A 4-year-old, female, Maltese dog with bilateral hind limb ataxia was brought to Gyeongsang National University Animal Medical Center (GAMC). Based on the previous medical and imaging records, the patient was presumptively diagnosed with a primary brain tumor of the right temporo-occipital lobe on magnetic resonance imaging (MRI) in a local animal hospital. Hydroxyurea and prednisolone therapy was initiated, and the neurological signs transiently improved. Approximately 5 months after the treatment, ataxia recurred and the patient was referred to GAMC. Upon admission, MRI at the same anatomic level as in the previous MRI was performed. Results showed inflammatory brain lesions, not brain neoplastic changes. Considering this finding, the dog was tentatively diagnosed with meningoencephalitis of unknown etiology (MUE). We added oral imatinib mesylate (10 mg/kg every 24 h), and the dosage of prednisolone was increased to 1 mg/kg twice daily. Hydroxyurea was discontinued. A rapid improvement in neurological signs was observed after the initiation of imatinib mesylate treatment. Approximately 2 months after the treatment, the size of the inflammatory lesion remarkably decreased on repeat MRI. The patient had been doing well, and there were no overt neurological signs 259 days after the initiation of imatinib mesylate therapy. We describe a case of MUE in a dog that was successfully managed with imatinib mesylate.

Gastrointestinal stromal tumor (GIST) is the most common soft tissue sarcoma of the gastrointestinal tract. Surgery is the primary treatment of choice for patients with localized or potentially resectable GIST, whereas imatinib is the main treatment for patients with advanced, unresectable, or metastatic GIST. Neoadjuvant treatment with imatinib is not routinely recommended unless there is significant justification for reducing the tumor size in order to improve surgical outcome. The authors describe a case of a 48-year-old man who confirmed huge rectal GIST, and received successful neoadjuvant treatment with imatinib for preserving anal sphincter function followed by transanal excision.

Metformin is the most commonly prescribed anti-diabetic drug with relatively minor side effect. Substantial evidence has suggested that metformin is associated with decreased cancer risk and anticancer activity against diverse cancer cells. The tyrosine kinase inhibitor imatinib has shown powerful activity for treatment of chronic myeloid leukemia and also induces growth arrest and apoptosis in colorectal cancer cells. In this study, we tested the combination of imatinib and metformin against HCT15 colorectal cancer cells for effects on cell viability, cell cycle and autophagy. Our data show that metformin synergistically enhances the imatinib cytotoxicity in HCT15 cells as indicated by combination and drug reduction indices. We also demonstrate that the combination causes synergistic down-regulation of pERK, cell cycle arrest in S and G2/M phases via reduction of cyclin B1 level. Moreover, the combination resulted in autophagy induction as revealed by increased acidic vesicular organelles and cleaved form of LC3-II. Inhibition of autophagic process by chloroquine led to decreased cell viability, suggesting that induction of autophagy seems to play a cell protective role that may act against anticancer effects. In conclusion, our present data suggest that metformin in combination with imatinib might be a promising therapeutic option in colorectal cancer.

Chronic myeloid leukemia (CML) was a well-known myeloproliferative neoplasm and a disease of haemopoietic stem cells due to BCR-ABL fusion protein arising from a translocation t(9;22), known as the Philadelphia chromosome. Imatinib (Gleevec), a selective small molecule inhibitor of Bcr-Abl kinase, has been confirmed as the standard drug therapy for CML. Discovery of imatinib led to the availability of a molecular-targeted therapy as a new model of cancer treatment and challenged the molecular target cancer treatment trend from non-targeted cytotoxic chemotherapy. We reviewed the advancement of chronic myeloid leukemia treatment in the area of imatinib.