58 research outputs found
HPV-associated cervical cancer: Current status and prospects
Every year, 570,000 new cases of cervical cancer (CC) are diagnosed in the world, and 311,000 people die from this disease. CC is the fourth most common type of cancer and therefore the fourth leading cause of cancer death in women worldwide. Numerous data on the occurrence and development of cervical cancer indicate an association in most cases (up to 90 %) with human papillomaviruses (HPV) of high carcinogenic risk (HCR).CC prevention strategies are based on screening, and deaths from this oncopathology can be prevented through vaccination and treatment with early detection of the disease.In this review, much attention is paid to current issues of detection and prevention of HPV-associated pathologies, and cervical cancer in particular, aiming to summarize and analyze the latest international literature data on this issue. As a result of this study, it was shown that for countries implementing the National program of vaccination against HPV of high carcinogenic risk, a decrease in the incidence of both cervical pathologies of varying severity and other cancers associated with the HPV carriage was registered.While effective implementation of actual experience and future advances in human papillomavirus vaccine prophylaxis may make it possible for all countries to move to the high levels of vaccination coverage required to eliminate HPV-associated pathologies, the results also suggest that the path to complete cervical cancer elimination as a global public health problem can be extremely difficult due to a number of existing limitations
Search for potential gastric cancer markers using miRNA databases and gene expression analysis
Aim: The aim of this study was to identify genes that are differentially expressed in gastric tumors and to analyze the association of their expression level with tumor clinicopathologic features. Methods: In the present research, we used bioinformatic-driven search to identify miRNA that are down-regulated in gastric tumors and to find their potential targets. Then, the expression levels of some of the target mRNAs were investigated using reverse transcription polymerase chain reaction (RT-PCR) analysis. Results: As a result of the bioinformatics analysis, fifteen genes were found to be potentially differentially expressed between the tumors and normal gastric tissue. Five of them were chosen for the further analysis (WNT4, FGF12, EFEMP1, CTGF, and HSPG2) due to their important role in cell proliferation and differentiation. Expression levels of these genes were evaluated in our collection of frozen tissue samples of gastric tumor and paired normal stomach epithelia. Increased FGF12 expression was observed in diffuse type of gastric cancer while WNT4 mRNA was found to be down-regulated in intestinal type of gastric cancer. Besides, CTGF gene overexpression was revealed in diffuse type of stomach cancer in comparison with that in intestinal type. Up-regulation of CTGF was also associated with lymph node metastasis. Conclusions: The findings show its expedient to perform further investigations in order to clarify diagnostic and prognostic value of CTGF, FGF12, and WNT4βs in stomach cancer as well as the role of these genes in carcinogenesis
Composite implants coated with biodegradable polymers prevent stimulating tumor progression
In this experiment we studied oncologic safety of model implants created using the solution blow spinning method with the use of the PURASORB PL-38 polylactic acid polymer and organic mineral filler which was obtained via laser ablation of a solid target made of dibasic calcium phosphate dihydrate. For this purpose the implant was introduced into the area of Wistar ratsβ iliums, and on day 17 after the surgery the Walker sarcoma was transplanted into the area of the implant. We evaluated the implantβs influence on the primary tumor growth, hematogenous and lymphogenous metastasis of the Walker sarcoma. In comparison with sham operated animals the implant group demonstrated significant inhibition of hematogenous metastasis on day 34 after the surgery. The metastasis inhibition index (MII) equaled 94% and the metastases growth inhibition index (MGII) equaled 83%. The metastasis frequency of the Walker sarcoma in para aortic lymph nodes in the implant group was not statistically different from the control frequency; there was also no influence of the implant on the primary tumor growth noted. In case of the Walker sarcoma transplantation into the calf and the palmar pad of the ipsilateral limb to the one with the implant in the ilium, we could not note any attraction of tumor cells to the implant area, i.e. stimulation of the Walker sarcoma relapse by the implant. Thus, the research concluded that the studied implant meets the requirements of oncologic safety
Composite implants coated with biodegradable polymers prevent stimulating tumor progression
In this experiment we studied oncologic safety of model implants created using the solution blow spinning method with the use of the PURASORB PL-38 polylactic acid polymer and organic mineral filler which was obtained via laser ablation of a solid target made of dibasic calcium phosphate dihydrate. For this purpose the implant was introduced into the area of Wistar ratsβ iliums, and on day 17 after the surgery the Walker sarcoma was transplanted into the area of the implant. We evaluated the implantβs influence on the primary tumor growth, hematogenous and lymphogenous metastasis of the Walker sarcoma. In comparison with sham operated animals the implant group demonstrated significant inhibition of hematogenous metastasis on day 34 after the surgery. The metastasis inhibition index (MII) equaled 94% and the metastases growth inhibition index (MGII) equaled 83%. The metastasis frequency of the Walker sarcoma in para aortic lymph nodes in the implant group was not statistically different from the control frequency; there was also no influence of the implant on the primary tumor growth noted. In case of the Walker sarcoma transplantation into the calf and the palmar pad of the ipsilateral limb to the one with the implant in the ilium, we could not note any attraction of tumor cells to the implant area, i.e. stimulation of the Walker sarcoma relapse by the implant. Thus, the research concluded that the studied implant meets the requirements of oncologic safety
ΠΠΠ’ΠΠ Π― ΠΠΠ’ΠΠ ΠΠΠΠΠΠ’ΠΠΠ‘Π’Π ΠΠΠΠ£Π‘ΠΠ ΠΠΠΠΠ BRCA1 Π BRCA2 Π ΠΠΠ£Π₯ΠΠΠ ΠΠΠΠΠ§ΠΠΠ ΠΠΠΠΠΠ«
One of the factors of variability of malignant neoplasms is the loss of heterozygosity (LOH). The biological meaning of LOH, in relation to carcinogenesis, is associated with the inactivation of heterozygous loci of pathogenetically significant genes. Thus, the aim of this work was to study BRCA1/2 LOH in breast tumors.Material and Methods. The study included 122 patients with stage IIAIIIC breast cancer. DNA was isolated from 122 biopsy samples of tumor tissue using the QIAamp DNA mini Kit (Qiagen, Germany). To assess the status of LOH, microarray analysis was performed on high-density DNA chips from Affymetrix CytoScanTM HD Array. To process the results of microchipping, we used the Chromosome Analysis Suite 3.3 program (Affymetrix, USA).Results. The loss of heterozygosity in the BRCA1 gene was found to be associated with response to NAC. It was shown that in 59 patients LOH in the BRCA1gene was associated with an objective response to treatment (p=0.005). The presence of LOH in the studied genes was associated with a favorable prognosis. The 5-year non-metastatic survival rates were 75 % and 100 % in patients with LOH in the BRCA1 and BRCA2 genes, respectively (log-rank test: p=0.003 and p=0.05, respectively).Conclusion. The phenomenon of LOH in the BRCA1/2 genes was shown to be associated with response to NACT. BRCA1/2. Further studies are needed to evaluate the frequency of BRCA1/2 LOH after NAC for choosing and changing treatment tactics.Β ΠΠ΄Π½ΠΈΠΌ ΠΈΠ· ΡΠ°ΠΊΡΠΎΡΠΎΠ² Π²Π°ΡΠΈΠ°Π±Π΅Π»ΡΠ½ΠΎΡΡΠΈ Π·Π»ΠΎΠΊΠ°ΡΠ΅ΡΡΠ²Π΅Π½Π½ΡΡ
Π½ΠΎΠ²ΠΎΠΎΠ±ΡΠ°Π·ΠΎΠ²Π°Π½ΠΈΠΉ ΡΠ²Π»ΡΠ΅ΡΡΡ ΠΏΠΎΡΠ΅ΡΡ Π³Π΅ΡΠ΅ΡΠΎΠ·ΠΈΠ³ΠΎΡΠ½ΠΎΡΡΠΈ (LOH β loss of heterozygosity). ΠΡΠ΅Π΄ΠΏΠΎΠ»Π°Π³Π°Π΅ΡΡΡ, ΡΡΠΎ Π±ΠΈΠΎΠ»ΠΎΠ³ΠΈΡΠ΅ΡΠΊΠΈΠΉ ΡΠΌΡΡΠ» LOH ΠΏΡΠΈΠΌΠ΅Π½ΠΈΡΠ΅Π»ΡΠ½ΠΎ ΠΊ ΠΊΠ°Π½ΡΠ΅ΡΠΎΠ³Π΅Π½Π΅Π·Ρ ΡΠ²ΡΠ·Π°Π½ Ρ ΠΈΠ½Π°ΠΊΡΠΈΠ²Π°ΡΠΈΠ΅ΠΉ Π³Π΅ΡΠ΅ΡΠΎΠ·ΠΈΠ³ΠΎΡΠ½ΡΡ
Π»ΠΎΠΊΡΡΠΎΠ² ΠΏΠ°ΡΠΎΠ³Π΅Π½Π΅ΡΠΈΡΠ΅ΡΠΊΠΈ Π·Π½Π°ΡΠΈΠΌΡΡ
Π³Π΅Π½ΠΎΠ².Π¦Π΅Π»ΡΡ ΠΈΡΡΠ»Π΅Π΄ΠΎΠ²Π°Π½ΠΈΡ ΡΠ²ΠΈΠ»ΠΎΡΡ ΠΈΡΡΠ»Π΅Π΄ΠΎΠ²Π°Π½ΠΈΠ΅ ΠΏΠΎΡΠ΅ΡΠΈ Π³Π΅ΡΠ΅ΡΠΎΠ·ΠΈΠ³ΠΎΡΠ½ΠΎΡΡΠΈ Π³Π΅Π½ΠΎΠ² BRCA1/2 Π² ΠΎΠΏΡΡ
ΠΎΠ»ΠΈ ΠΌΠΎΠ»ΠΎΡΠ½ΠΎΠΉ ΠΆΠ΅Π»Π΅Π·Ρ.ΠΠ°ΡΠ΅ΡΠΈΠ°Π» ΠΈ ΠΌΠ΅ΡΠΎΠ΄Ρ. Π ΠΈΡΡΠ»Π΅Π΄ΠΎΠ²Π°Π½ΠΈΠ΅ Π±ΡΠ»ΠΈ Π²ΠΊΠ»ΡΡΠ΅Π½Ρ 122 Π±ΠΎΠ»ΡΠ½ΡΡ
ΡΠ°ΠΊΠΎΠΌ ΠΌΠΎΠ»ΠΎΡΠ½ΠΎΠΉ ΠΆΠ΅Π»Π΅Π·Ρ IIAβIIIC ΡΡΠ°Π΄ΠΈΠΈ. ΠΠΠ Π²ΡΠ΄Π΅Π»ΡΠ»ΠΈ ΠΈΠ· 122 Π±ΠΈΠΎΠΏΡΠΈΠΉΠ½ΡΡ
ΠΎΠ±ΡΠ°Π·ΡΠΎΠ² ΠΎΠΏΡΡ
ΠΎΠ»Π΅Π²ΠΎΠΉ ΡΠΊΠ°Π½ΠΈ Ρ ΠΏΠΎΠΌΠΎΡΡΡ Π½Π°Π±ΠΎΡΠ° QIAamp DNA mini Kit (Qiagen, Germany). ΠΠ»Ρ ΠΎΡΠ΅Π½ΠΊΠΈ ΡΡΠ°ΡΡΡΠ° LOH ΠΏΡΠΎΠ²Π΅Π΄Π΅Π½ ΠΌΠΈΠΊΡΠΎΠΌΠ°ΡΡΠΈΡΠ½ΡΠΉ Π°Π½Π°Π»ΠΈΠ· Π½Π° ΠΠΠ-ΡΠΈΠΏΠ°Ρ
Π²ΡΡΠΎΠΊΠΎΠΉ ΠΏΠ»ΠΎΡΠ½ΠΎΡΡΠΈ ΡΠΈΡΠΌΡ Affymetrix CytoScanTM HD Array. ΠΠ»Ρ ΠΎΠ±ΡΠ°Π±ΠΎΡΠΊΠΈ ΡΠ΅Π·ΡΠ»ΡΡΠ°ΡΠΎΠ² ΠΌΠΈΠΊΡΠΎΡΠΈΠΏΠΈΡΠΎΠ²Π°Π½ΠΈΡ ΠΈΡΠΏΠΎΠ»ΡΠ·ΠΎΠ²Π°Π»ΠΈ ΠΏΡΠΎΠ³ΡΠ°ΠΌΠΌΡ Β«Chromosome Analysis Suite 3.3Β» (Affymetrix, USA).Π Π΅Π·ΡΠ»ΡΡΠ°ΡΡ. Π ΡΠ΅Π·ΡΠ»ΡΡΠ°ΡΠ΅ ΠΏΡΠΎΠ²Π΅Π΄Π΅Π½Π½ΠΎΠ³ΠΎ ΠΈΡΡΠ»Π΅Π΄ΠΎΠ²Π°Π½ΠΈΡ Π±ΡΠ»ΠΎ ΡΡΡΠ°Π½ΠΎΠ²Π»Π΅Π½ΠΎ, ΡΡΠΎ Π½Π°Π»ΠΈΡΠΈΠ΅ ΠΏΠΎΡΠ΅ΡΠΈ Π³Π΅ΡΠ΅ΡΠΎΠ·ΠΈΠ³ΠΎΡΠ½ΠΎΡΡΠΈ Π² Π³Π΅Π½Π΅ BRCA1 ΡΠΎΠΏΡΡΠΆΠ΅Π½ΠΎ Ρ ΠΎΡΠ²Π΅ΡΠΎΠΌ Π½Π° Π½Π΅ΠΎΠ°Π΄ΡΡΠ²Π°Π½ΡΠ½ΡΡ Ρ
ΠΈΠΌΠΈΠΎΡΠ΅ΡΠ°ΠΏΠΈΡ. ΠΠΎΠΊΠ°Π·Π°Π½ΠΎ, ΡΡΠΎ Ρ 59 Π±ΠΎΠ»ΡΠ½ΡΡ
Π½Π°Π»ΠΈΡΠΈΠ΅ LOH Π² Π³Π΅Π½Π΅ BRCA1 ΡΠΎΠΏΡΡΠΆΠ΅Π½ΠΎ Ρ ΠΎΠ±ΡΠ΅ΠΊΡΠΈΠ²Π½ΡΠΌ ΠΎΡΠ²Π΅ΡΠΎΠΌ Π½Π° Π»Π΅ΡΠ΅Π½ΠΈΠ΅ (p=0,005). ΠΠ°Π»ΠΈΡΠΈΠ΅ ΠΏΠΎΡΠ΅ΡΠΈ Π³Π΅ΡΠ΅ΡΠΎΠ·ΠΈΠ³ΠΎΡΠ½ΠΎΡΡΠΈ Π² ΠΈΠ·ΡΡΠ°Π΅ΠΌΡΡ
Π³Π΅Π½Π°Ρ
ΡΠΎΠΏΡΡΠΆΠ΅Π½ΠΎ Ρ Π±Π»Π°Π³ΠΎΠΏΡΠΈΡΡΠ½ΡΠΌ ΠΏΡΠΎΠ³Π½ΠΎΠ·ΠΎΠΌ. ΠΠΎΠΊΠ°Π·Π°ΡΠ΅Π»Ρ 5-Π»Π΅ΡΠ½Π΅ΠΉ Π±Π΅Π·ΠΌΠ΅ΡΠ°ΡΡΠ°ΡΠΈΡΠ΅ΡΠΊΠΎΠΉ Π²ΡΠΆΠΈΠ²Π°Π΅ΠΌΠΎΡΡΠΈ Ρ ΠΏΠ°ΡΠΈΠ΅Π½ΡΠΎΠ² Ρ ΠΏΠΎΡΠ΅ΡΠ΅ΠΉ Π³Π΅ΡΠ΅ΡΠΎΠ·ΠΈΠ³ΠΎΡΠ½ΠΎΡΡΠΈ Π΄Π»Ρ Π³Π΅Π½Π° BRCA1 ΡΠΎΡΡΠ°Π²Π»ΡΠ΅Ρ 75 % (log-rank test p=0,003), Π΄Π»Ρ Π³Π΅Π½Π° BRCA2 Π²ΡΠ΅ ΠΏΠ°ΡΠΈΠ΅Π½ΡΡ ΠΈΠΌΠ΅Π»ΠΈ 100 % Π±Π΅Π·ΠΌΠ΅ΡΠ°ΡΡΠ°ΡΠΈΡΠ΅ΡΠΊΡΡ Π²ΡΠΆΠΈΠ²Π°Π΅ΠΌΠΎΡΡΡ, log-rank test p=0,05.ΠΠ°ΠΊΠ»ΡΡΠ΅Π½ΠΈΠ΅. ΠΠΎΠΊΠ°Π·Π°Π½ΠΎ, ΡΡΠΎ ΠΏΠΎΡΠ΅ΡΡ Π³Π΅ΡΠ΅ΡΠΎΠ·ΠΈΠ³ΠΎΡΠ½ΠΎΡΡΠΈ Π² Π³Π΅Π½Π°Ρ
BRCA1/2 ΡΠ²ΡΠ·Π°Π½Π° Ρ ΡΡΡΠ΅ΠΊΡΠΈΠ²Π½ΠΎΡΡΡΡ Π½Π΅ΠΎΠ°Π΄ΡΡΠ²Π°Π½ΡΠ½ΠΎΠΉ Ρ
ΠΈΠΌΠΈΠΎΡΠ΅ΡΠ°ΠΏΠΈΠΈ, Π° ΡΠ°ΠΊΠΆΠ΅ ΡΠ²Π»ΡΠ΅ΡΡΡ Π½Π΅Π·Π°Π²ΠΈΡΠΈΠΌΡΠΌ ΠΏΡΠΎΠ³Π½ΠΎΡΡΠΈΡΠ΅ΡΠΊΠΈΠΌ ΡΠ°ΠΊΡΠΎΡΠΎΠΌ. Π‘ ΡΡΠ΅ΡΠΎΠΌ ΠΏΠΎΠ»ΡΡΠ΅Π½Π½ΡΡ
ΡΠ΅Π·ΡΠ»ΡΡΠ°ΡΠΎΠ² ΠΌΠΎΠΆΠ½ΠΎ ΠΏΡΠ΅Π΄ΠΏΠΎΠ»ΠΎΠΆΠΈΡΡ, ΡΡΠΎ ΠΈΠ½Π°ΠΊΡΠΈΠ²Π°ΡΠΈΡ BRCA1/2 Π΄ΠΎΠ»ΠΆΠ½Π° ΠΊΠΎΡΡΠ΅Π»ΠΈΡΠΎΠ²Π°ΡΡ Ρ ΡΡΠ²ΡΡΠ²ΠΈΡΠ΅Π»ΡΠ½ΠΎΡΡΡΡ ΠΊ ΡΠ΅ΡΠ°ΠΏΠΈΠΈ Π½Π° ΠΎΡΠ½ΠΎΠ²Π΅ ΠΏΠ»Π°ΡΠΈΠ½Ρ, ΡΡΠΎ, Π½Π΅ΡΠΎΠΌΠ½Π΅Π½Π½ΠΎ, Π΄Π΅Π»Π°Π΅Ρ Π΄Π°Π»ΡΠ½Π΅ΠΉΡΠ΅Π΅ ΠΈΠ·ΡΡΠ΅Π½ΠΈΠ΅ Π΄Π°Π½Π½ΠΎΠ³ΠΎ Π²ΠΎΠΏΡΠΎΡΠ° Π°ΠΊΡΡΠ°Π»ΡΠ½ΡΠΌ.
ΠΠΎΠ»Π½ΠΎΡΡΠ°Π½ΡΠΊΡΠΈΠΏΡΠΎΠΌΠ½ΡΠΉ Π°Π½Π°Π»ΠΈΠ· ΠΎΠΏΡΡ ΠΎΠ»ΠΈ ΠΌΠΎΠ»ΠΎΡΠ½ΠΎΠΉ ΠΆΠ΅Π»Π΅Π·Ρ Π² ΠΏΡΠΎΡΠ΅ΡΡΠ΅ Π½Π΅ΠΎΠ°Π΄ΡΡΠ²Π°Π½ΡΠ½ΠΎΠΉ Ρ ΠΈΠΌΠΈΠΎΡΠ΅ΡΠ°ΠΏΠΈΠΈ: ΡΠ²ΡΠ·Ρ Ρ ΠΎΡΠ²Π΅ΡΠΎΠΌ Π½Π° ΠΏΡΠ΅Π΄ΠΎΠΏΠ΅ΡΠ°ΡΠΈΠΎΠ½Π½ΡΡ Ρ ΠΈΠΌΠΈΠΎΡΠ΅ΡΠ°ΠΏΠΈΡ
Introduction. Treatment of breast cancer often includes systemic neoadjuvant chemotherapy. The frequency of complete morphological response varies significantly depending on the molecular subtype of tumor. However, even in triple negative breast cancer, which is considered the most sensitive, it does not exceed 50 %. Therefore, the search for new genetic predictors of tumor response to preoperative treatment, as well as the assessment of tumor changes during neoadjuvant chemotherapy are highly relevant.Objective β to perform whole-transcriptome analysis of breast cancer during neoadjuvant chemotherapy depending on tumor response to preoperative treatment.Materials and methods. This study included 39 patients with luminal B HER2-positive (human epidermal growth factor receptor 2) breast cancer who received 6 to 8 cycles of neoadjuvant chemotherapy. We performed whole-transcriptome analysis of paired biopsy and surgical specimens using the Clariomβ’ S Assay, human (Affymetrix, USA).Results. We observed significant differences in the pretreatment expression of 166 genes (13 were up-regulated and 153 were down-regulated) between patients with objective response to therapy and those without it. Comparison of preand post-treatment expression profiles demonstrated 680 differentially expressed genes in patients with complete and partial response and 3240 differentially expressed genes in patients with stable or progressive disease. Venn diagram showed that patients with and without objective response to neoadjuvant chemotherapy shared 105 differentially expressed genes.Conclusion. We performed primary screening of genes in breast tumors before therapy and identified genes whose pretreatment expression differed significantly between patients with objective response to neoadjuvant chemotherapy and those without it. Further validation of these genes in an independent sample will allow the development of a genetic panel to evaluate the response to neoadjuvant chemotherapy. Assessment of changes in the expression of tumor genes during treatment depending on patientβs response to therapy can be useful for further development of a panel of genes, which will enable the evaluation of clinical response to chemotherapy, as well as identification of key cellular processes that change the activity of genes during therapy.ΠΠ²Π΅Π΄Π΅Π½ΠΈΠ΅. ΠΠ΅ΡΠ΅Π½ΠΈΠ΅ ΡΠ°ΠΊΠ° ΠΌΠΎΠ»ΠΎΡΠ½ΠΎΠΉ ΠΆΠ΅Π»Π΅Π·Ρ Π²ΠΎ ΠΌΠ½ΠΎΠ³ΠΈΡ
ΡΠ»ΡΡΠ°ΡΡ
Π²ΠΊΠ»ΡΡΠ°Π΅Ρ ΡΠΈΡΡΠ΅ΠΌΠ½ΡΡ Ρ
ΠΈΠΌΠΈΠΎΡΠ΅ΡΠ°ΠΏΠΈΡ Π² Π½Π΅ΠΎΠ°Π΄ΡΡΠ²Π°Π½ΡΠ½ΠΎΠΌ ΡΠ΅ΠΆΠΈΠΌΠ΅. Π‘ΠΎΠ³Π»Π°ΡΠ½ΠΎ Π΄Π°Π½Π½ΡΠΌ Π»ΠΈΡΠ΅ΡΠ°ΡΡΡΡ ΡΠ°ΡΡΠΎΡΠ° ΠΏΠΎΠ»Π½ΠΎΠ³ΠΎ ΠΌΠΎΡΡΠΎΠ»ΠΎΠ³ΠΈΡΠ΅ΡΠΊΠΎΠ³ΠΎ ΠΎΡΠ²Π΅ΡΠ° ΠΎΠΏΡΡ
ΠΎΠ»ΠΈ Π·Π½Π°ΡΠΈΡΠ΅Π»ΡΠ½ΠΎ Π²Π°ΡΡΠΈΡΡΠ΅Ρ Π² Π·Π°Π²ΠΈΡΠΈΠΌΠΎΡΡΠΈ ΠΎΡ Π΅Π΅ ΠΌΠΎΠ»Π΅ΠΊΡΠ»ΡΡΠ½ΠΎΠ³ΠΎ ΠΏΠΎΠ΄ΡΠΈΠΏΠ°, ΠΎΠ΄Π½Π°ΠΊΠΎ Π΄Π°ΠΆΠ΅ ΠΏΡΠΈ ΡΠ°ΠΌΠΎΠΌ ΡΡΠ²ΡΡΠ²ΠΈΡΠ΅Π»ΡΠ½ΠΎΠΌ, ΡΡΠΈΠΆΠ΄Ρ Π½Π΅Π³Π°ΡΠΈΠ²Π½ΠΎΠΌ ΠΏΠΎΠ΄ΡΠΈΠΏΠ΅ ΠΎΠ½Π° Π½Π΅ ΠΏΡΠ΅Π²ΡΡΠ°Π΅Ρ 50 %. Π² ΡΠ²ΡΠ·ΠΈ Ρ ΡΡΠΈΠΌ Π°ΠΊΡΡΠ°Π»ΡΠ½Ρ ΠΏΠΎΠΈΡΠΊ Π³Π΅Π½Π΅ΡΠΈΡΠ΅ΡΠΊΠΈΡ
ΠΏΡΠ΅Π΄ΠΈΠΊΡΠΎΡΠΎΠ² ΠΎΡΠ²Π΅ΡΠ° ΠΎΠΏΡΡ
ΠΎΠ»ΠΈ Π½Π° ΠΏΡΠ΅Π΄ΠΎΠΏΠ΅ΡΠ°ΡΠΈΠΎΠ½Π½ΠΎΠ΅ Π»Π΅ΡΠ΅Π½ΠΈΠ΅ ΠΈ ΠΎΡΠ΅Π½ΠΊΠ° ΠΈΠ·ΠΌΠ΅Π½Π΅Π½ΠΈΠΉ, ΠΊΠΎΡΠΎΡΡΠ΅ ΠΏΡΠΎΠΈΡΡ
ΠΎΠ΄ΡΡ Π² ΠΎΠΏΡΡ
ΠΎΠ»ΠΈ Π² ΠΏΡΠΎΡΠ΅ΡΡΠ΅ Π½Π΅ΠΎΠ°Π΄ΡΡΠ²Π°Π½ΡΠ½ΠΎΠΉ Ρ
ΠΈΠΌΠΈΠΎΡΠ΅ΡΠ°ΠΏΠΈΠΈ.Π¦Π΅Π»Ρ ΠΈΡΡΠ»Π΅Π΄ΠΎΠ²Π°Π½ΠΈΡ β ΠΏΡΠΎΠ²Π΅Π΄Π΅Π½ΠΈΠ΅ ΠΏΠΎΠ»Π½ΠΎΡΡΠ°Π½ΡΠΊΡΠΈΠΏΡΠΎΠΌΠ½ΠΎΠ³ΠΎ Π°Π½Π°Π»ΠΈΠ·Π° ΠΎΠΏΡΡ
ΠΎΠ»ΠΈ ΠΌΠΎΠ»ΠΎΡΠ½ΠΎΠΉ ΠΆΠ΅Π»Π΅Π·Ρ Π² Ρ
ΠΎΠ΄Π΅ Π½Π΅ΠΎΠ°Π΄ΡΡΠ²Π°Π½ΡΠ½ΠΎΠΉ Ρ
ΠΈΠΌΠΈΠΎΡΠ΅ΡΠ°ΠΏΠΈΠΈ Π² Π·Π°Π²ΠΈΡΠΈΠΌΠΎΡΡΠΈ ΠΎΡ ΠΎΡΠ²Π΅ΡΠ° Π½Π° ΠΏΡΠ΅Π΄ΠΎΠΏΠ΅ΡΠ°ΡΠΈΠΎΠ½Π½ΠΎΠ΅ Π»Π΅ΡΠ΅Π½ΠΈΠ΅.ΠΠ°ΡΠ΅ΡΠΈΠ°Π»Ρ ΠΈ ΠΌΠ΅ΡΠΎΠ΄Ρ. Π ΠΈΡΡΠ»Π΅Π΄ΠΎΠ²Π°Π½ΠΈΠ΅ Π²ΠΊΠ»ΡΡΠ΅Π½Ρ 39 ΠΏΠ°ΡΠΈΠ΅Π½ΡΠΎΠ² Ρ ΡΠ°ΠΊΠΎΠΌ ΠΌΠΎΠ»ΠΎΡΠ½ΠΎΠΉ ΠΆΠ΅Π»Π΅Π·Ρ Π»ΡΠΌΠΈΠ½Π°Π»ΡΠ½ΠΎΠ³ΠΎ Π² HER2-ΠΏΠΎΠ·ΠΈΡΠΈΠ²Π½ΠΎΠ³ΠΎ ΠΏΠΎΠ΄ΡΠΈΠΏΠ° (human epidermal growth factor receptor 2, ΡΠ΅ΡΠ΅ΠΏΡΠΎΡ ΡΠΏΠΈΠ΄Π΅ΡΠΌΠ°Π»ΡΠ½ΠΎΠ³ΠΎ ΡΠ°ΠΊΡΠΎΡΠ° ΡΠΎΡΡΠ°, ΡΠΈΠΏ 2), ΠΏΠΎΠ»ΡΡΠ°Π²ΡΠΈΠ΅ 6β8 ΠΊΡΡΡΠΎΠ² Π½Π΅ΠΎΠ°Π΄ΡΡΠ²Π°Π½ΡΠ½ΠΎΠΉ Ρ
ΠΈΠΌΠΈΠΎΡΠ΅ΡΠ°ΠΏΠΈΠΈ. ΠΡΠ»ΠΈ ΠΈΡΡΠ»Π΅Π΄ΠΎΠ²Π°Π½Ρ ΠΏΠ°ΡΠ½ΡΠ΅ ΠΎΠ±ΡΠ°Π·ΡΡ Π±ΠΈΠΎΠΏΡΠΈΠΉΠ½ΠΎΠ³ΠΎ ΠΈ ΠΎΠΏΠ΅ΡΠ°ΡΠΈΠΎΠ½Π½ΠΎΠ³ΠΎ ΠΌΠ°ΡΠ΅ΡΠΈΠ°Π»Π°. ΠΠΎΠ»Π½ΠΎΡΡΠ°Π½ΡΠΊΡΠΈΠΏΡΠΎΠΌΠ½ΡΠΉ ΠΌΠΈΠΊΡΠΎΠΌΠ°ΡΡΠΈΡΠ½ΡΠΉ Π°Π½Π°Π»ΠΈΠ· ΠΏΡΠΎΠ²ΠΎΠ΄ΠΈΠ»ΡΡ Ρ ΠΈΡΠΏΠΎΠ»ΡΠ·ΠΎΠ²Π°Π½ΠΈΠ΅ΠΌ ΠΏΠ»Π°ΡΡΠΎΡΠΌΡ Clariomβ’ S Assay, human (Affymetrix, Π‘Π¨Π).Π Π΅Π·ΡΠ»ΡΡΠ°ΡΡ. ΠΡΠΈ ΡΡΠ°Π²Π½Π΅Π½ΠΈΠΈ ΡΠΊΡΠΏΡΠ΅ΡΡΠΈΠΎΠ½Π½ΠΎΠ³ΠΎ ΠΏΡΠΎΡΠΈΠ»Ρ ΠΏΠ°ΡΠΈΠ΅Π½ΡΠΎΠ² Ρ Π½Π°Π»ΠΈΡΠΈΠ΅ΠΌ ΠΈ ΠΎΡΡΡΡΡΡΠ²ΠΈΠ΅ΠΌ ΠΎΠ±ΡΠ΅ΠΊΡΠΈΠ²Π½ΠΎΠ³ΠΎ ΠΎΡΠ²Π΅ΡΠ° Π½Π° Π»Π΅ΡΠ΅Π½ΠΈΠ΅ Π΄ΠΎ ΠΏΡΠΎΠ²Π΅Π΄Π΅Π½ΠΈΡ Π½Π΅ΠΎΠ°Π΄ΡΡΠ²Π°Π½ΡΠ½ΠΎΠΉ Ρ
ΠΈΠΌΠΈΠΎΡΠ΅ΡΠ°ΠΏΠΈΠΈ Π±ΡΠ»ΠΎ Π²ΡΡΠ²Π»Π΅Π½ΠΎ 166 Π΄ΠΈΡΡΠ΅ΡΠ΅Π½ΡΠΈΠ°Π»ΡΠ½ΠΎ ΡΠΊΡΠΏΡΠ΅ΡΡΠΈΡΡΡΡΠΈΡ
ΡΡ Π³Π΅Π½ΠΎΠ² (13 up-regulated, 153 down-regulated). ΠΡΠΈ ΡΡΠ°Π²Π½Π΅Π½ΠΈΠΈ ΡΠΊΡΠΏΡΠ΅ΡΡΠΈΠΎΠ½Π½ΠΎΠ³ΠΎ ΠΏΡΠΎΡΠΈΠ»Ρ Π΄ΠΎ ΠΈ ΠΏΠΎΡΠ»Π΅ Π»Π΅ΡΠ΅Π½ΠΈΡ Ρ Π±ΠΎΠ»ΡΠ½ΡΡ
Ρ ΠΏΠΎΠ»Π½ΠΎΠΉ ΠΈ ΡΠ°ΡΡΠΈΡΠ½ΠΎΠΉ ΡΠ΅Π³ΡΠ΅ΡΡΠΈΠ΅ΠΉ Π²ΡΡΠ²Π»Π΅Π½ΠΎ 680 Π΄ΠΈΡΡΠ΅ΡΠ΅Π½ΡΠΈΠ°Π»ΡΠ½ΠΎ ΡΠΊΡΠΏΡΠ΅ΡΡΠΈΡΡΡΡΠΈΡ
ΡΡ Π³Π΅Π½ΠΎΠ², Π° Ρ Π±ΠΎΠ»ΡΠ½ΡΡ
ΡΠΎ ΡΡΠ°Π±ΠΈΠ»ΠΈΠ·Π°ΡΠΈΠ΅ΠΉ ΠΈΠ»ΠΈ ΠΏΡΠΎΠ³ΡΠ΅ΡΡΠΈΡΠΎΠ²Π°Π½ΠΈΠ΅ΠΌ β 3240 ΡΡΠΈΡ
Π³Π΅Π½ΠΎΠ². Π‘ ΠΏΠΎΠΌΠΎΡΡΡ ΠΏΠΎΡΡΡΠΎΠ΅Π½ΠΈΡ Π΄ΠΈΠ°Π³ΡΠ°ΠΌΠΌΡ Π²Π΅Π½Π½Π° Π±ΡΠ»ΠΎ ΠΏΠΎΠΊΠ°Π·Π°Π½ΠΎ, ΡΡΠΎ 105 Π΄ΠΈΡΡΠ΅ΡΠ΅Π½ΡΠΈΠ°Π»ΡΠ½ΠΎ ΡΠΊΡΠΏΡΠ΅ΡΡΠΈΡΡΡΡΠΈΡ
ΡΡ Π³Π΅Π½ΠΎΠ² ΡΠ²Π»ΡΡΡΡΡ ΠΎΠ±ΡΠΈΠΌΠΈ Π΄Π»Ρ ΠΏΠ°ΡΠΈΠ΅Π½ΡΠΎΠ² Ρ Π½Π°Π»ΠΈΡΠΈΠ΅ΠΌ/ΠΎΡΡΡΡΡΡΠ²ΠΈΠ΅ΠΌ ΠΎΠ±ΡΠ΅ΠΊΡΠΈΠ²Π½ΠΎΠ³ΠΎ ΠΎΡΠ²Π΅ΡΠ° Π½Π° Π½Π΅ΠΎΠ°Π΄ΡΡΠ²Π°Π½ΡΠ½ΡΡ Ρ
ΠΈΠΌΠΈΠΎΡΠ΅ΡΠ°ΠΏΠΈΡ Π΄ΠΎ ΠΈ ΠΏΠΎΡΠ»Π΅ Π»Π΅ΡΠ΅Π½ΠΈΡ.ΠΠ°ΠΊΠ»ΡΡΠ΅Π½ΠΈΠ΅. ΠΡΠ» ΠΏΡΠΎΠ²Π΅Π΄Π΅Π½ ΠΏΠ΅ΡΠ²ΠΈΡΠ½ΡΠΉ ΡΠΊΡΠΈΠ½ΠΈΠ½Π³ Π³Π΅Π½ΠΎΠ² Π² ΠΎΠΏΡΡ
ΠΎΠ»ΠΈ ΠΌΠΎΠ»ΠΎΡΠ½ΠΎΠΉ ΠΆΠ΅Π»Π΅Π·Ρ Π΄ΠΎ Π»Π΅ΡΠ΅Π½ΠΈΡ. ΠΡΡΠ²Π»Π΅Π½Ρ Π³Π΅Π½Ρ, ΡΠΊΡΠΏΡΠ΅ΡΡΠΈΡ ΠΊΠΎΡΠΎΡΡΡ
Π΄ΠΎ ΡΠ΅ΡΠ°ΠΏΠΈΠΈ ΡΡΠ°ΡΠΈΡΡΠΈΡΠ΅ΡΠΊΠΈ Π·Π½Π°ΡΠΈΠΌΠΎ ΡΠ°Π·Π»ΠΈΡΠ°Π»Π°ΡΡ Ρ Π±ΠΎΠ»ΡΠ½ΡΡ
Ρ ΠΎΠ±ΡΠ΅ΠΊΡΠΈΠ²Π½ΡΠΌ ΠΎΡΠ²Π΅ΡΠΎΠΌ Π½Π° Π½Π΅ΠΎΠ°Π΄ΡΡΠ²Π°Π½ΡΠ½ΡΡ Ρ
ΠΈΠΌΠΈΠΎΡΠ΅ΡΠ°ΠΏΠΈΡ ΠΈ Π΅Π³ΠΎ ΠΎΡΡΡΡΡΡΠ²ΠΈΠ΅ΠΌ. ΠΠ°Π»ΡΠ½Π΅ΠΉΡΠ°Ρ Π²Π°Π»ΠΈΠ΄Π°ΡΠΈΡ Π΄Π°Π½Π½ΡΡ
Π³Π΅Π½ΠΎΠ² Π½Π° Π½Π΅Π·Π°Π²ΠΈΡΠΈΠΌΠΎΠΉ Π²ΡΠ±ΠΎΡΠΊΠ΅ Π΄Π°ΡΡ Π²ΠΎΠ·ΠΌΠΎΠΆΠ½ΠΎΡΡΡ ΡΠ°Π·ΡΠ°Π±ΠΎΡΠ°ΡΡ Π³Π΅Π½Π΅ΡΠΈΡΠ΅ΡΠΊΡΡ ΠΏΠ°Π½Π΅Π»Ρ Π΄Π»Ρ ΠΎΠΏΡΠ΅Π΄Π΅Π»Π΅Π½ΠΈΡ ΠΎΡΠ²Π΅ΡΠ° Π½Π° Π½Π΅ΠΎΠ°Π΄ΡΡΠ²Π°Π½ΡΠ½ΡΡ Ρ
ΠΈΠΌΠΈΠΎΡΠ΅ΡΠ°ΠΏΠΈΡ. ΠΡΠ΅Π½ΠΊΠ° ΠΈΠ·ΠΌΠ΅Π½Π΅Π½ΠΈΡ ΡΠΊΡΠΏΡΠ΅ΡΡΠΈΠΈ ΠΎΠΏΡΡ
ΠΎΠ»Π΅Π²ΡΡ
Π³Π΅Π½ΠΎΠ² Π² Ρ
ΠΎΠ΄Π΅ Π»Π΅ΡΠ΅Π½ΠΈΡ Ρ Π±ΠΎΠ»ΡΠ½ΡΡ
Π² Π·Π°Π²ΠΈΡΠΈΠΌΠΎΡΡΠΈ ΠΎΡ ΠΎΡΠ²Π΅ΡΠ° Π½Π° ΡΡΡ ΡΠ΅ΡΠ°ΠΏΠΈΡ ΠΌΠΎΠΆΠ΅Ρ Π±ΡΡΡ ΠΏΠΎΠ»Π΅Π·Π½Π° Π΄Π»Ρ ΡΠ°Π·ΡΠ°Π±ΠΎΡΠΊΠΈ Π² Π΄Π°Π»ΡΠ½Π΅ΠΉΡΠ΅ΠΌ ΠΏΠ°Π½Π΅Π»ΠΈ Π³Π΅Π½ΠΎΠ², Π²ΡΡΠ²Π»Π΅Π½ΠΈΠ΅ ΠΈΠ·ΠΌΠ΅Π½Π΅Π½ΠΈΠΉ ΠΊΠΎΡΠΎΡΡΡ
ΠΏΠΎΠ·Π²ΠΎΠ»ΠΈΡ ΡΡΠ΄ΠΈΡΡ ΠΎ ΠΊΠ»ΠΈΠ½ΠΈΡΠ΅ΡΠΊΠΎΠΌ ΠΎΡΠ²Π΅ΡΠ΅ ΠΎΠΏΡΡ
ΠΎΠ»ΠΈ Π½Π° Ρ
ΠΈΠΌΠΈΠΎΡΠ΅ΡΠ°ΠΏΠΈΡ, Π° ΡΠ°ΠΊΠΆΠ΅ Π²ΡΠ΄Π΅Π»ΠΈΡΡ ΠΊΠ»ΡΡΠ΅Π²ΡΠ΅ ΠΊΠ»Π΅ΡΠΎΡΠ½ΡΠ΅ ΠΏΡΠΎΡΠ΅ΡΡΡ, ΠΌΠ΅Π½ΡΡΡΠΈΠ΅ Π°ΠΊΡΠΈΠ²Π½ΠΎΡΡΡ Π³Π΅Π½ΠΎΠ² Π² ΠΏΡΠΎΡΠ΅ΡΡΠ΅ ΡΠ΅ΡΠ°ΠΏΠΈΠΈ
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