 discordance between primary breast cancer, synchronous axillary lymph node metastasis, and other metastatic sites. We reviewed these data related to (1) relevance of discordance rates in clinical practice and (2) therapeutic consequences of discordance rate. Results were analyzed qualitatively. Changes in ER and particularly in PR are observed in locoregional and in distant metastases reaching a rate of 10% to 30% for ER and 20% to 50% for PR. The loss of PR is more frequent than ER loss. High HER2 concordance between primary tumors and axillary lymph node or distant metastases has been demonstrated in many studies; in the discordant cases, it is more frequent to have HER2-positive metastases with negative primary tumors than the opposite. A reassessment of biomolecular status in residual tumors after neoadjuvant treatment or in metastatic sites is advisable, whenever it is possible, to correct/modify the treatment schedule and to estimate the actual prognosis. Copyright © 2015 Elsevier Inc. All rights reserved.
    Clinical Breast Cancer 03/2015; DOI:10.1016/j.clbc.2015.03.010 · 2.63 Impact Factor
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    ABSTRACT: The purpose of this study was to evaluate feasibility, safety, tolerance, and efficacy of drug-eluting beads loaded with irinotecan (DEBIRI) in combination with capecitabine in the treatment of mCRC refractory to chemotherapy in patients affected by liver predominant metastatic disease. Twenty patients affected by CRC hepatic metastasis with liver-dominant disease, who had progression after two or more lines of chemotherapy, were enrolled. TACE with 100 mg of Irinotecan loaded into 2-ml of 70-150 µm drug-eluting beads was administrated every 4 weeks in patients with unilobar disease (2 treatments) and every 2 weeks in patients with bilobar disease (4 treatments). All patients assumed capecitabine 1000 mg/m(2) twice daily on days 1-14 every 3 weeks, until disease progression. Primary endpoints were safety, tolerance and overall disease control (ODC); secondary endpoints were progression free survival (PFS) and overall survival (OS). A total of 54 treatments were performed (54/66, 82 %). No intra/peri-procedural death occurred. During the mean follow-up of 11 months, two partial responses (PR) were reported with ODC of 60 % (2 PR + 10 stable disease). PFS and OS were 4 and 7.3 months, respectively. Univariate analysis showed that patients presenting with KRAS wild-type, good ECOG performance status and unilobar disease had a better prognosis. Only performance status (ECOG) correlated with OS in multivariate analysis (p = 0.03). DEBIRI with capecitabine seem to be a safe, technically feasible and well-tolerated treatment in chemotherapy refractory liver prevalent colorectal metastases.
    CardioVascular and Interventional Radiology 03/2015; DOI:10.1007/s00270-015-1080-9 · 1.97 Impact Factor
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    ABSTRACT: Background and aims: Treatment with sorafenib of patients with advanced hepatocellular carcinoma (HCC) is challenged by anticipated discontinuation due to tumor progression, liver decompensation or adverse effects (AE). While post-progression survival is clearly determined by the pattern of tumor progression, understanding the factors that drive prognosis in patients who discontinued sorafenib for any reason may help to improve patient management and second line trial design. Methods: Patients consecutively admitted to 3 referral centers who were receiving best supportive care following permanent discontinuation of sorafenib for any reason, were included. Post-sorafenib survival (PSS) was calculated from the last day of treatment to death or last visit available. Results: Two-hundred and sixty patients were included in this prospective study, 67 year old, 60% hepatitis C, 51% Child-Pugh A, 83% Performance Status (PS) ≥1, 41% macroscopic vascular invasion and 38% extrahepatic tumor spread. Overall, median PSS was 4.1 (3.3-4.9) months, resulting from 4.6 (3.3-5.7) months for 123 progressors, 7.3 (6.0-10.0) months in 77 with AE and 1.8 (1.6-2.4) months in 60 decompensated patients (p<0.001). PSS was independently predicted by PS, prothrombin time, extrahepatic tumor spread and macrovascular invasion and reason for discontinuation. Two hundred patients potentially eligible to second line therapy, had a PSS of 5.3 (4.6-7.1) months, which was dependent on reasons of discontinuation (p=0.004), PS (p<0.001), macrovascular invasion (p<0.001) and extrahepatic metastases (p<0.002). Conclusion: discontinuation due to AE in the absence of macrovascular invasion, extrahepatic metastases and deteriorated PS, predicts the best PSS in compensated patients, thereby setting the stage for both improved patient counseling and selection second line therapy. This article is protected by copyright. All rights reserved.
    Hepatology 02/2015; DOI:10.1002/hep.27729 · 11.19 Impact Factor
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    ABSTRACT: Oxaliplatin (Oxa) is widely used in metastatic colorectal cancer (mCRC), but currently there are not valid predictors of response to this drug. In the control arms both of OPUS and PRIME studies Oxa seems more active in patients with mCRC with mutated (mt) KRAS than in those with wild type (wt) KRAS. Recently we have retrospectively confirmed this suggestion, therefore we have hypothesized that the mutational status of KRAS could influence the expression of ERCC1, one of the main mechanisms of Oxa resistance. We used four cell lines of colorectal cancer: two KRAS wild type (wt) (HCT-8 and HT-29) and two KRAS mt (SW620 and SW480). We evaluated the sensitivity of these cell lines to Oxa by MTT-test as well the ERCC1 levels before and after 24 h exposure to Oxa by Real-Time PCR. We silenced KRAS in a KRAS mt cell line (SW620LV) to evaluate the impact on Oxa sensitivity and ERCC1 levels. Lastly, ERCC1 was also silenced in order to confirm the importance of this protein as an Oxa resistance factor. The KRAS mt cell lines resulted more sensitive to Oxa (OR 2.68; IC 95% 1.511-4.757 p<0.001). The basal levels of ERCC1 did not show significant differences between KRAS mt and wt cell lines, however, after 24 h exposure to Oxa, only the wt KRAS lines showed the ability to induce ERCC1, with a statistically significant difference (OR 42.9 IC 95% 17.260-106.972 p<0.0005). By silencing KRAS, sensitivity to Oxa was reduced in mt KRAS cell lines and this effect was associated with the acquisition of ability to induce ERCC1. Silencing of ERCC1, in turn, enhanced the sensitivity to Oxa in wt KRAS cell lines and restored sensitivity to Oxa in SW620LV cell line. KRAS mutated cell lines were more sensitive to Oxa. This feature seems secondary to the inability of these cells to induce ERCC1 after exposure to Oxa. Thus, KRAS mutational status might be a predictor of response to Oxa in CRC surrogating the cell ability to induce ERCC1.
  • Journal of Hepatology 04/2014; 60(1):S51. DOI:10.1016/S0168-8278(14)60125-2 · 10.40 Impact Factor
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    ABSTRACT: Gastric cancer represents one of the most common cancer worldwide. Unfortunately, the majority of patients still present in advanced stage and, despite advances in diagnostic and treatment strategies, outcome still remains poor with high mortality rate despite decreasing incidence. Although utility of classical chemotherapy agents has been widely explored, advances have been slow and the efficacy of these agents has reached a plateau of median overall survival not higher than 12 months. Therefore, researchers focused their attention on better understanding molecular biology of carcinogenesis and of acquisition of the cancer cell phenotype, as well on development of rationally designed drugs that would target specific molecular aberrancies in signal transduction pathways. These targets include cell surface receptors, circulating growth and angiogenic factors and other molecules involved in downstream intracellular signalling pathways, including receptor tyrosine kinases. Therapeutic advances in gastric cancer are not so encouraging when compared to other solid organ malignanciessuch as breast and colorectal cancer. This article reviews the role of targeted agents in gastric cancer as single-agent therapy or in combination regimens, including their rational and emerging mechanism of action, current and emerging data. We focused our attention mainly on published phase III studies, therefore cornerstone clinical trials with trastuzumab and bevacizumab have been largely discussed. Phase III studies presented in important international meetings are also reviewed as well phase II published studies and promising new therapies investigated in preclinical or phase I studies. Todate, only trastuzumab has shown significantly increased survival in combination with chemotherapy in first-line and ramucirumab as single agent in second-line treatment, but - despite other disappointing results - these are the proof of principle that targeting the proper molecular aberration is the best way for implementing outcome of therapy.
    Current Medicinal Chemistry 11/2013; DOI:10.2174/0929867321666131129124054 · 3.72 Impact Factor
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    ABSTRACT: BACKGROUND: In 2007, sorafenib was the first drug able to improve overall survival in patients with advanced hepatocellular carcinoma. AIM: In 2005 we designed a phase II study to assess safety and efficacy of sunitinib. METHODS: This is a single arm, open-label, single-centre phase II trial. Eligibility criteria were advanced hepatocellular carcinoma; no prior chemotherapy, performance status 0-1; and Child≤B8. The treatment schedule was 50mg each day orally, 4 weeks on, 2 weeks off. RESULTS: Between 10/2007 and 10/2010, 34 patients were enrolled. A significant worsening of liver functional reserve after sunitinib was observed. Grade 3/4 adverse effects occurred in 80% of patients and included fatigue (47%), nausea (15%), liver failure (15%), encephalopathy (12%) and upper gastrointestinal bleeding (12%). Six patients (18%) died within 60 days of enrolment. A partial response was observed in 4 patients (12%). Median time to tumour progression was 2.8 months and median overall survival was 5.8 months. CONCLUSION: A dose of 50mg/d induces a high rate of severe adverse events. Toxicity remains a key concern also at the dose of 37.5mg/d. However, sunitinib is able to induce a prolonged response in some patients. Positron Emission Tomography/Computed Tomography scans may select good responders.
    Digestive and Liver Disease 02/2013; 45(8). DOI:10.1016/j.dld.2013.01.002 · 2.89 Impact Factor
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    ABSTRACT: Background:In this study, we evaluated the possibility that KRAS mutational status might be predictive of oxaliplatin (OXA) efficacy. We also explored the role of excision repair cross complementing group-1 (ERCC-1).Methods:Ninety anti-epidermal growth factor receptor-naive advanced colorectal cancer patients were retrospectively analysed. In all patients KRAS mutational status was assessed. In 60 patients mRNA ERCC-1 expression was also investigated. Response rate (RR) and progression-free survival (PFS) after FOLFOX-6±bevacizumab were evaluated according to KRAS status and mRNA ERCC-1 expression.Results:Among 90 patients 47% wild-type (wt) and 53% mutated (mt) KRAS tumours were found. Response rate was 26% in the wt KRAS group, whereas it was 56% in the mt KRAS group; the difference is statistically significant in the total sample (P=0.008) and when only patients receiving FOLFOX-6±bevacizumab as first-line are considered (P=0.01). Progression-free survival was longer in mt than in wt KRAS patients over all patients (10 vs 8 months, respectively, P=0.001) and in those treated as first-line (10 vs 8 months, respectively, P=0.0069). Mt KRAS patients experienced a longer survival (24 vs 18 months; P=0.01). ERCC-1 mRNA expression was not found to correlate with FOLFOX activity in our analysis.Conclusion:Our results suggest that activating mutation of KRAS oncogene may predict response to OXA. Basal expression of ERCC-1 mRNA does not explain the high efficacy of FOLFOX-6 in mt KRAS patients.British Journal of Cancer advance online publication, 22 November 2012; doi:10.1038/bjc.2012.526 www.bjcancer.com.
    British Journal of Cancer 11/2012; 108(1). DOI:10.1038/bjc.2012.526 · 4.82 Impact Factor
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    Michele Basso, Maria Basso, Carlo Barone
    Hepatology 04/2012; 55(4):1305; author reply 1305-6. DOI:10.1002/hep.25541 · 11.19 Impact Factor
  • Journal of Hepatology 04/2012; 56:S65-S66. DOI:10.1016/S0168-8278(12)60164-0 · 10.40 Impact Factor
  • Digestive and Liver Disease 02/2012; 44:S39. DOI:10.1016/S1590-8658(12)60113-3 · 2.89 Impact Factor
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    ABSTRACT: Gingival metastases are very rare and generally occur in disseminated tumors. We report a case of solitary gingival metastasis of lung cancer. We report the case of a 74-year-old asymptomatic Caucasian woman affected by a rapidly growing, painless gingival swelling. Histopathologic examination of the excisional biopsy showed metastasis of poorly differentiated thyroid transcription factor 1-positive adenocarcinoma. A total-body computed tomographic scan revealed a tumor of the right lung lower lobe with ipsilateral, mediastinal lymph node swelling. Moreover, bone scintigraphy revealed no bone metastases. No other metastases were found, so we planned a multi-modal therapeutic approach with a curative intent. However, the tumor proved to be intrinsically resistant and highly aggressive. The presentation of solitary gingival metastasis is exceptional. In view of its rapid clinical evolution, our case confirms that gingival metastasis is an important prognostic factor. This behavior raises the question whether the poor prognosis for patients with tumors with oral metastases depends on its diffuse spread or on its highly malignant nature.
    Journal of Medical Case Reports 05/2011; 5:202. DOI:10.1186/1752-1947-5-202
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    ABSTRACT: There is no agreement on which channel is involved in oxaliplatin neurotoxicity, most investigators favouring voltage-gated sodium channels. However, the small conductance Ca(++) activated K(+) channels, encoded by the SK1-3 genes, are also involved in membrane excitability, playing a role in after-hyperpolarization at the motor nerve terminal. As the SK3 gene is characterized in Caucasians by a highly polymorphic CAG motif within the exon 1, we hypothesize that SK3 gene polymorphism may influence the development of acute nerve hyperexcitability in oxaliplatin-treated patients. Patients eligible for an oxaliplatin-containing regimen were enrolled. Detailed neurological examination, nerve conduction studies and needle electromyography were performed before and after oxaliplatin administration. DNA was extracted by polymerase chain reaction, and each allele was isolated and sequenced. We evaluated 40 patients. After oxaliplatin administration, 28 patients developed symptoms of neurotoxicity, which were severe in 11. Patients were divided into three groups according to neurophysiological data: G0 (normal peripheral nerve excitability [PNE]), 16 patients; G1 (mild PNE), 15 patients; G2 (severe PNE), 9 patients. Genetic analysis showed different alleles ranging from 13 to 23 CAG repeats. Patients carrying alleles containing 13-15 CAG repeats experienced a significantly higher incidence of severe nerve hyperexcitability (chi-square 48.6; df 16; P = 0.0001). The results suggest that OXA-neurotoxicity may be related to distribution of the polymorphic CAG motif of the SK3 gene, which might modulate nerve after-hyperpolarization. The 13-14 CAG repeat allele could mark patients susceptible to acute OXA neurotoxicity.
    Cancer Chemotherapy and Pharmacology 05/2011; 67(5):1179-87. DOI:10.1007/s00280-010-1466-y · 2.57 Impact Factor
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    ABSTRACT: Two cases of acute hepatitis occurring during treatment with anastrozole have previously been reported, but the underlying mechanisms of liver injury are still uncertain. We report the case of anastrozole-related acute hepatitis with some autoimmune features. A 70-year-old woman developed acute hepatitis associated with serum antinuclear antibodies during anastrozole treatment; after drug withdrawal, liver function parameters rapidly improved and serum auto-antibodies were no longer detectable. Anastrozole-induced hepatotoxicity is a very rare event. Drug-drug interactions or metabolically-mediated damage might be involved, with a possible role of individual susceptibility. Our report suggests that an immune-mediated mechanism may also be considered in anastrozole-related liver injury.
    BMC Gastroenterology 03/2011; 11:32. DOI:10.1186/1471-230X-11-32 · 2.11 Impact Factor
  • Article: In reply.
    Cancer Chemotherapy and Pharmacology 02/2011; DOI:10.1007/s00280-011-1578-z · 2.57 Impact Factor
  • Lung Cancer 02/2011; 71. DOI:10.1016/S0169-5002(11)70197-0 · 3.74 Impact Factor
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    ABSTRACT: The prognosis of patients with advanced hepatocellular carcinoma (HCC) is very poor. The outcome of these patients is particularly bleak when the disease is complicated by portal vein tumor thrombosis (PVTT), since the increased portal pressure often causes serious gastrointestinal bleedings. Before the introduction of sorafenib (SOR), a tyrosine kinase inhibitor, no effective treatment was available for patients with advanced disease. SOR is now considered the standard treatment even for patients with tumor thrombosis, although the well-known interference between tyrosine kinase inhibitors and the coagulation pathway calls for caution against their use in this setting. Here, we report the case of a 74-year-old male patient with advanced HCC and PVTT treated with sunitinib (SUN), another multikinase inhibitor. During the third cycle, our patient experienced a life-threatening hematemesis with hemorrhagic shock that required intensive care treatment and SUN discontinuation. However, he completely recovered, and the PET/CT scan performed 1 year after the adverse effect demonstrated no evidence of the tumor together with portal vein recanalization. The short course of SUN causing both tumor response and gastrointestinal bleeding warrants further studies on the effectiveness of SUN in this setting as well as on the duration of treatment with multikinase inhibitors in patients with tumor thrombosis.
    Case Reports in Oncology 11/2010; 3(3):391-396. DOI:10.1159/000322135
  • Cancer Treatment Reviews 11/2010; 36. DOI:10.1016/S0305-7372(10)70074-8 · 6.47 Impact Factor
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    The Oncologist 07/2010; 15(7):790-1; author reply 792. DOI:10.1634/theoncologist.2010-0099 · 4.54 Impact Factor

Publication Stats

351 Citations
140.89 Total Impact Points


  • 2007–2015
    • Catholic University of the Sacred Heart
      • School of Internal Medicine
      Milano, Lombardy, Italy
  • 2005–2008
    • The Catholic University of America
      Washington, Washington, D.C., United States
  • 2004
    • Sacred Heart University
      Феърфилд, Connecticut, United States