A combinatorial approach incorporating anti cancer drugs targeting different pathway for treatment regimens is often used to improve medical outcomes. The synergistic effects of TAI 1 with commercial anti cancer agents suggest that TAI 1 or its analogues may be very easily incorporated to current multi drug treat ment regimens. A small pilot study using clinical data base analysis shows that Hec1 expression may correlate with established patient subtypes, which may further aid in the building of the parameters for response in clinical applications. Further studies in the clinical development of Hec 1 inhibitors will determine whether selection based on these subtypes will aid in the identification of patients who are more likely to respond to Hec1 targeted therapy.

Conclusion In conclusion, this study demonstrates the potential of the improved anticancer selleck inhibitor agent targeting Hec1 for clin ical utility. The potency, safety, and translational impli cations show that a Hec1 targeted small molecule agent can be developed for clinical utility and that a variety of potential clinical applications may be available to sup port clinical development. Background c Jun NH2 terminal kinases are strongly activated by a variety of stressful cellular environments, such as chemotherapy and oxidative stress, and induce growth in hibition or cell death. The JNK signaling pathway has also been involved in stress induced apoptosis, includ ing neuronal death in models of excitotoxicity and stroke.

JNK is a stress activated protein kinase and plays a pivotal role in both inflammation and cell death, with the JNK induced apoptotic response being mediated, in part, by the expression and or phosphorylation of proteins belonging to the Bcl 2 buy inhibitor related family. JNK have a number of targets, including the transcription factor c Jun, the forkhead transcription factor, and other pro or anti apoptotic factors, such as Bax and Bcl 2. Autophagy is a lysosomal pathway involved in the deg radation of cytoplasmic macromolecules, and organelles. This process was well preserved during evo lution. Although autophagy became a very seductive topic in cancer treatment research, the current literature about autophagy is very confusing due to the association of au tophagy with both cell survival and death. Some studies demonstrated that autophagy is induced by stressful condi tions, such as metabolic stress, energy need, and chemo therapy. Furthermore, several recent reports indicated that reactive oxygen species induced au tophagy in response to chemotherapy. Studies also showed that autophagy promoted cancer cell survival through the generation of metabolic substrates maintaining cellular activity, thereby limiting chemotherapy cytotoxicity.