OBJECTIVETo evaluate the anti-inflammatory and analgesic activities of leaf extract of Melanthera scandens (M. scandens).

METHODSThe crude leaf extract (39-111 mg/kg) of M. scandens was investigated for anti-inflammatory and analgesic activities using various experimental models. The anti-inflammatory activity was investigated using carragenin, egg-albumin induced oedema models, while acetic acid, formalin-induced paw licking and thermal-induced pain models were used to evaluate the antinociceptive property.

RESULTSThe extract caused a significant (P<0.05 - 0.001) dose-dependent reduction of inflammation and pains induced by different agents used.

CONCLUSIONSThe leaf extract possesses anti-inflammatory and analgesic effects which may be mediated through the phytochemical constituents of the plant.

Acetic Acid ; toxicity ; Albumins ; adverse effects ; Analgesics ; therapeutic use ; Animals ; Anti-Inflammatory Agents ; therapeutic use ; Asteraceae ; metabolism ; Carrageenan ; toxicity ; Edema ; drug therapy ; Formaldehyde ; toxicity ; Inflammation ; chemically induced ; drug therapy ; Mice ; Pain ; chemically induced ; drug therapy ; Phytochemicals ; therapeutic use ; Phytotherapy ; Plant Extracts ; therapeutic use ; Plant Leaves ; metabolism

Commonly observed aberrations in epidermal growth factor receptor (EGFR) signaling have led to the development of EGFR-targeted therapies for various cancers, including non-small cell lung cancer (NSCLC). EGFR mutations and overexpression have further been shown to modulate sensitivity to these EGFR-targeted therapies in NSCLC and several other types of cancers. However, it is clear that mutations and/or genetic variations in EGFR alone cannot explain all of the variability in the responses of patients with NSCLC to EGFR-targeted therapies. For instance, in addition to EGFR genotype, genetic variations in other members of the signaling pathway downstream of EGFR or variations in parallel receptor tyrosine kinase (RTK) pathways are now recognized to have a significant impact on the efficacy of certain EGFR-targeted therapies. In this review, we highlight the mutations and genetic variations in such genes downstream of EGFR and in parallel RTK pathways. Specifically, the directional effects of these pharmacogenetic factors are discussed with a focus on two commonly prescribed EGFR inhibitors: cetuximab and erlotinib. The results of this comprehensive review can be used to optimize the treatment of NSCLC with EGFR inhibitors. Furthermore, they may provide the rationale for the design of subsequent combination therapies that involve the inhibition of EGFR.
Antineoplastic Agents ; Carcinoma, Non-Small-Cell Lung ; Cetuximab ; Erlotinib Hydrochloride ; Genes, erbB-1 ; Humans ; Lung Neoplasms ; Mutation ; Pharmacogenetics ; Quinazolines ; Receptor, Epidermal Growth Factor