Comparison of abluminal biodegradable polymer biolimus-eluting stents and durable polymer everolimus-eluting stents in the treatment of coronary bifurcations.

Comparison of abluminal biodegradable polymer biolimus-eluting stents and durable polymer everolimus-eluting stents in the treatment of coronary bifurcations.

Catheter Cardiovasc Interv. 2013 Jun 27;

Authors: Costopoulos C, Latib A, Naganuma T, Sticchi A, Ferrarello S, Regazzoli D, Chieffo A, Figini F, Carlino M, Montorfano M, Naim C, Kawaguchi M, Gerasimou A, Giannini F, Godino C, Colombo A

Abstract
OBJECTIVES: To compare biodegradable polymer biolimus-eluting (BES) with abluminal drug elution and durable polymer everolimus-eluting (EES) stents in the treatment of bifurcation lesions.
BACKGROUND: The persistence of a polymer in drug-eluting stents (DES) following drug elution has been viewed as a possible culprit for restenosis. DES with biodegradable polymer may thus be associated with improved clinical outcomes, especially in high-risk lesions such as those at bifurcation sites.
METHODS: We performed a retrospective study of consecutive de novo bifurcation lesions treated with EES between October 2006-October 2011 and BES between February 2008-March 2012. Study endpoints included major adverse cardiac events (MACE) defined as all cause-death, myocardial infarction (MI), including peri-procedural MI, and target vessel revascularization (TVR) as well as target lesion revascularization separately (TLR).
RESULTS: We analyzed 236 bifurcation lesions treated with either BES (79 lesions in 69 patients) or EES (157 lesions in 154 patients). Patient and procedural characteristics were broadly similar between the two groups. Estimated MACE and TVR rates at 2-year follow-up were similar between the BES and EES groups (MACE=13.6 � 4.6% vs. 14.6 � 3.2% (p=0.871); TVR=6.9 � 3.5% vs. 8.0 � 2.7% (p=0.889). No significant differences were noted between the two groups following propensity-score matched analysis. There was no probable or definite stent thrombosis.
CONCLUSION: BES use in the treatment of bifurcation lesions appears to be associated with good clinical outcomes, comparable to those seen with EES, at long-term follow-up. These results are hypothesis-generating and need to be validated with larger studies. � 2013 Wiley Periodicals, Inc.

PMID: 23804318 [PubMed - as supplied by publisher]

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Preserving Flow in Liver Transplant Recipients: mTOR Inhibitors Everolimus and Sirolimus Are Not Peas From a Pod.

Preserving Flow in Liver Transplant Recipients: mTOR Inhibitors Everolimus and Sirolimus Are Not Peas From a Pod.

Am J Transplant. 2013 Jul;13(7):1633-1635

Authors: Bhat M, Charlton M

PMID: 23802724 [PubMed - as supplied by publisher]

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Clinical modes of EGFR tyrosine kinase inhibitor failure and subsequent management in advanced non-small cell lung cancer.

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Clinical modes of EGFR tyrosine kinase inhibitor failure and subsequent management in advanced non-small cell lung cancer.

Lung Cancer. 2013 Jan;79(1):33-9

Authors: Yang JJ, Chen HJ, Yan HH, Zhang XC, Zhou Q, Su J, Wang Z, Xu CR, Huang YS, Wang BC, Yang XN, Zhong WZ, Nie Q, Liao RQ, Jiang BY, Dong S, Wu YL

Abstract
BACKGROUND: There is no published overview of epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI) failure modes in advanced non-small-cell lung cancer (NSCLC). This study aimed to classify the diversity of EGFR-TKI failure, and to investigate the usefulness of clinical modes in subsequent management and prognosis.
METHODS: One-hundred and twenty consecutive clinical trial patients with EGFR-TKI failure were enrolled as the training set to establish a clinical model based on clinical factors. Another 107 routine patients were enrolled as the validating set according to a Bayes discriminant analysis. EGFR mutations and c-MET amplification were analyzed. Kaplan-Meier survival analysis was used to test the differences among three clinical modes and subsequent management.
RESULTS: The duration of disease control, evolution of tumor burden, and clinical symptom were verified as feasible grouping variables. A correct grouping rate achieved 87.9%. The cohort was classified into three groups, as follows: 130 patients with dramatic progression, 42 with gradual progression, and 55 with local progression. Progression-free survivals (PFSs) for the dramatic progression, gradual progression, and local progression groups were 9.3, 12.9, and 9.2 months, respectively (P = 0.007). Overall survivals for the groups (OSs) were 17.1, 39.4, and 23.1 months, respectively (P < 0.001). TKI continuation was superior to switching chemotherapy in a subsequent setting for gradual progression (39.4 months vs. 17.8 months; P = 0.02). The difference of EGFR or c-MET among the three groups was not significant.
CONCLUSIONS: Clinical modes of EGFR-TKI failure could favor strategies for subsequent treatment and predicting a survival benefit in advanced NSCLC.

PMID: 23079155 [PubMed - indexed for MEDLINE]

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Clinical modes of EGFR tyrosine kinase inhibitor failure and subsequent management in advanced non-small cell lung cancer.

Related Articles

Clinical modes of EGFR tyrosine kinase inhibitor failure and subsequent management in advanced non-small cell lung cancer.

Lung Cancer. 2013 Jan;79(1):33-9

Authors: Yang JJ, Chen HJ, Yan HH, Zhang XC, Zhou Q, Su J, Wang Z, Xu CR, Huang YS, Wang BC, Yang XN, Zhong WZ, Nie Q, Liao RQ, Jiang BY, Dong S, Wu YL

Abstract
BACKGROUND: There is no published overview of epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI) failure modes in advanced non-small-cell lung cancer (NSCLC). This study aimed to classify the diversity of EGFR-TKI failure, and to investigate the usefulness of clinical modes in subsequent management and prognosis.
METHODS: One-hundred and twenty consecutive clinical trial patients with EGFR-TKI failure were enrolled as the training set to establish a clinical model based on clinical factors. Another 107 routine patients were enrolled as the validating set according to a Bayes discriminant analysis. EGFR mutations and c-MET amplification were analyzed. Kaplan-Meier survival analysis was used to test the differences among three clinical modes and subsequent management.
RESULTS: The duration of disease control, evolution of tumor burden, and clinical symptom were verified as feasible grouping variables. A correct grouping rate achieved 87.9%. The cohort was classified into three groups, as follows: 130 patients with dramatic progression, 42 with gradual progression, and 55 with local progression. Progression-free survivals (PFSs) for the dramatic progression, gradual progression, and local progression groups were 9.3, 12.9, and 9.2 months, respectively (P = 0.007). Overall survivals for the groups (OSs) were 17.1, 39.4, and 23.1 months, respectively (P < 0.001). TKI continuation was superior to switching chemotherapy in a subsequent setting for gradual progression (39.4 months vs. 17.8 months; P = 0.02). The difference of EGFR or c-MET among the three groups was not significant.
CONCLUSIONS: Clinical modes of EGFR-TKI failure could favor strategies for subsequent treatment and predicting a survival benefit in advanced NSCLC.

PMID: 23079155 [PubMed - indexed for MEDLINE]

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Aspirin antagonizes the cytotoxic effect of methotrexate in lung cancer cells.

Aspirin antagonizes the cytotoxic effect of methotrexate in lung cancer cells.

Oncol Rep. 2013 Jun 21;

Authors: Yan KH, Lee LM, Hsieh MC, Yan MD, Yao CJ, Chang PY, Chen TL, Chang HY, Cheng AL, Lai GM, Chuang SE

Abstract
Methotrexate (MTX) has been widely used for the treatment of cancer and rheumatoid arthritis (RA). Aspirin (ASA) is a non-selective cyclooxygenase (COX) inhibitor that contributes to the treatment of inflammatory conditions such as RA. It has been observed that the antitumor effect of ASA can be attributed to inhibition of cell cycle progression, induction of apoptosis and inhibition of angiogenesis. In the present study, we revealed that the treatment with a combination of MTX and ASA resulted in antagonism of the cytotoxic effect as demonstrated by SRB and colony formation assays. ASA alleviated the MTX-mediated S�phase accumulation and recovered the G1�phase. MTX-mediated accumulation of the S�phase marker cyclin�A was also alleviated by ASA. Notably, FAS protein levels were upregulated by MTX in A549 cells. The antagonism of MTX efficacy caused by ASA was accompanied by altered expression of caspase-3, Bcl-2 and FAS but not dihydrofolate reductase (DHFR). This suggests that the alteration of caspase-3, Bcl-2 and FAS was involved in the antagonism between ASA and MTX. Exogenously added folic acid reversed the MTX-mediated DHFR inhibition following either MTX or MTX�+�ASA treatments. Most importantly, we demonstrated for the first time that the commonly used non-steroidal anti-inflammatory drug for headache ASA and possibly other COX-1/2 inhibitors can produce a strong antagonistic effect on the growth inhibition of lung cancer cells when administered in combination with MTX. The clinical implication of our finding is obvious, i.e., the clinical efficacy of MTX therapy can be compromised by ASA and their concomitant use should be avoided.

PMID: 23799623 [PubMed - as supplied by publisher]

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Antiangiogenic agents in advanced, persistent or recurrent endometrial cancer: a novel treatment option.

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Antiangiogenic agents in advanced, persistent or recurrent endometrial cancer: a novel treatment option.

Gynecol Endocrinol. 2013 Jun 14;

Authors: Gadducci A, Sergiampietri C, Guiggi I

Abstract
Abstract The limited efficacy of endocrine therapy and chemotherapy has stimulated several researches aimed to detect novel molecularly target therapies for advanced, persistent or recurrent endometrial cancer. Prior attempts to block vascular endothelial growth factor (VEGF) with sunitinib, sorafenib and thalidomide have obtained disappointing results. Bevacizumab has shown a promising activity in a phase II study. The percentages of patients with progression-free survival ?6 months were similar for endometrioid (35%) and serous carcinoma (36%), but the number of cases was too small to assess the relevance of histological type for response to bevacizumab. In a phase II study, aflibercept was administered every 2 weeks to women with recurrent or persistent disease after chemotherapy. Forty-one percent of the patients were progression-free at 6 months, but 32% of the women had been removed from study because of toxicity. The detection of activating mutations of Fibroblast Growth Factor Receptor (FGFR)-2 in primary endometrial carcinoma has generated a new avenue for the development of molecularly target agents. Dovitinib, a tyrosine kinase inhibitor targeting both VEGF receptor (VEGFR) and FGFRs, is under clinical investigation in different malignancies including endometrial cancer.

PMID: 23767831 [PubMed - as supplied by publisher]

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Antiangiogenic agents in advanced, persistent or recurrent endometrial cancer: a novel treatment option.

Related Articles

Antiangiogenic agents in advanced, persistent or recurrent endometrial cancer: a novel treatment option.

Gynecol Endocrinol. 2013 Jun 14;

Authors: Gadducci A, Sergiampietri C, Guiggi I

Abstract
Abstract The limited efficacy of endocrine therapy and chemotherapy has stimulated several researches aimed to detect novel molecularly target therapies for advanced, persistent or recurrent endometrial cancer. Prior attempts to block vascular endothelial growth factor (VEGF) with sunitinib, sorafenib and thalidomide have obtained disappointing results. Bevacizumab has shown a promising activity in a phase II study. The percentages of patients with progression-free survival ?6 months were similar for endometrioid (35%) and serous carcinoma (36%), but the number of cases was too small to assess the relevance of histological type for response to bevacizumab. In a phase II study, aflibercept was administered every 2 weeks to women with recurrent or persistent disease after chemotherapy. Forty-one percent of the patients were progression-free at 6 months, but 32% of the women had been removed from study because of toxicity. The detection of activating mutations of Fibroblast Growth Factor Receptor (FGFR)-2 in primary endometrial carcinoma has generated a new avenue for the development of molecularly target agents. Dovitinib, a tyrosine kinase inhibitor targeting both VEGF receptor (VEGFR) and FGFRs, is under clinical investigation in different malignancies including endometrial cancer.

PMID: 23767831 [PubMed - as supplied by publisher]

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