In BMC Cancer this week, researchers in Japan say that expression of the TKTL1 gene can predict disease-free survival in rectal cancer patients undergoing neoadjuvant chemoradiotherapy. The team analyzed tumor and corresponding normal tissue pairs from 33 patient with locally advanced rectal cancer, treated in phase I and phase II trials with neoadjuvant chemotherapy. The researchers found that there was significantly higher expression of VEGFR in tumor tissue pre- and post-treatment compared to normal tissue, and that high expression levels of TKTL1 was significantly correlated with survival. "High TKTL1 expression correlates with poor prognosis in terms of three year disease-free survival in patients with [locally advanced rectal cancer] treated with intensified neoadjuvant chemoradiotherapy and may therefore serve as a molecular prognostic marker which should be further evaluated in randomized clinical trials," the authors write. "None of the markers had influence on early response parameters such as tumor regression grading."
Also in BMC Cancer this week, researchers in Germany use BH3 mimetic molecules like ABT-737 to increase the treatment efficiency of paclitaxel in hepatoblastoma, a cancer where drug resistance remains a challenge. The team analyzed hepatoblastoma cells from the HUH6 and HepT1 cells lines treated with paclitaxel alone, ABT-737 alone, and a combination of both. ABT-737 reduced the viability of the cancer cells and enhanced the cytotoxic effects of paclitaxel, when used in combination. "Paclitaxel could be reduced tenfold to achieve similar reduction of viability of tumor cells," the team writes. "Our results demonstrate enhancement of chemotherapy by using modulators of apoptosis. Further analyses should include improved pharmacological formulations of paclitaxel and BH3 mimetics in order to reduce toxicological effects. Sensitizing hepatoblastoma to apoptosis may also render resistant hepatoblastoma susceptible to established chemotherapy regimens."
Finally in BMC Cancer this week, another group of researchers in Japan write of a novel Transferrin receptor-targeted hybrid peptide that disintegrates cancer cell membranes, allowing for the induction of rapid cancer cell death. The team assessed the cytotoxicity of the TfR-lytic hybrid peptide in 12 cancer and two normal cell lines in vitro, and administered the peptide in an athymic mouse model in vivo. The analysis showed that the peptide had cytotoxic effects in 12 cancer cell lines. "In addition, it was revealed that this molecule can disintegrate the cell membrane of T47D cancer cells just in 10 minutes, to effectively kill these cells and induce approximately 80 percent apoptotic cell death but not in normal cells," the authors write. "The intravenous administration of TfR-lytic peptide in the athymic mice model significantly inhibited tumor progression."