6035 Background: Photodynamic therapy (PDT) is an effective treatment for various cancers ensuring maximum preservation of the viability of healthy tissues surrounding the tumor. The purpose of the study was to reveal the effectiveness of PDT in treatment for preinvasive cervical cancer. Methods: The study included 45 patients aged 22-53 years with preinvasive cervical cancer. The patients were divided into two groups depending on the type of the transformation area and the tumor site: group 1–on the exocervix (type I-II), n=24; group 2–on the endocervix (type III), n=21. Infection with high-risk genotypes of HPV (16, 18, 31, 33, 35, 45, 56) was detected with PCR in 37 (82%) women. All patients received PDT with the semiconductor Latus laser up to 3 W, a single-use diffusing fiber for the exocervix irradiation and a single-use cylindrical diffusing fiber for tumors in the cervical canal. Photoditazine and photolon were used as photosensitizers. Effectiveness criteria included the normalization of the colposcopic picture, the absence of atypical cells, and the pathogen elimination confirmed by PCR. Results: A normal cytogram profile was observed after PDT in 84% of group 1 and in 88% of group 2. PCR 3 months after PDT showed a positive HPV reaction in 9.1%. Neither group of patients had negative changes in cytogram after 6 and 12 months. Repeated HPV DNA tests detected HPV DNAs in 2.8% in group 1 and 3.2% in group 2. The effectiveness of PDT did not depend on the photosensitizer. The maximum follow-up period has lasted for 4.5 years, with no recurrences registered. During this period, three young women successfully gave birth to healthy children. Conclusions: PDT is an alternative treatment for pre-tumor and initial tumor pathology of the cervix with preservation of the anatomical and functional integrity of the organ, which is important for the female reproductive function. The results support the use of PDT in treatment for preinvasive cervical cancer.
Purpose of the study. To evaluate the role of chronic chlamydial infection in the genesis of proliferative processes in the female genital area.Materials and methods. The study involved 267 women aged from 27 to 43 years. Depending on the severity of the pathological process in the genital tract and the presence of the Chlamydia trachomatis infection, 6 groups were distinguished: 1st — 30 somatically healthy women without pathologies of the female reproductive system; 2nd and 3rd — those with inflammatory processes in the reproductive organs of non-chlamydial (36) and chlamydial nature (38); 4th and 5th — those with proliferative processes in the pelvic organs of non-chlamydial (50) and chlamydial nature (58); 6th — patients with cervical cancer (55). The PCR and ELISA (Chem Well, USA) methods were used to identify the presence of Chlamydia trachomatis. The concentration of estradiol (E) and progesterone (P) (ELISA) in the blood, as well as their ratio (E/P), was determined. The as-obtained data were compared with the results of cytomorphological and ultrasound studies.Results. Proliferative processes in the genital tract are accompanied by a change in the level of female sex hormones, in particular, by a sharp decrease in progesterone in the luteal phase of the cycle against the background of absolute or relative hyperestrogenism. These changes are more pronounced in women with chronic chlamydial infection. A connection between the presence of the infectious agent in question and the severity of hyperplastic processes in the female genital tract is established. A comparison of the obtained morphological data with the blood progesterone content in women without Chlamydia trachomatis showed that an increase in the severity of disorders correlates with a decrease in the level of female hormones. In women infected with Chlamydia trachomatis, the severity of hyperplastic processes shifts to the right, i. e. towards normal progesterone values. Therefore, even at maximal progesterone concentrations close to the reference values, a greater severity of pathological changes is observed.Conclusion. The obtained results demonstrate the undeniable role of chronic chlamydial infection in initiating a hormonal imbalance towards absolute or relative hyperestrogenia with a severe progesterone deficiency. A causal relationship of the Chlamydia trachomatis infectious agent with the severity of hyperplastic processes in the pelvic organs is established. It is concluded that the detection of chlamydial infection should be considered as an essential element in the screening and prevention of hyperplastic processes.
e17549 Background: The question of the mechanisms of platinum resistance development in advanced ovarian cancer (OC) remains open. The aim of the study was to reveal the relationship between the proliferative activity of OC cells, the disruption of apoptosis processes and the changes in the activity of transporter proteins that provide the efflux of chemotherapy drugs. Methods: Patients with advanced OC (T3-4N0-3M0-1) of postmenopausal age, sensitive (SPtPs, n = 23) and resistant to platinum drugs (RPtPs, n = 17), operated on after 3-6 cycles of neoadjuvant chemotherapy, were retrospectively studied. The parameters of proliferative activity (ki67), apoptosis disturbances (p53), as well as the expression of BCRP and Pgp transporter proteins were evaluated in OC tissue using immunohistochemistry methods. Statistical analysis was performed using the Mann-Whitney and Pearson tests (χ2), as well as the Spearman's rank correlation coefficient (SC). Results: In total, the dominance of the RPtPs over the SPtPs was noted in terms of intensity of the studied indicators (p < 0.05-0.003), the most significant for Pgp expression. At the same time, moderate and high values of these indicators were observed in SPtPs in 42-61% of cases, which reduced the predictive value of the revealed differences. It was of interest that statistically significant correlations between the indicators in SPtPs differed from those in RPtPs. Thus, the following values of the SC were observed in SPtPs: +0.848 (ki67-p53), -0.675 (ki67-BCRP), -0.575 (p53-BCR). In RPtPs, another intensity and/or direction of these relations were noted: +0.521 (ki 67-p53), +0.500 (ki 67-BCRP), +0.705 (p53-BCR). There were no statistically significant relationships between ki67-Pgp expression in SPtPs and RPtPs. The direction and intensity of the studied relationships could indicate changes in cell regulation in primary OC in SPtPs compared to RPtPs. Thus, in SPtPs, they reflected a significant contribution of apoptotic disturbances to the enhancement of OC cell proliferation, which was limited by the negative feedback mechanism via BCRP activity suppression indicated by the presence of an inverse correlation ki67-BCRP. In RPtPs, this mechanism was apparently already lost, which resulted in a change in the direction of the statistical relationship ki67-BCRP from reverse to direct one. Under these conditions, the positive contribution of apoptosis disruption to the proliferative activity of OC cells could obviously be supplemented by a synergistic increase in the activity of the BCRP transporter protein, which removes platinum drugs from OC cells. Conclusions: Patients with advanced OC may develop platinum resistance due to discoordination of proliferation, apoptosis, and regulation of the activity of the BCRP transporter protein.
The article provides a modern vision of the problem of cardiotoxicity in oncology. Integrity and generality of nodal pathogenetic events in the body in case of carcinogenesis, antitumor therapy and cardiopathology are caused by similar mechanisms at different hierarchical levels. Identity of potential risk factors, including inflammation, aging, obesity, diabetes and smoking, has been noted. Similarly, in the development of metabolic syndrome and carcinogenesis, the level of growth factors (IGF-1), neoangiogenesis, hormones and other triggers of oncological and cardiovascular pathology is increasing. It is important that a variety of clinical manifestations of cardiotoxicity are due to the rapid expansion of the number of therapeutic options for effects. This thesis is illustrated by vivid examples of the use of anthracycline-based drugs whose mechanism of action is aimed at damaging genetic targets. The use of monoclonal antibodies -trastuzumab, is directed against HER2 / ErB2 receptors in breast cancer and is accompanied by distinct signs of cardiotoxicity especially in the elderly. A new strategy to enhance the targeted cytotoxic immune response to cancer cells (Ipilimumab, Nivolumab) has a chance to cause autoimmune myocarditis and myositis. Modern anti-angiogenic methods of cancer therapy, including inhibition of VEGF, significantly increase the risk of myocardial ischemia, hypertension and atherosclerosis. This indicates the need for monitoring of complications, a targeted selection of preventive and curative strategies, as well as attention to the mechanisms of tissue homeostasis in the implementation of the antitumor effect.
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