histone methyltransferase inhibitor Another recent study als
Another recent study also concluded that presence of EMD at diagnosis, rather than any treatment modalities ever used, was the only significant predictor of extramedullary recurrence. This finding suggests that the development of EMD, even during treatment, may possibly reflect different tumor biology. One issue raised about the MVD is the histological specimen was obtained usually from the posterior iliac crest and not the vertebral column. This is of some concern, because MM may grow in a patchy rather than diffuse pattern; therefore, the degree of infiltration of the BM by MCs cannot be expected to be equal throughout the skeleton.
However, controversy still surrounds the possible correlation between parameters of DCE-MRI and angiogenesis histone methyltransferase inhibitor in MM patients. Authors concluded that among MM patients, the angiogenesis parameter Amp was strongly correlated with the tissue MVD of BM obtained from the posterior iliac crest. This finding possibly reflects not only the tissue-specific vascularity, but also the vascular permeability in a more sizable area than the MVD of BM. As a result, Amp rather than MVD may correlate with the development of EMD among MM patients. Thus, high Amp might be a risk factor that could help identify MM patients with the potential to develop EMD. When compared with patients without EMD, patients with EMD displayed significantly greater infiltration of MCs in BM and higher levels of angiogenesis parameter “Amp”. Multiple logistic regression model showed that Amp was the only significant factor associated with EMD.
Limitation and future direction
Conclusions Bone marrow angiogenesis can be measured by DCE-MRI. DCE-MRI may provide dynamic and functional tumor angiogenesis and may help identify high-risk patients for tailored anti-antigenic therapy and monitoring treatment response. Increased bone marrow perfusion as reflected by higher Peak value can independently predict adverse clinical outcome in patients with AML. All DCE-MR parameters were significantly associated with overall survival. In addition, DCE-MRI data of bone marrow in AML patients at remission status can provide useful information on clinical outcome of patients who achieve CR. High Kep is an independent factor of overall and relapse free survival in these patients in whom CR was achieved. Patients with a higher value for Kep at CR would have shorter relapse-free duration and may need to undergo additional therapy. Multi-parametric DCE-MR data was illustrated as below: Fig. 1a–c were the time intensity curve (a), peak (b) and Kep (c) acquired from patient before chemotherapy (day 0). Fig. 2a–c were the time intensity curve (a), peak (b) and Kep (c) were acquired from patient after complete the induction chemotherapy (as day 7). The difference was significant and well demonstrated.
Conflict of interest
Introduction Previously, cancer had been viewed primarily as a genetic disorder. However, it has recently become generally accepted that cancer is not only influenced by genetic factors but also by the consequences of abnormal epigenetic events. Genetic alterations and aneuploidy are linked to changes in the DNA sequence, and are true hallmarks of malignant pathogenesis. Epigenetic changes commonly exist in human cancers as a consequence of heritable alterations in gene expression and chromatin structure, which are transmitted to several cell generations without alterations in DNA sequence. This results in functional costs which correspond to those induced by genetic changes. Significantly, intriguing evidence has emerged indicating that epigenetic modifications may lead and actually provoke genetic alterations. In this scenario, the epigenetic events are main events while genetic changes (for example mutations) are basically a consequence of the epigenetic disruption. This information may clarify why numerous genetic screens proved to be imperfect with regard to cancer pathogenesis and causality. Aberrant epigenetic events influence cellular pathways and multiple genes in a non-random fashion, and thus can predispose the beginning and accumulation of genetic alterations in the course of tumor initiation and development. These considerations are crucial for a better understanding of tumor pathogenesis, cellular and molecular processes underlying the acquisition of drug resistance, in addition to the development of cancer therapy, control and prevention strategies.