Your browser doesn't support javascript.
loading
Show: 20 | 50 | 100
Results 1 - 4 de 4
Filter
Add more filters










Database
Language
Publication year range
1.
Clin Pharmacol Ther ; 101(5): 577-579, 2017 May.
Article in English | MEDLINE | ID: mdl-28073148

ABSTRACT

In the development of highly active anticancer drugs, the European situation may be viewed as paradoxical. Limited data may support marketing authorization, but may be insufficient for the health economic appraisal needed for reimbursement and market uptake. To achieve this, conventional confirmatory studies may be needed. For products of special interest, studies aimed at optimizing cost-effectiveness may be warranted. Efficient designs of studies to meet these objectives constitute challenges to all stakeholders.


Subject(s)
Drug Approval , Government Agencies , Medical Oncology/trends , Research Design , Antineoplastic Agents/economics , Antineoplastic Agents/therapeutic use , Cost-Benefit Analysis , European Union , Humans , Marketing/standards , Medical Oncology/economics
3.
Ann Oncol ; 27(1): 96-105, 2016 Jan.
Article in English | MEDLINE | ID: mdl-26487583

ABSTRACT

Patient access to new cancer drugs in the EU involves centralised licensing decisions by regulators as well as reimbursement recommendations in the context of national healthcare systems. Differences in assessment criteria and evidence requirements may result in divergent decisions at central and national levels, ultimately compromising effective access to patients. Early access decisions are particularly challenging due to the limited clinical evidence available to conclude on the benefit-risk and relative (cost-) effectiveness of new high-priced cancer drugs. We describe mechanisms to accelerate approval of promising anticancer drugs that fulfil an unmet medical need, review the experience from the European Medicines Agency, compare timelines and outcomes of reimbursement decisions in major EU markets, and discuss shortcomings of the current system, ongoing initiatives, and future steps to facilitate effective early access.


Subject(s)
Antineoplastic Agents/therapeutic use , Drug Approval , Neoplasms/drug therapy , European Union , Health Services Accessibility , Humans
4.
Oncogene ; 26(55): 7665-74, 2007 Dec 06.
Article in English | MEDLINE | ID: mdl-17599058

ABSTRACT

Cell-cycle inhibitors of the Cip/Kip and INK4 families are involved in cellular senescence and tumor suppression. Some of these proteins, p21(Cip1), p16(INK4a) and p15(INK4b), are coexpressed in response to antiproliferative signals such as cellular senescence resulting in cell-cycle arrest. To understand the roles of these inhibitors and their synergistic effect, we have characterized the growth properties and senescent behavior of primary cells deficient in p21(Cip1) and expressing an endogenous Cdk4(R24C) (cyclin-dependent kinase) mutant (Cdk4(R24C) knock-in cells) insensitive to INK4 proteins. Inactivation of both p21(Cip1) and INK4 pathways strongly cooperate in suppressing cellular senescence in vitro. These double mutant cells behavior as immortal cultures and display high sensitivity to cellular transformation by oncogenes. Moreover, mice double mutant in the INK4 and p21(Cip1) pathways (Cdk4(R24C); p21(Cip1)-null mice) display an increased incidence of specific sarcomas, suggesting a significant cooperation between these two families of cell-cycle inhibitors in senescence responses and tumor suppression in vivo.


Subject(s)
Cellular Senescence/genetics , Cyclin-Dependent Kinase Inhibitor Proteins/physiology , Sarcoma/genetics , Animals , Cyclin-Dependent Kinase 4/genetics , Cyclin-Dependent Kinase Inhibitor Proteins/genetics , Cyclin-Dependent Kinase Inhibitor p15/genetics , Cyclin-Dependent Kinase Inhibitor p15/physiology , Cyclin-Dependent Kinase Inhibitor p16/genetics , Cyclin-Dependent Kinase Inhibitor p16/physiology , Cyclin-Dependent Kinase Inhibitor p21/genetics , Cyclin-Dependent Kinase Inhibitor p21/physiology , Mice , Mice, Mutant Strains , Sarcoma/metabolism , Sarcoma/pathology
SELECTION OF CITATIONS
SEARCH DETAIL
...