In the British Journal of Cancer this week, an international team of researchers suggests that carboplatin-paclitaxel-induced leukopenia and neuropathy can predict progression-free survival in patients with recurrent ovarian cancer. The researchers analyzed 608 patients that did not receive growth factors and found that 72 percent had leukopenia, which was prognostic of survival in those receiving carboplatin-paclitaxel. "Efficacy of carboplatin-paclitaxel treatment was similar to carboplatin-liposomal doxorubicin in patients who developed leukopenia," the team writes. "These findings support further research to understand the mechanisms of treatment-related toxicity."
Also in the British Journal of Cancer this week, researchers in France write that T-bet expression in intratumoral lymphoid structures after neoadjuvant trastuzumab plus docetaxel therapy predicts survival in HER2 over-expressing breast carcinoma. In HER2 cancers, evidence suggests that some chemotherapies trigger a Th1 anticancer immune response, characterized by the expression of the T-bet transcription factor in CD4 T-lymphocytes. In this study, the researchers studied 102 HER2 over-expressing breast cancer patients treated with neoadjuvant chemotherapy incorporating antracyclines or taxane and trastuzumab. They found that the presence of T-bet-positive lymphocytes in peritumoral lymphoid structures after chemotherapy was elevated in the group treated with trastuzumab and a taxane-like docetaxel. "After a median follow-up of 40 months, the presence of T-bet+ lymphocytes after neoadjuvant chemotherapy confers significantly better relapse-free survival only in patients treated with trastuzumab–taxane," the authros write. "These findings indicate that the tumor infiltration by T-bet+ Th1 lymphocytes following neoadjuvant trastuzumab–taxane may represent a new independent prognostic factor of improved outcome in HER2 over-expressing breast carcinoma."
And finally in the British Journal of Cancer this week, researchers in Italy and the US examine the anti-tumor efficacy of MEK inhibitors in human lung cancer cells with acquired resistance to different tyrosine kinase inhibitors, called TKIs. The researchers developed an in vitro model of acquired resistance to four different TKIs by continuously treating human lung adenocarcinoma cells from the CALU-3 cell line with escalating doses of the drugs. All four TKI-resistant CALU-3 cell lines "showed increased invasion, migration and anchorage-independent growth," the authors write. In contrast, when TKI-resistant cells were treated with MEK inhibitors, cell proliferation, invasion, and migration were inhibited in all cell lines. "These data suggest that resistance to four different TKIs is characterised by epithelial to mesenchymal transition, which is MEK-inhibitor sensitive in human CALU-3 lung adenocarcinoma."