On 2015 Jul 12, Miguel Lopez-Lazaro commented:

The authors discuss that their results provide preclinical evidence proposing the use of SYK inhibitors in combination with paclitaxel in cancer patients, and that this combination warrants future clinical studies to assess its clinical benefit.

Before initiating clinical studies, it would be interesting to evaluate if inhibition of STK can also potentiate paclitaxel-induced cytotoxicity in nonmalignant cells from a variety of tissues (including those responsible for the dose-limiting toxicity of paclitaxel). This is important because a drug combination that induces a potentiation effect in cancer cells will not be clinically useful if it induces a higher potentiation effect in nonmalignant cells. What matters is if the new treatment improves the selectivity of the standard treatment, and not if it improves its cytotoxic potency in cancer cells.

It would also be interesting to test if the combination of a STK inhibitor + paclitaxel improves the survival rate induced by paclitaxel when tested under equivalent experimental conditions (e.g., equitoxic doses, determined in mice) in animal models representative of the patients who are expected to receive the new treatment (e.g., animal models of metastasis). Patients with localized and resectable tumors are usually treated successfully with surgery and are not expected to benefit from this pharmacological treatment.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4381701/pdf/oncoscience-02-0091.pdf

On 2015 Jul 12, Miguel Lopez-Lazaro commented:

The authors discuss that their results provide preclinical evidence proposing the use of SYK inhibitors in combination with paclitaxel in cancer patients, and that this combination warrants future clinical studies to assess its clinical benefit.

Before initiating clinical studies, it would be interesting to evaluate if inhibition of STK can also potentiate paclitaxel-induced cytotoxicity in nonmalignant cells from a variety of tissues (including those responsible for the dose-limiting toxicity of paclitaxel). This is important because a drug combination that induces a potentiation effect in cancer cells will not be clinically useful if it induces a higher potentiation effect in nonmalignant cells. What matters is if the new treatment improves the selectivity of the standard treatment, and not if it improves its cytotoxic potency in cancer cells.

It would also be interesting to test if the combination of a STK inhibitor + paclitaxel improves the survival rate induced by paclitaxel when tested under equivalent experimental conditions (e.g., equitoxic doses, determined in mice) in animal models representative of the patients who are expected to receive the new treatment (e.g., animal models of metastasis). Patients with localized and resectable tumors are usually treated successfully with surgery and are not expected to benefit from this pharmacological treatment.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4381701/pdf/oncoscience-02-0091.pdf