EGFR family signaling and its association with breast cancer development and resistance to chemotherapy (Review)

Mechanistic Analysis of Taxol-induced Multidrug Resistance in an Ovarian Cancer Cell Line

“…The MAPK family has been classified into 3 distinct subfamilies: the extracellular signal-regulated protein kinases (ERKs) including ERK1/2, the stress-activated c-Jun N-terminal protein kinase (JNKs) and p38 kinase (Hoshino et al, 1999;Doddareddy et al, 2012). The MAP kinase cascade and PI3K/Akt are all effectors of Ras signaling (Downward, 2003;McCubrey et al, 2012), which have been implicated in a wide range of cellular functions, including proliferation, survival, migration, malignant transformation (Wee et al, 2008;Yang et al, 2013), and also in the development of drug resistance (Navolanic et al, 2003;Sui et al, 2012). In our study, we found that JNK and ERK1/2 were activated in A2780/ Taxol cells.…”

Targeted Therapy in Breast Cancer

“…Utilizing cell lines, it was possible to establish a standardized immunohistochemical procedure and scoring system in which cells containing less than 20,000 receptors would show no staining (0), cells containing ϳ100,000 receptors would show partial membrane staining with less than 10% of the cells showing complete membrane staining (1ϩ), cells containing ϳ500,000 receptors would show light to moderate complete membrane staining in more than 10% of the cells (2ϩ), and cells containing ϳ2,300,000 receptors would show strong, complete membrane staining in more than 10% of the cells (3ϩ). Studies have shown that when a standardized IHC assay is performed on specimens that are carefully fixed, processed, and embedded, there is excellent correlation between gene copy status and protein expression levels (1,51,52,139). However, alterations can be significantly impacted by technical issues, especially in archival fixed paraffin-embedded tissues.…”

“…amplification and/or protein overexpression has been identified in 10 -34% of invasive breast cancers (1).…”

Targeting survival cascades induced by activation of Ras/Raf/MEK/ERK, PI3K/PTEN/Akt/mTOR and Jak/STAT pathways for effective leukemia therapy

“…Although various cytotoxic drugs differ in their mechanism of action, each ultimately relies upon built in apoptotic machinery to elicit cell death. [34][35][36][37][38][39] Caspase family cysteine proteases are responsible for proteolytic cleavage of cellular proteins C terminus to aspartate residues. Drug resistance has often been linked with the altered expression of proteins involved in the regulation of apoptosis (for example, Bcl-2, caspase 3 44 This pathway is also induced after chemotherapy due to the induction of reactive oxygen species.…”