Inflammation and cancer: back to Virchow?
F Balkwill, A Mantovani - The lancet, 2001 - thelancet.com
The response of the body to a cancer is not a unique mechanism but has many parallels
with inflammation and wound healing. This article reviews the links between cancer and …
with inflammation and wound healing. This article reviews the links between cancer and …
[HTML][HTML] Review of therapeutic drug monitoring of anticancer drugs part two–targeted therapies
Most of oral targeted therapies are tyrosine kinase inhibitors (TKIs). Oral administration
generates a complex step in the pharmacokinetics (PK) of these drugs. Inter-individual PK …
generates a complex step in the pharmacokinetics (PK) of these drugs. Inter-individual PK …
Clinical resistance to STI-571 cancer therapy caused by BCR-ABL gene mutation or amplification
ME Gorre, M Mohammed, K Ellwood, N Hsu… - Science, 2001 - science.org
Clinical studies with the Abl tyrosine kinase inhibitor STI-571 in chronic myeloid leukemia
demonstrate that many patients with advanced stage disease respond initially but then …
demonstrate that many patients with advanced stage disease respond initially but then …
Reciprocal Regulation Between TOC1 and LHY/CCA1 Within the Arabidopsis Circadian Clock
D Alabadı́, T Oyama, MJ Yanovsky, FG Harmon, P Más… - Science, 2001 - science.org
The interactive regulation between clock genes is central for oscillator function. Here, we
show interactions between the Arabidopsis clock genes LATE ELONGATED HYPOCOTYL …
show interactions between the Arabidopsis clock genes LATE ELONGATED HYPOCOTYL …
[PDF][PDF] Multiple BCR-ABL kinase domain mutations confer polyclonal resistance to the tyrosine kinase inhibitor imatinib (STI571) in chronic phase and blast crisis …
NP Shah, JM Nicoll, B Nagar, ME Gorre, RL Paquette… - Cancer cell, 2002 - cell.com
Through sequencing analysis of blood or bone marrow samples from patients with chronic
myeloid leukemia, we identified BCR-ABL kinase domain mutations in 29 of 32 patients …
myeloid leukemia, we identified BCR-ABL kinase domain mutations in 29 of 32 patients …
The development of imatinib as a therapeutic agent for chronic myeloid leukemia
M Deininger, E Buchdunger, BJ Druker - Blood, 2005 - ashpublications.org
Imatinib has revolutionized drug therapy of chronic myeloid leukemia (CML). Preclinical
studies were promising but the results of clinical trials by far exceeded expectations …
studies were promising but the results of clinical trials by far exceeded expectations …
[HTML][HTML] Imatinib mesylate—a new oral targeted therapy
DG Savage, KH Antman - New England Journal of Medicine, 2002 - Mass Medical Soc
This review discusses the development and uses of imatinib mesylate, a protein tyrosine
kinase inhibitor useful in the treatment of chronic myelogenous leukemia and …
kinase inhibitor useful in the treatment of chronic myelogenous leukemia and …
Transmembrane transport of endo-and xenobiotics by mammalian ATP-binding cassette multidrug resistance proteins
Multidrug Resistance Proteins (MRPs), together with the cystic fibrosis conductance
regulator (CFTR/ABCC7) and the sulfonylurea receptors (SUR1/ABCC8 and SUR2/ABCC9) …
regulator (CFTR/ABCC7) and the sulfonylurea receptors (SUR1/ABCC8 and SUR2/ABCC9) …
Acquired resistance to imatinib in gastrointestinal stromal tumor occurs through secondary gene mutation
CR Antonescu, P Besmer, T Guo, K Arkun, G Hom… - Clinical cancer …, 2005 - AACR
Most gastrointestinal stromal tumors (GIST) have an activating mutation in either KIT or
PDGFRA. Imatinib is a selective tyrosine kinase inhibitor and achieves a partial response or …
PDGFRA. Imatinib is a selective tyrosine kinase inhibitor and achieves a partial response or …
Imatinib induces hematologic and cytogenetic responses in patients with chronic myelogenous leukemia in myeloid blast crisis: results of a phase II study: Presented …
CL Sawyers, A Hochhaus, E Feldman… - Blood, The Journal …, 2002 - ashpublications.org
Blast crisis is the most advanced stage of chronic myelogenous leukemia (CML) and is
highly refractory to therapy. CML is caused by expression of the chimeric BCR-ABL tyrosine …
highly refractory to therapy. CML is caused by expression of the chimeric BCR-ABL tyrosine …