Dual Role of p73 in Cancer Microenvironment and DNA Damage Response.

Understanding the mechanisms that regulate cancer progression is pivotal for the development of new therapies. Although p53 is mutated in half of human cancers, its family member p73 is not. At the same time, isoforms of p73 are often overexpressed in cancers and p73 can overtake many p53 functions to kill abnormal cells.

The p53 family member p73 in the regulation of cell stress response.

During oncogenesis, cells become unrestrictedly proliferative thereby altering the tissue homeostasis and resulting in subsequent hyperplasia. This process is paralleled by resumption of cell cycle, aberrant DNA repair and blunting the apoptotic program in response to DNA damage. In most human cancers these processes are associated with malfunctioning of tumor suppressor p53.

[2-year follow-up of the use of a new fistulization operation in patients with refractory glaucoma].

A new full-thickness operation is described and its results in 45 patients (46 eyes) with refractory glaucoma are analyzed. The patients were observed for 18.6 months after the intervention.

[Use of Naclof in combined intervention for cataract and glaucoma].

Two aspects of using eye drops of a nonsteroid antiinflammatory drug Naclof (sodium diclofenac) are analyzed: maintenance of mydriasis during an intervention (extracapsular cataract extraction with implantation of an intraocular lens and trabeculectomy and arrest of postoperative inflammation. The study was carried out in 40 patients, 20 of which were controls. In the naclof group the diameter of the pupil during the intervention was reliably larger, exudative inflammatory reactions were rarer, and the postoperative vision acuity higher.