Implementación del diagnóstico molecular del VPH: experiencia chilena en curso / Molecular diagnosis of human papillomavirus infection: the Chilean experience

Cervical Cancer (CaCu) has a heterogeneous epidemiological behavior throughout the planet, depending on regional socioeconomic development level. Some developed countries predict a potential eradication of this cancer in the next 100 years, while in Chile it still constitutes a pending challenge. Incidence rates show a slow but sustained downward prob, however, mortality has continued to fluctuate between 500-600 cases per year. A few years ago, vaccination against Human Papillomavirus (HPV), the main causal agent for this tumor, was consolidated as a public policy, both in girls and in boys. However, the technological leap in the screening prob was pending, from cytology to molecular diagnosis of the agent (HPV). In this report, we update our most recent data (2018) regarding CaCu mortality, then review global guidelines and experiences in HPV screening. Finally, we offer an account of the strategies that our health system is promoting to address the screening of the disease and whose molecular approach generates the widest worldwide scientific consensus. We also recognize the main barriers and future challenges, which, if overcome, would allow us to be in line with the mandate of WHO to control this women's health problema.

[Molecular diagnosis of human papillomavirus infection. The Chilean experience]. / Implementación del diagnóstico molecular del VPH: experiencia chilena en curso.

Cervical Cancer (CaCu) has a heterogeneous epidemiological behavior throughout the planet, depending on regional socioeconomic development level. Some developed countries predict a potential eradication of this cancer in the next 100 years, while in Chile it still constitutes a pending challenge. Incidence rates show a slow but sustained downward prob, however, mortality has continued to fluctuate between 500-600 cases per year. A few years ago, vaccination against Human Papillomavirus (HPV), the main causal agent for this tumor, was consolidated as a public policy, both in girls and in boys. However, the technological leap in the screening prob was pending, from cytology to molecular diagnosis of the agent (HPV). In this report, we update our most recent data (2018) regarding CaCu mortality, then review global guidelines and experiences in HPV screening. Finally, we offer an account of the strategies that our health system is promoting to address the screening of the disease and whose molecular approach generates the widest worldwide scientific consensus. We also recognize the main barriers and future challenges, which, if overcome, would allow us to be in line with the mandate of WHO to control this women's health problema.

Diabetic concentrations of metformin inhibit platelet-mediated ovarian cancer cell progression.

Clinical studies have suggested a survival benefit in ovarian cancer patients with type 2 diabetes mellitus taking metformin, however the mechanism by which diabetic concentrations of metformin could deliver this effect is still poorly understood. Platelets not only represent an important reservoir of growth factors and angiogenic regulators, they are also known to participate in the tumor microenvironment implicated in tumor growth and dissemination. Herein, we investigated if diabetic concentrations of metformin could impinge upon the previously reported observation that platelet induces an increase in the tube forming capacity of endothelial cells (angiogenesis) and upon ovarian cancer cell aggressiveness. We demonstrate that metformin inhibits the increase in angiogenesis brought about by platelets in a mechanism that did not alter endothelial cell migration. In ovarian cancer cell lines and primary cultured cancer cells isolated from the ascitic fluid of ovarian cancer patients, we assessed the effect of combinations of platelets and metformin upon angiogenesis, migration, invasion and cancer sphere formation. The enhancement of each of these parameters by platelets was abrogated by the present of metformin in the vast majority of cancer cell cultures tested. Neither metformin nor platelets altered proliferation; however, metformin inhibited the increase in phosphorylation of focal adhesion kinase induced by platelets. We present the first evidence suggesting that concentrations of metformin present in diabetic patients may reduce the actions of platelets upon both endothelial cells and cancer cell survival and dissemination.