Chromatid recommensuration after segmental duplication

<p>Abstract</p> <p>Background</p> <p>Midsegment duplication (dup) of chromatid arms may be symmetric or asymmetric. It can be argued that every dup should yield a discommensured RC with (a) loss of at least one duplicated unit to the template counterpart and; (b) deletion of all sections of the replicating chromatid arm that are distal to both the gap left by the duplicating process and the segment closest to the centromere.</p> <p>Hypothesis</p> <p>Mechanisms capable of recommensuring the stack of chromatids after topological shifts of duplicated units (dups) are discussed. The mechanics might fail in few cases, which are discussed in terms of statistics and scalability.</p> <p>Conclusion</p> <p>The dynamics of the highly non-linear processes discussed here may be relevant to duplications of smaller (epsilon) subunits such as telomeric units within malignant genomes.</p

Immunotherapy using slow-cycling tumor cells prolonged overall survival of tumor-bearing mice

<p>Abstract</p> <p>Background</p> <p>Despite considerable progress in the development of anticancer therapies, there is still a high mortality rate caused by cancer relapse and metastasis. Dormant or slow-cycling residual tumor cells are thought to be a source of tumor relapse and metastasis, and are therefore an obstacle to therapy. In this study, we assessed the drug resistance of tumor cells in mice, and investigated whether vaccination could promote survival.</p> <p>Methods</p> <p>The mouse colon carcinoma cell line CT-26 was treated with 5-fluorouracil to assess its sensitivity to drug treatment. Mice with colon tumors were immunized with inactivated slow-cycling CT-26 cells to estimate the efficacy of this vaccine.</p> <p>Results</p> <p>We identified a small population of slow-cycling tumor cells in the mouse colon carcinoma CT-26 cell line, which was resistant to conventional chemotherapy. To inhibit tumor recurrence and metastasis more effectively, treatments that selectively target the slow-cycling tumor cells should be developed to complement conventional therapies. We found that drug-treated, slow-cycling tumor cells induced a more intense immune response <it>in vitro</it>. Moreover, vaccination with inactivated slow-cycling tumor cells caused a reduction in tumor volume and prolonged the overall survival of tumor-bearing mice.</p> <p>Conclusions</p> <p>These findings suggest that targeting of slow-cycling tumor cells application using immunotherapy is a possible treatment to complement traditional antitumor therapy.</p