Gastric Cancer: Current Status of Diagnosis and Treatment

Gastric cancer is the second leading cause of death from malignant disease worldwide and most frequently discovered in advanced stages. Because curative surgery is regarded as the only option for cure, early detection of resectable gastric cancer is extremely important for good patient outcomes. Therefore, noninvasive diagnostic modalities such as evolutionary endoscopy and positron emission tomography are utilized as screening tools for gastric cancer. To date, early gastric cancer is being treated using minimally invasive methods such as endoscopic treatment and laparoscopic surgery, while in advanced cancer it is necessary to consider multimodality treatment including chemotherapy, radiotherapy, and surgery. Because of the results of large clinical trials, surgery with extended lymphadenectomy could not be recommended as a standard therapy for advanced gastric cancer. Recent clinical trials had shown survival benefits of adjuvant chemotherapy after curative resection compared with surgery alone. In addition, recent advances of molecular targeted agents would play an important role as one of the modalities for advanced gastric cancer. In this review, we summarize the current status of diagnostic technology and treatment for gastric cancer

Antitumor effect of the tyrosine kinase inhibitor nilotinib on gastrointestinal stromal tumor (GIST) and imatinib-resistant GIST cells

<p>Antitumor effect of the tyrosine kinase inhibitor nilotinib on gastrointestinal stromal tumor (GIST) and imatinib-resistant GIST cells</p

apoptosis assay

<p>apoptosis assay date</p

in vivo drug assay

<p>in vivo drug assay date</p

Figure4

<p>Figure 4</p> <p>Quantitative phosphorylation analysis. Parental (GK1C and GK3C; red histograms) or imatinib-resistant GIST cell lines (GK1C-IR and GK3C-IR, blue histograms) were fixed and stained with anti phospho-KIT (Tyr719), anti phospho-PDGFRA (Tyr754), anti phospho-SRC (Tyr416), anti phospho-AKT (Ser473) and anti phospho-ERK1/2 (Thr202/Tyr204). Finally, cells were detected with Alexa Fluor 488 donkey anti-rabbit IgG antibody (Isotype control was reacted only with the secondary antibody). The MFI (mean of fluorescence intensity) values were calculated by FlowJo. GK1C: p-KIT=3.21, p-PDGFRA=10.3, p-SRC=7.19, p-AKT=20.3, p-ERK1/2=37.8. GK1C-IR: p-KIT=3.30, p-PDGFRA=12.8, p-SRC=9.35, p-AKT=20.5, p-ERK1/2=94.4. GK3C: p-KIT=2.65, p-PDGFRA=7.29, p-SRC=5.35, p-AKT=19.5, p-ERK1/2=32.2. GK3C-IR: p-KIT=3.89, p-PDGFRA=9.82, p-SRC=8.31, p-AKT=21.3, p-ERK1/2=115.</p

in vitro drug assay

<p>in vitro drug assay date</p