Current Angiogenesis (Discontinued) - Current Issue

Background/Objective: The role of circulating endothelial cells in tumor progression was noted by many researchers. The purpose of this research was to study the relationship of free (unrelated to the wall of vessel) CD34 positive cells (F-CD34+) located in the lumen of tumor vessels with features of angiogenesis, clinical and morphological characteristics of breast cancer (BC). Materials and Methods: The tumor samples received from 45 patients with T1-T2 stages of ductal invasive carcinomas were included in this study. The sections were stained immunohistochemically using antibodies to CD34. The presence of F-CD34+ was assessed microscopically and compared with clinical characteristics of BC, hormone receptors and HER2/neu status, with the number of different tumor vessels and with the presence of lymphovascular invasion (LVI). Results: F-CD34+ were revealed in 35 cases (77,8%). Their presence correlated with the number of atypical dilated capillaries (p=0.00001) and “cavitary” structures (CS) type-1 (p=0,001) having been described by us earlier, with the presence of LVI (p=0,02), tumor grade (p=0,01), estrogen receptor (p=0,0002) and progesterone receptor (p=0,002) status. FCD34+ were more often observed in the cases with multiple atypical dilated capillaries (p=0,001) and CS type-1 (p=0,04), in the presence of LVI (p=0,1), in G2-G3 (p=0,09), in negative estrogen (p=0,01) and progesterone (p=0,03) receptors status. The correlations of F-CD34+ with Her2/new status, microvessel density and other types of tumor vessels were not detected. Conclusion: The presence of F-CD34+ in tumor vessels is associated with clinical, morphological and biological characteristics of BC and its evaluation may be important for the prognosis.

Background: The development of drugs capable of enhance or inhibit the cell proliferation is an area in expansion at modern biomedical sciences. Recent researches have shown that latex has strong angiogenic potential. Methods: We performed a bibliometric analysis on the global literature trying to identify: the main scientometrics data, the botanical families and species, the angiogenic or antiangiogenic properties and also discussed the results obtained on this topic up to now. Results: The different bibliometric approaches, showed a continuous increase of both quantitative and qualitative parameters in the studies of latex utilization in the angiogenesis process. From more than 35,000 lactiferous species existing only 29 have been studied and showed angiogenic potential. Then, the potential for finding new therapeutic compounds in latex is a new and promising field that needs to be better explored. Regarding the biological activity, 59% of articles have reported the angiogenic activity and 41% the antiangiogenic property. The most articles identified in this research, have been used in their experimental analysis the crude latex (73.41%). Only 26.52% of the articles used biocompounds isolated from latex. Among the weaknesses in this field, it is necessary to point: the molecular characterization of latex; the establishment of molecular mechanism of action; and demonstration of latex biocompunds safety and effectiveness in clinical trials. Conclusion: Those results are important to spread knowledge about the use of latex as a new biomaterial employed in medicine, indicate trends, point out the technical difficult on the development of new drugs.

Vascular endothelial growth factor is a signaling protein, which is responsible for the angiogenesis process. Variation in its expression leads to various disorders like cancer, diabetes, psoriasis and neuronal imbalance (depression) etc. The abundance of VEGF (VEGF-A, B, C) concentration is present in the kidney, heart, lung, ovary, thyroid gland, neurons, embryonic tissue etc. The regulation of VEGF expression is controlled by the hypoxia condition, hormonal regulation, inflammatory mediator cytokines and growth hormone. The VEGF binds to the VEGFR1, and VEGFR2 tyrosine kinase receptors causing conformational changes resulting in the endothelial cell proliferation, increased vascular permeability, and formation of new blood vessel. The high level of VEGF- A activity found in the synovial fluid leads to rheumatoid arthritis, whereas in the retinal cell it results in diabetic retinopathy. The tumor growth factor induced VEGF A expression in keratin cell lead to psoriasis. The higher level of VEGF activity increased neovascularization which is beneficial in cerebral ischemia, as well as in the growth of the neurons. VEGF is also considered to be an important factor in tumor invasion and metastasis. Various growth factors stimulate or participated in tumor angiogenesis. Therefore, the Anti-VEGF therapy can be a potential option for treatment of psoriasis, rheumatoid arthritis, diabetic retinopathy, and cancer. The (VEGF) gene expression modulation will lead to the new therapeutic possibilities in the future.

Gastrointestinal [GI] malignancies are common and frequently lethal neoplasms. As our understanding of GI cancers deepens, more pathways are discovered that play key roles in tumorigenesis and metastasis. Angiogenesis has emerged as a critical pathway in many cancers, particularly in GI cancers. The discovery of a complex network of signals, including vascular epithelial growth factor [VEGF], led to the emergence of a new class of cancer therapies targeting angiogenesis. Bevacizumab was the first to emerge, gaining US Food and Drug Administration [FDA] approval in 2004 for the treatment of advanced colorectal cancer; since then, several antiangiogenic agents have become clinically available, and numerous others are in clinical or preclinical testing. This review will focus on anti-angiogenesis therapies in GI malignancies.

Background: Vascular smooth muscle cells (VSMCs) show eminently plasticity during physiological and pathological processes. VSMCs undergo from contractile phenotype to proliferative, matrigenic, inflammatory or osteogenic phenotype during the pathogenesis of hypertension, atherosclerosis, and vascular calcification etc. Methods: Here we reviewed the research papers regarding to the respective effects of extracellular matrix (ECM) on VSMC phenotypic switching. Results: The ECM including collagens, elastins, proteoglycans and glycoproteins etc, via complex protein-protein interaction, constitute a complicated microenvironment for VSMCs. Each component regulates VSMC phenotypic switching via various signaling pathways and cell surface receptor. On the other hand, ECM can be dynamic degraded or proteolysed by a variety of extracellular proteinases such as matrix metalloproteinases (MMPs) and a disintegrin and metalloprotease with thrombospondin motifs (ADAMTS). Thus, these extracellular proteinases are able to modulate VSMC phenotypes partially via degrading ECM. Moreover, the ECM-modulated VSMC phenotypic switching also plays a critical role in various vascular diseases, such as hypertension, atherosclerosis and vascular calcification. Conclusion: Various ECM compositions including fibrous proteins, glycoproteins and proteoglycans exhibit the ability to modulate the VSMC phenotypic switching.