Reconstruction of a Traumatic Bone Defect from Distal Femur.

INTRODUCTION: Bone defect is a difficult problem in orthopedics. The treatment conventionally relies on techniques such as induced membrane, grafts, and elongations. The reintegration of an externalized osseous fragment involves significant infectious risks but is essential in certain situations. CASE REPORT: We report the case of a 10 cm traumatic bone loss of the right distal femur in a 35-year-old woman. Treatment consisted of paring, reintegration and stabilization by the external fixative. The 5-year follow-up was satisfactory with good consolidation and good function of the limb. CONCLUSION: The reintegration of a bone fragment of limb expelled onto the soil is rare. We tried it because the response time was very short, but also and especially because the fragment was expelled on very hot bitumen. These two elements limited the risk of infection and favored the osseointegration of the fragment. We have not found a similar case reported in the literature allowing comparisons and recommendations.

An intergenic regulatory region mediates Drosophila Myc-induced apoptosis and blocks tissue hyperplasia.

Induction of cell-autonomous apoptosis following oncogene-induced overproliferation is a major tumor-suppressive mechanism in vertebrates. However, the detailed mechanism mediating this process remains enigmatic. In this study, we demonstrate that dMyc-induced cell-autonomous apoptosis in the fruit fly Drosophila melanogaster relies on an intergenic sequence termed the IRER (irradiation-responsive enhancer region). The IRER mediates the expression of surrounding proapoptotic genes, and we use an in vivo reporter of the IRER chromatin state to gather evidence that epigenetic control of DNA accessibility within the IRER is an important determinant of the strength of this response to excess dMyc. In a previous work, we showed that the IRER also mediates P53-dependent induction of proapoptotic genes following DNA damage, and the chromatin conformation within IRER is regulated by polycomb group-mediated histone modifications. dMyc-induced apoptosis and the P53-mediated DNA damage response thus overlap in a requirement for the IRER. The epigenetic mechanisms controlling IRER accessibility appear to set thresholds for the P53- and dMyc-induced expression of apoptotic genes in vivo and may have a profound impact on cellular sensitivity to oncogene-induced stress.

The flower code and cancer development

It has been postulated that the preliminary steps of cancer known as "cancerization field" could be mediated by a competitive mechanism among mutated and wild-type cells. Cell competition is a process of selection among populations of cells with different fitness: the best adapted cells (winners) survive and proliferate in the tissue at the expense of the less well adapted cells (losers), and these loser cells are eliminated from the tissue by apoptosis. However, the molecular mechanisms mediating this process and the genes involved are still unknown. A mechanism of cell-to-cell communication during cell competition known as the "flower code" has been recently proposed to distinguish loser from winner cells: fwe(ubi) isoform is expressed ubiquitously in the imaginal disc while fwe(Lose) isoforms are expressed specifically during cell competition in the cells to be eliminated. Cell competition has been postulated to have implications in development, tissue homeostasis, regeneration and tumour development; the process of cell competition does not affect the total cell number and organ morphology is maintained because winner cells compensate for the loss. A role of cell competition as the mechanism occurring during initial stages of tumour formation is currently under study (AU)