4 research outputs found
ΠΠΎΡΡΠ΅Π»ΡΡΠΈΡ ΠΏΠ»ΠΎΡΠ½ΠΎΡΡΠΈ ΠΌΠ°ΠΊΡΠΎΡΠ°Π³ΠΎΠ² Ρ ΡΡΠΆΠ΅ΡΡΡΡ Π½Π΅ΠΎΠΏΠ»Π°Π·ΠΈΠΈ ΡΠ΅ΠΉΠΊΠΈ ΠΌΠ°ΡΠΊΠΈ
Despite all recent efforts, cancer of the uterine cervix still remains one of the most frequent malignancies among women. Lymphatic vessels represent the primary route of tumor cells dissemination in cervical cancer. It has been demonstrated that cervical neoplasia actively participates in the recruitment of new blood and lymphatic vessels. Macrophages are extremely versatile cells which have a significant contribution to tumor progression. The aim: 1) To establish the correlation between tumor-associated macrophages (TAM) and the grade of the uterine cervix neoplasia; 2) To evaluate the distribution of TAM within both intratumoral and peritumoral areas. Material and Methods: Ninety-six cases were studied. The specimens were fixed in buffered formalin and paraffin embedded. Step sections, 5ΞΌm thick, were performed for each case. Initial sections were stained with haematoxylin-eosin, for the pathological diagnosis and grading of the tumor. Lesions were classified as follows: squamous cell metaplasia (n = 12), CIN I (n = 8), CIN II (n = 6), CIN III (n = 24), microinvasive carcinoma (n = 16) and invasive squamous cell carcinoma (n = 26). Additional sections for each case were stained for CD68 antibody, in order to highlight the macrophages. Quantification of macrophage population has been made based on hot-spot technique. The arithmetic media of 3 (Γ 200) fields represented the final result. Results: We found a statistical correlation between peritumoral macrophages (PTM) and intratumoral macrophages in all stages of cervical neoplasia, macrophage density and tumor stage (p = 0.01). In 16 cases we found vascular invasion. Almost in all these cases (87.5%) intravascular tumor emboli were embedded with CD68 cells. Conclusions: based on these findings, we consider that macrophages are key regulators of cervical cancer progression. TAM targeted management could be an essential therapeutic strategy, not only in order to suppress the progression of cervical neoplasia, but also to inhibit macrophage-mediated vascular invasion.Π Π°ΠΊ ΡΠ΅ΠΉΠΊΠΈ ΠΌΠ°ΡΠΊΠΈ ΠΎΡΡΠ°Π΅ΡΡΡ ΠΎΠ΄Π½ΠΎΠΉ ΠΈΠ· ΡΠ°ΠΌΡΡ
ΡΠ°ΡΡΠΎ Π²ΡΡΡΠ΅ΡΠ°ΡΡΠΈΡ
ΡΡ Π·Π»ΠΎΠΊΠ°ΡΠ΅ΡΡΠ²Π΅Π½Π½ΡΡ
Π·Π°Π±ΠΎΠ»Π΅Π²Π°Π½ΠΈΠΉ ΠΆΠ΅Π½ΡΠΊΠΎΠ³ΠΎ Π½Π°ΡΠ΅Π»Π΅Π½ΠΈΡ. ΠΠΈΠΌΡΠ°ΡΠΈΡΠ΅ΡΠΊΠΈΠ΅ ΡΠΎΡΡΠ΄Ρ ΡΠ²Π»ΡΡΡΡΡ ΠΏΠ΅ΡΠ²ΠΈΡΠ½ΡΠΌ ΠΏΡΡΠ΅ΠΌ ΠΌΠ΅ΡΠ°ΡΡΠ°Π·ΠΈΡΠΎΠ²Π°Π½ΠΈΡ ΠΏΡΠΈ Π΄Π°Π½Π½ΠΎΠΌ Π·Π°Π±ΠΎΠ»Π΅Π²Π°Π½ΠΈΠΈ. ΠΡΠ»ΠΎ Π΄ΠΎΠΊΠ°Π·Π°Π½ΠΎ, ΡΡΠΎ ΠΊΠ»Π΅ΡΠΊΠΈ ΡΠ΅ΡΠ²ΠΈΠΊΠ°Π»ΡΠ½ΠΎΠΉ Π½Π΅ΠΎΠΏΠ»Π°Π·ΠΈΠΈ Π°ΠΊΡΠΈΠ²Π½ΠΎ ΡΡΠ°ΡΡΠ²ΡΡΡ Π² ΠΎΠ±ΡΠ°Π·ΠΎΠ²Π°Π½ΠΈΠΈ Π½ΠΎΠ²ΡΡ
Π»ΠΈΠΌΡΠ°ΡΠΈΡΠ΅ΡΠΊΠΈΡ
ΡΠΎΡΡΠ΄ΠΎΠ². ΠΠ°ΠΊΡΠΎΡΠ°Π³ΠΈ β ΠΌΠ½ΠΎΠ³ΠΎΡΡΠ½ΠΊΡΠΈΠΎΠ½Π°Π»ΡΠ½ΡΠ΅ ΠΊΠ»Π΅ΡΠΊΠΈ, ΠΎΠΊΠ°Π·ΡΠ²Π°ΡΡΠΈΠ΅ Π±ΠΎΠ»ΡΡΠΎΠ΅ Π²Π»ΠΈΡΠ½ΠΈΠ΅ Π½Π° ΠΏΡΠΎΠ³ΡΠ΅ΡΡΠΈΡΠΎΠ²Π°Π½ΠΈΠ΅ ΠΎΠΏΡΡ
ΠΎΠ»ΠΈ. Π¦Π΅Π»Ρ: 1). ΠΡΡΠ²Π»Π΅Π½ΠΈΠ΅ ΠΊΠΎΡΡΠ΅Π»ΡΡΠΈΠΈ ΠΌΠ΅ΠΆΠ΄Ρ ΠΌΠ°ΠΊΡΠΎΡΠ°Π³Π°ΠΌΠΈ ΠΈ ΡΡΠ°Π΄ΠΈΠ΅ΠΉ ΠΏΡΠΎΠ³ΡΠ΅ΡΡΠΈΠΈ Π½Π΅ΠΎΠΏΠ»Π°Π·ΠΈΠΈ ΡΠ΅ΠΉΠΊΠΈ ΠΌΠ°ΡΠΊΠΈ; 2). ΠΠΏΡΠ΅Π΄Π΅Π»Π΅Π½ΠΈΠ΅ ΠΎΡΠΎΠ±Π΅Π½Π½ΠΎΡΡΠ΅ΠΉ ΡΠ°ΡΠΏΡΠ΅Π΄Π΅Π»Π΅Π½ΠΈΡ ΠΌΠ°ΠΊΡΠΎΡΠ°Π³ΠΎΠ² Π²Π½ΡΡΡΠΈ ΠΎΠΏΡΡ
ΠΎΠ»Π΅Π²ΠΎΠΉ ΠΌΠ°ΡΡΡ ΠΈ Π²ΠΎΠΊΡΡΠ³ Π½Π΅Π΅. ΠΠ°ΡΠ΅ΡΠΈΠ°Π» ΠΈ ΠΌΠ΅ΡΠΎΠ΄Ρ. ΠΡΠ»ΠΎ ΠΈΠ·ΡΡΠ΅Π½ΠΎ 96 ΡΠ»ΡΡΠ°Π΅Π². ΠΠ°ΡΠ΅ΡΠΈΠ°Π» ΡΠΈΠΊΡΠΈΡΠΎΠ²Π°Π»ΠΈ Π² ΡΠΎΡΠΌΠ°Π»ΠΈΠ½Π΅ Ρ ΠΏΠΎΡΠ»Π΅Π΄ΡΡΡΠΈΠΌ Π·Π°ΠΊΠ»ΡΡΠ΅Π½ΠΈΠ΅ΠΌ Π² ΠΏΠ°ΡΠ°ΡΠΈΠ½. ΠΠ»Ρ ΠΊΠ°ΠΆΠ΄ΠΎΠ³ΠΎ ΡΠ»ΡΡΠ°Ρ ΠΏΡΠΎΠΈΠ·Π²ΠΎΠ΄ΠΈΠ»ΠΈ ΡΡΠ΅Π·Ρ, ΡΠΎΠ»ΡΠΈΠ½ΠΎΠΉ Π² 5 ΠΌΠΊΠΌ. ΠΠ·Π½Π°ΡΠ°Π»ΡΠ½ΠΎ, ΡΡΠ΅Π·Ρ ΠΎΠΊΡΠ°ΡΠΈΠ²Π°Π»ΠΈ Π³Π΅ΠΌΠ°ΡΠΎΠΊΡΠΈΠ»ΠΈΠ½-ΡΠΎΠ·ΠΈΠ½ΠΎΠΌ Π΄Π»Ρ ΠΎΠΏΡΠ΅Π΄Π΅Π»Π΅Π½ΠΈΡ Π³ΠΈΡΡΠΎΠΏΠ°ΡΠΎΠ»ΠΎΠ³ΠΈΡΠ΅ΡΠΊΠΎΠ³ΠΎ Π΄ΠΈΠ°Π³Π½ΠΎΠ·Π°. ΠΡΠ»ΠΈ ΠΏΠΎΠ»ΡΡΠ΅Π½Ρ ΡΠ»Π΅Π΄ΡΡΡΠΈΠ΅ Π³ΡΡΠΏΠΏΡ ΠΏΠΎΡΠ°ΠΆΠ΅Π½ΠΈΠΉ: ΠΏΠ»ΠΎΡΠΊΠΎΠΊΠ»Π΅ΡΠΎΡΠ½Π°Ρ ΠΌΠ΅ΡΠ°ΠΏΠ»Π°Π·ΠΈΡ (n = 12), CIN I (n = 8), CIN II (n = 6), CIN III (n = 24), ΠΌΠΈΠΊΡΠΎΠΊΠ°ΡΡΠΈΠ½ΠΎΠΌΠ° (n = 16), ΠΈΠ½Π²Π°Π·ΠΈΠ²Π½ΡΠΉ ΡΠ°ΠΊ (n = 26). ΠΠ»Ρ Π²ΡΡΠ²Π»Π΅Π½ΠΈΡ ΠΌΠ°ΠΊΡΠΎΡΠ°Π³ΠΎΠ², ΠΏΡΠΎΠΈΠ·Π²oΠ΄ΠΈΠ»ΠΈ ΠΈΠΌΠΌΡΠ½ΠΎΠ³ΠΈΡΡΠΎΡ
ΠΈΠΌΠΈΡΠ΅ΡΠΊΠΎΠ΅ ΠΈΡΡΠ»Π΅Π΄ΠΎΠ²Π°Π½ΠΈΠ΅ Ρ ΠΈΡΠΏΠΎΠ»ΡΠ·ΠΎΠ²Π°Π½ΠΈΠ΅ΠΌ ΠΌΠ°ΡΠΊΠ΅ΡΠ° CD68. ΠΠΎΠ΄ΡΡΠ΅Ρ ΠΏΠΎΠΏΡΠ»ΡΡΠΈΠΈ ΠΌΠ°ΠΊΡΠΎΡΠ°Π³ΠΎΠ² ΠΏΡΠΎΠΈΠ·Π²ΠΎΠ΄ΠΈΠ»ΠΈ ΠΏΠΎ ΠΌΠ΅ΡΠΎΠ΄ΠΈΠΊΠ΅ hot-spot. Π Π΅Π·ΡΠ»ΡΡΠ°ΡΡ. ΠΡ ΠΏΠΎΠ»ΡΡΠΈΠ»ΠΈ ΡΡΠ°ΡΠΈΡΡΠΈΡΠ΅ΡΠΊΠΈ Π·Π½Π°ΡΠΈΠΌΡΡ ΠΊΠΎΡΡΠ΅Π»ΡΡΠΈΡ ΠΌΠ΅ΠΆΠ΄Ρ Π²Π½ΡΡΡΠΈΡΡΠΌΠΎΡΠ°Π»ΡΠ½ΡΠΌΠΈ ΠΈ ΠΏΠ΅ΡΠΈΡΡΠΌΠΎΡΠ°Π»ΡΠ½ΡΠΌΠΈ ΠΌΠ°ΠΊΡΠΎΡΠ°Π³Π°ΠΌΠΈ Π²ΠΎ Π²ΡΠ΅Ρ
ΡΡΠ°Π΄ΠΈΡΡ
ΠΏΡΠΎΠ³ΡΠ΅ΡΡΠΈΠΈ Π½Π΅ΠΎΠΏΠ»Π°Π·ΠΈΠΈ ΡΠ΅ΠΉΠΊΠΈ ΠΌΠ°ΡΠΊΠΈ, ΠΌΠ΅ΠΆΠ΄Ρ ΠΏΠ»ΠΎΡΠ½ΠΎΡΡΡΡ ΠΌΠ°ΠΊΡΠΎΡΠ°Π³ΠΎΠ² ΠΈ ΡΡΠ°Π΄ΠΈΠ΅ΠΉ ΠΎΠΏΡΡ
ΠΎΠ»ΠΈ (p = 0,01). Π 16 ΡΠ»ΡΡΠ°ΡΡ
Π²ΡΡΠ²ΠΈΠ»ΠΈ ΡΠΎΡΡΠ΄ΠΈΡΡΡΠ΅ ΡΠΌΠ±ΠΎΠ»Ρ. ΠΠΎΡΡΠΈ Π²ΠΎ Π²ΡΠ΅Ρ
ΡΠ»ΡΡΠ°ΡΡ
(87,5%) Π²Π½ΡΡΡΠΈΡΠΎΡΡΠ΄ΠΈΡΡΡΠ΅ ΡΠΌΠ±ΠΎΠ»Ρ ΡΠΎΠ΄Π΅ΡΠΆΠ°Π»ΠΈ Π² ΡΠ΅Π±Π΅ CD68 ΠΊΠ»Π΅ΡΠΊΠΈ. ΠΡΠ²ΠΎΠ΄Ρ: ΠΡΠ½ΠΎΠ²ΡΠ²Π°ΡΡΡ Π½Π° ΠΏΠΎΠ»ΡΡΠ΅Π½Π½ΡΡ
ΡΠ΅Π·ΡΠ»ΡΡΠ°ΡΠ°Ρ
, ΠΌΡ ΡΡΠΈΡΠ°Π΅ΠΌ, ΡΡΠΎ ΠΌΠ°ΠΊΡΠΎΡΠ°Π³ΠΈ Π²ΠΎΠ²Π»Π΅ΡΠ΅Π½Ρ Π² ΠΏΡΠΎΠ³ΡΠ΅ΡΡΠΈΡ ΡΠ°ΠΊΠ° ΡΠ΅ΠΉΠΊΠΈ ΠΌΠ°ΡΠΊΠΈ
Histological and immunohistochemical evaluation of mandibular bone tissue regeneration
The purpose of the study was to perform an immunohistochemical and histological evaluation of samples taken from different bone regeneration procedures in atrophic human mandible. 30 patients (15 men and 15 women, age range of 35-60βyears), non-smokers, with good general and oral health were recruited in this study and divided into three groups. The first group included patients who were treated with blood Concentration Growth Factors (bCGF), the second group included patients who were treated with a mixture of bCGF and autologous bone, while the third group of patients was treated with bCGF and tricalcium phosphate/hydroxyapatite (TCP-HA). Six months after the regenerative procedures, all patients undergone implant surgery, and a bone biopsy was carried out in the site of implant insertion. Each sample was histologically and immunohistochemically examined. Histological evaluation showed a complete bone formation for group II, partial ossification for group I, and moderate ossification for group III. Immunohistochemical analysis demonstrated a statistically significant difference between the three groups, and the best clinical result was obtained with a mixture of bCGF and autologous bone
Π ΠΎΠ»Ρ ΡΠ΅ΡΠ΅ΠΏΡΠΎΡΠ° ΡΠΎΡΡΠ΄ΠΈΡΡΠΎΠ³ΠΎ ΡΠ½Π΄ΠΎΡΠ΅Π»ΠΈΠ°Π»ΡΠ½ΠΎΠ³ΠΎ ΡΠ°ΠΊΡΠΎΡΠ° ΡΠΎΡΡΠ° (VEGFR-3) Π² ΠΏΡΠΎΡΠ΅ΡΡΠ΅ ΠΊΠ°Π½ΡΠ΅ΡΠΎΠ³Π΅Π½Π΅Π·Π° ΡΠ΅ΠΉΠΊΠΈ ΠΌΠ°ΡΠΊΠΈ
In spite of the huge achievements made in the early detection of uterine cervix cancer, this disease remains one of the most widespread human malignancies throughout the world. Nowadays, there is a tendency of cervical cancer to affect the youth population. Early metastasizing is a critical point in evolution of this disease. Lymphatic vessels (LV) represents the primary route of cancer cells spreading towards the distant sites. That is why understanding of new lymphatics recruitment by the tumor, at molecular level, could be a potent support in solving of metastasizing. VEGFR-3 is a tyrosine-kinase receptor, specific for lymphatic endothelial cells, that being activated provides their proliferation, surviving and migration. It has been demonstrated that VEGF-R3 mediates invasion activity of tumor cells into surrounding stroma and vascular structures. The aim of this research was to study the importance of VEGFR-3 in cervical carcinogenesis. Material and methods: We studied biological material, taken by targeted biopsy and conization, from women with detectable cervical lesions. Detection VEGFR-3 was made using monoclonal antibody anti VEGF-R3 through Avidin-Biotin working system, LSAB technique. Lymphatic microvascular density was assessed by podoplanin labeling, using anti D2-40. A statistical analysis was made with SPSS 13.0. Results: We obtained VEGFR-3 expression in LV, blood vessels, tumor mass and stromal cells. The highest density of VEGFR-3 LV was in CIN III with gradually decreasing in invasive stages. In invasive carcinoma we obtained statistically significant correlation between tumor VEGFR-3 expression and vascular invasion. Conclusions: VEGFR-3 is not specific for lymphatic endothelium. It can not be used for alone lymphatic microvascular density assessing. It is actively involved in vascular invasion.ΠΠ΅ΡΠΌΠΎΡΡΡ Π½Π° ΠΎΠ³ΡΠΎΠΌΠ½ΡΠΉ ΡΡΠΏΠ΅Ρ
, Π΄ΠΎΡΡΠΈΠ³Π½ΡΡΡΠΉ Π² Π²ΡΡΠ²Π»Π΅Π½ΠΈΠ΅ ΡΠ°ΠΊΠ° ΡΠ΅ΠΉΠΊΠΈ ΠΌΠ°ΡΠΊΠΈ (Π Π¨Π) Π½Π° ΡΠ°Π½Π½ΠΈΡ
ΡΡΠ°Π΄ΠΈΡΡ
ΡΠ°Π·Π²ΠΈΡΠΈΡ, Π΄Π°Π½Π½ΠΎΠ΅ Π·Π°Π±ΠΎΠ»Π΅Π²Π°Π½ΠΈΠ΅ ΠΎΡΡΠ°Π΅ΡΡΡ ΠΎΠ΄Π½ΠΎΠΉ ΠΈΠ· ΡΠ°ΠΌΡΡ
ΡΠ°ΡΡΠΎ Π²ΡΡΡΠ΅ΡΠ°ΡΡΠΈΡ
ΡΡ Π·Π»ΠΎΠΊΠ°ΡΠ΅ΡΡΠ²Π΅Π½Π½ΡΡ
Π½ΠΎΠ²ΠΎΠΎΠ±ΡΠ°Π·ΠΎΠ²Π°Π½ΠΈΠΉ Π²ΠΎ Π²ΡΠ΅ΠΌ ΠΌΠΈΡΠ΅. ΠΠ° ΡΠ΅Π³ΠΎΠ΄Π½ΡΡΠ½ΠΈΠΉ Π΄Π΅Π½Ρ Π½Π°Π±Π»ΡΠ΄Π°Π΅ΡΡΡ ΡΠ΅Π½Π΄Π΅Π½ΡΠΈΡ ΠΎΠΌΠΎΠ»ΠΎΠΆΠ΅Π½ΠΈΡ Π Π¨Π. Π Π°Π½Π½Π΅Π΅ ΠΌΠ΅ΡΠ°ΡΡΠ°Π·ΠΈΡΠΎΠ²Π°Π½ΠΈΠ΅ ΡΠ²Π»ΡΠ΅ΡΡΡ ΠΊΠ»ΡΡΠ΅Π²ΡΠΌ ΠΌΠΎΠΌΠ΅Π½ΡΠΎΠΌ Π² ΡΠ²ΠΎΠ»ΡΡΠΈΠΈ Π·Π°Π±ΠΎΠ»Π΅Π²Π°Π½ΠΈΡ. ΠΠΈΠΌΡΠ°ΡΠΈΡΠ΅ΡΠΊΠΈΠ΅ ΡΠΎΡΡΠ΄Ρ ΠΏΡΠ΅Π΄ΡΡΠ°Π²Π»ΡΡΡ ΡΠΎΠ±ΠΎΠΉ ΠΏΠ΅ΡΠ²ΠΈΡΠ½ΡΠΉ ΠΏΡΡΡ ΡΠ°ΡΠΏΡΠΎΡΡΡΠ°Π½Π΅Π½ΠΈΡ ΠΎΠΏΡΡ
ΠΎΠ»Π΅Π²ΡΡ
ΠΊΠ»Π΅ΡΠΎΠΊ. Π ΡΠ²ΡΠ·ΠΈ Ρ ΡΡΠΈΠΌ, ΠΏΠΎΠ½ΠΈΠΌΠ°Π½ΠΈΠ΅ ΠΌΠ΅Ρ
Π°Π½ΠΈΠ·ΠΌΠΎΠ² ΠΎΠ±ΡΠ°Π·ΠΎΠ²Π°Π½ΠΈΡ Π»ΠΈΠΌΡΠ°ΡΠΈΡΠ΅ΡΠΊΠΈΡ
ΡΠΎΡΡΠ΄ΠΎΠ² Π½Π° ΠΌΠΎΠ»Π΅ΠΊΡΠ»ΡΡΠ½ΠΎΠΌ ΡΡΠΎΠ²Π½Π΅, ΠΌΠΎΠΆΠ΅Ρ ΠΏΠΎΠΌΠΎΡΡ ΡΠ΅ΡΠΈΡΡ ΡΡΡ ΠΏΡΠΎΠ±Π»Π΅ΠΌΡ. VEGFR-3 ΡΠ²Π»ΡΠ΅ΡΡΡ ΡΠΈΡΠΎΠ·ΠΈΠ½-ΠΊΠΈΠ½Π°Π·Π½ΡΠΌ ΡΠ΅ΡΠ΅ΠΏΡΠΎΡΠΎΠΌ. ΠΠ½ Π½Π°Ρ
ΠΎΠ΄ΠΈΡΡΡ Π½Π° ΠΏΠΎΠ²Π΅ΡΡ
Π½ΠΎΡΡΠΈ Π»ΠΈΠΌΡΠ°ΡΠΈΡΠ΅ΡΠΊΠΈΡ
ΡΠ½Π΄ΠΎΡΠ΅Π»ΠΈΠ°Π»ΡΠ½ΡΡ
ΠΊΠ»Π΅ΡΠΎΠΊ, ΠΏΡΠΈ Π°ΠΊΡΠΈΠ²Π°ΡΠΈΠΈ ΠΊΠΎΡΠΎΡΠΎΠ³ΠΎ ΠΏΡΠΎΠΈΡΡ
ΠΎΠ΄ΠΈΡ ΠΈΡ
ΠΏΡΠΎΠ»ΠΈΡΠ΅ΡΠ°ΡΠΈΡ, ΠΌΠΈΠ³ΡΠ°ΡΠΈΡ ΠΈ Π²ΡΠΆΠΈΠ²Π°Π½ΠΈΠ΅. ΠΡΠ»ΠΎ Π΄ΠΎΠΊΠ°Π·Π°Π½ΠΎ, ΡΡΠΎ VEGFR-3 ΡΠ΅Π³ΡΠ»ΠΈΡΡΠ΅Ρ ΠΈΠ½Π²Π°Π·ΠΈΡ ΡΠ°ΠΊΠΎΠ²ΡΡ
ΠΊΠ»Π΅ΡΠΎΠΊ Π² ΡΡΡΠΎΠΌΡ ΠΈ ΡΠΎΡΡΠ΄Ρ. Π¦Π΅Π»Ρ ΡΠ°Π±ΠΎΡΡ: ΠΈΠ·ΡΡΠΈΡΡ ΡΠΎΠ»Ρ VEGFR-3 Π² ΠΊΠ°Π½ΡΠ΅ΡΠΎΠ³Π΅Π½Π΅Π·Π΅ Π Π¨Π. ΠΠ°ΡΠ΅ΡΠΈΠ°Π» ΠΈ ΠΌΠ΅ΡΠΎΠ΄Ρ: Π±ΡΠ» ΠΈΠ·ΡΡΠ΅Π½ Π±ΠΈΠΎΠ»ΠΎΠ³ΠΈΡΠ΅ΡΠΊΠΈΠΉ ΠΌΠ°ΡΠ΅ΡΠΈΠ°Π», ΠΏΠΎΠ»ΡΡΠ΅Π½Π½ΡΠΉ ΠΏΠΎΡΡΠ΅Π΄ΡΡΠ²ΠΎΠΌ ΠΏΡΠΈΡΠ΅Π»ΡΠ½ΡΡ
Π±ΠΈΠΎΠΏΡΠΈΠΉ ΠΈ ΠΊΠΎΠ½ΠΈΠ·Π°ΡΠΈΠΉ Ρ ΠΏΠ°ΡΠΈΠ΅Π½ΡΠΎΠΊ Ρ ΠΌΠ°ΠΊΡΠΎΡΠΊΠΎΠΏΠΈΡΠ΅ΡΠΊΠΈ Π²ΡΡΠ²Π»Π΅Π½Π½ΡΠΌ ΠΏΠΎΡΠ°ΠΆΠ΅Π½ΠΈΠ΅ΠΌ ΡΠ΅ΠΉΠΊΠΈ ΠΌΠ°ΡΠΊΠΈ. ΠΠ»Ρ ΠΎΠΏΡΠ΅Π΄Π΅Π»Π΅Π½ΠΈΡ VEGFR-3 Π±ΡΠ»Π° ΠΈΡΠΏΠΎΠ»ΡΠ·ΠΎΠ²Π°Π½Π° ΡΠΈΡΡΠ΅ΠΌΠ° Avidin-Biotin, ΡΠ΅Ρ
Π½ΠΈΠΊΠ° LSAB , Ρ ΠΏΡΠΈΠΌΠ΅Π½Π΅Π½ΠΈΠ΅ΠΌ ΠΏΠ΅ΡΠ²ΠΈΡΠ½ΠΎΠ³ΠΎ Π°Π½ΡΠΈΡΠ΅Π»Π° Π°Π½ΡΠΈ VEGFR-3. ΠΠ»Ρ ΠΎΠΏΡΠ΅Π΄Π΅Π»Π΅Π½ΠΈΡ Π»ΠΈΠΌΡΠ°ΡΠΈΡΠ΅ΡΠΊΠΈΡ
ΡΠΎΡΡΠ΄ΠΎΠ² Π±ΡΠ»ΠΈ ΠΈΡΠΏΠΎΠ»ΡΠ·ΠΎΠ²Π°Π½Ρ ΠΌΠΎΠ½ΠΎΠΊΠ»ΠΎΠ½Π°Π»ΡΠ½ΡΠ΅ Π°Π½ΡΠΈΡΠ΅Π»Π° Π°Π½ΡΠΈ D2-40. Π‘ΡΠ°ΡΠΈΡΡΠΈΡΠ΅ΡΠΊΠΈΠΉ Π°Π½Π°Π»ΠΈΠ· Π΄Π°Π½Π½ΡΡ
Π±ΡΠ» ΠΏΡΠΎΠΈΠ·Π²Π΅Π΄Π΅Π½ ΠΏΡΠΈ ΠΏΠΎΠΌΠΎΡΠΈ SPSS 13.0. Π Π΅Π·ΡΠ»ΡΡΠ°ΡΡ: ΠΌΡ Π²ΡΡΠ²ΠΈΠ»ΠΈ ΡΠΊΡΠΏΡΠ΅ΡΡΠΈΡ VEGFR-3 Π½Π΅ ΡΠΎΠ»ΡΠΊΠΎ Π² Π»ΠΈΠΌΡΠ°ΡΠΈΡΠ΅ΡΠΊΠΈΡ
ΡΠΎΡΡΠ΄Π°Ρ
, Π° ΡΠ°ΠΊΠΆΠ΅ Π² ΠΊΡΠΎΠ²Π΅Π½ΠΎΡΠ½ΡΡ
ΡΠΎΡΡΠ΄Π°Ρ
, Π² ΠΎΠΏΡΡ
ΠΎΠ»Π΅Π²ΠΎΠΉ ΠΌΠ°ΡΡΠ΅ ΠΈ ΠΊΠ»Π΅ΡΠΊΠ°Ρ
ΡΡΡΠΎΠΌΡ. ΠΠ°ΠΈΠ±ΠΎΠ»ΡΡΠ°Ρ ΠΏΠ»ΠΎΡΠ½ΠΎΡΡΡ Π»ΠΈΠΌΡΠ°ΡΠΈΡΠ΅ΡΠΊΠΈΡ
ΡΠΎΡΡΠ΄ΠΎΠ² Π±ΡΠ»Π° ΠΎΠΏΡΠ΅Π΄Π΅Π»Π΅Π½Π° Π½Π° ΡΡΠ°Π΄ΠΈΠΈ CIN III (ΠΈΠ½ΡΡΠ°ΡΠΏΠΈΡΠ΅Π»ΠΈΠ°Π»ΡΠ½Π°Ρ ΡΠ΅ΡΠ²ΠΈΠΊΠ°Π»ΡΠ½Π°Ρ Π½Π΅ΠΎΠΏΠ»Π°Π·ΠΈΡ), Ρ ΠΏΠΎΡΠ»Π΅Π΄ΡΡΡΠΈΠΌ ΠΏΡΠΎΠ³ΡΠ΅ΡΡΠΈΠ²Π½ΡΠΌ ΡΠΌΠ΅Π½ΡΡΠ΅Π½ΠΈΠ΅ΠΌ. ΠΠ° ΡΡΠ°Π΄ΠΈΠΈ ΠΈΠ½Π²Π°Π·ΠΈΠ²Π½ΠΎΠ³ΠΎ ΡΠ°ΠΊΠ° ΠΌΡ ΠΏΠΎΠ»ΡΡΠΈΠ»ΠΈ ΡΡΠ°ΡΠΈΡΡΠΈΡΠ΅ΡΠΊΠΈ Π·Π½Π°ΡΠΈΠΌΡΡ ΠΊΠΎΡΡΠ΅Π»ΡΡΠΈΡ ΠΌΠ΅ΠΆΠ΄Ρ ΠΈΠ½ΡΠ΅Π½ΡΠΈΠ²Π½ΠΎΡΡΡΡ ΡΠΊΡΠΏΡΠ΅ΡΡΠΈΠΈ VEGFR-3 ΠΎΠΏΡΡ
ΠΎΠ»ΡΡ ΠΈ ΡΠΎΡΡΠ΄ΠΈΡΡΠΎΠΉ ΠΈΠ½Π²Π°Π·ΠΈΠ΅ΠΉ, Π° ΡΠ°ΠΊΠΆΠ΅ ΠΌΠ΅ΠΆΠ΄Ρ ΠΈΠ½ΡΠ΅Π½ΡΠΈΠ²Π½ΠΎΡΡΡΡ ΡΠΊΡΠΏΡΠ΅ΡΡΠΈΠΈ VEGFR-3 ΠΎΠΏΡΡ
ΠΎΠ»ΡΡ ΠΈ Π²Π½ΡΡΡΠΈΡΠΎΡΡΠ΄ΠΈΡΡΡΠΌΠΈ ΠΎΠΏΡΡ
ΠΎΠ»Π΅Π²ΡΠΌΠΈ ΡΠΌΠ±ΠΎΠ»Π°ΠΌΠΈ. ΠΡΠ²ΠΎΠ΄Ρ: VEGFR-3 Π½Π΅ ΡΠ²Π»ΡΠ΅ΡΡΡ ΡΠΏΠ΅ΡΠΈΡΠΈΡΠ΅ΡΠΊΠΈΠΌ ΠΌΠ°ΡΠΊΠ΅ΡΠΎΠΌ Π΄Π»Ρ Π»ΠΈΠΌΡΠ°ΡΠΈΡΠ΅ΡΠΊΠΎΠ³ΠΎ ΡΠ½Π΄ΠΎΡΠ΅Π»ΠΈΡ. ΠΠ°Π½Π½ΡΠΉ ΠΌΠ°ΡΠΊΠ΅Ρ Π½Π΅ ΠΌΠΎΠΆΠ΅Ρ ΠΈΡΠΏΠΎΠ»ΡΠ·ΠΎΠ²Π°ΡΡΡΡ ΡΠ°ΠΌΠΎΡΡΠΎΡΡΠ΅Π»ΡΠ½ΠΎ Π΄Π»Ρ ΠΎΠΏΡΠ΅Π΄Π΅Π»Π΅Π½ΠΈΡ Π»ΠΈΠΌΡΠ°ΡΠΈΡΠ΅ΡΠΊΠΎΠΉ ΠΌΠΈΠΊΡΠΎΡΠΎΡΡΠ΄ΠΈΡΡΠΎΠΉ ΠΏΠ»ΠΎΡΠ½ΠΎΡΡΠΈ. VEGFR-3 Π°ΠΊΡΠΈΠ²Π½ΠΎ Π²ΠΎΠ²Π»Π΅ΡΠ΅Π½ Π² ΠΏΡΠΎΡΠ΅ΡΡ ΡΠΎΡΡΠ΄ΠΈΡΡΠΎΠΉ ΠΈΠ½Π²Π°Π·ΠΈΠΈ
Expression of CK5 basal cytokeratin in primary breast carcinoma
Department of Histology, Cytology and Embryology,
Laboratory of Morphology, Nicolae Testemitsanu State University of Medicine and Pharmacy, Chisinau, the Republic of MoldovaBackground: CK5 positive cells represent progenitors for glandular and myoepithelial lineages of mammary epithelium. During epithelial differentiation there is a gradual decrease of CK5 expression. In case of benign lesions the proliferating luminal cells show a high expression of CK5. Contrary, the majority of malignancies which are derived from differentiated glandular cells line do not reveal immunohistochemical staining with CK5 marker. The aim of this study was to compare the expression of basal cytokeratin CK5 vs hormone receptors, HER2, Ki67 and molecular subtypeβs immunohistochemically defined in the primary breast carcinomas of NST type. Material and methods: We processed 108 invasive breast carcinomas of NST type. The specimens were formalin-fixed and paraffin-embedded as traditionally. Sections were immunostained (ER, PR, HER2, CK5 and Ki67) automatically with Leica Bond-Max autostainer. Results: Breast carcinoma of NST type was in majority of cases CK5 negative (94 cases/87%). The positive CK5 cases had a high grade of differentiation. CK5 negative tumors were usually hormone positive, but in 8 cases/6.5% a combined simultaneous CK5-ER (PR) positive expression was determined. From 22 HER2 positive cases, 16 were CK5 negative. CK5 value correlated statistically significant with all used markers, except grade of differentiation: a positive Pearson coefficient was determined in relation to HER2 and Ki67, and a negative one compared to hormone receptors and molecular subtype. Conclusions: We support CK5 potential value in molecular subtypeβs differentiation. Breast carcinoma of NST type is usually CK5 negative and hormone positive. The presence of cases with simultaneous expression of CK5 and hormone receptors is an open field to debate the existence of other, transient molecular subtypes and we expect a further confirmation in larger study groups