The Aqua Melafen Solutions’ Influences on the Parameters of the Mice’s Solid Carcinoma Luis Development

Author(s):  
A Krementsova ◽  
V Erokhin ◽  
V Semenov ◽  
O Alekseeva
Keyword(s):  
Author(s):  
А.А. Раецкая ◽  
С.В. Калиш ◽  
С.В. Лямина ◽  
Е.В. Малышева ◽  
О.П. Буданова ◽  
...  

Цель исследования. Доказательство гипотезы, что репрограммированные in vitro на М3 фенотип макрофаги при введении в организм будут существенно ограничивать развитие солидной карциномы in vivo . Методика. Рост солидной опухоли инициировали у мышей in vivo путем подкожной инъекции клеток карциномы Эрлиха (КЭ). Инъекцию макрофагов с нативным М0 фенотипом и с репрограммированным M3 фенотипом проводили в область формирования солидной КЭ. Репрограммирование проводили с помощью низких доз сыворотки, блокаторов факторов транскрипции STAT3/6 и SMAD3 и липополисахарида. Использовали две схемы введения макрофагов: раннее и позднее. При раннем введении макрофаги вводили на 1-е, 5-е, 10-е и 15-е сут. после инъекции клеток КЭ путем обкалывания макрофагами с четырех сторон область развития опухоли. При позднем введении, макрофаги вводили на 10-е, 15-е, 20-е и 25-е сут. Через 15 и 30 сут. после введения клеток КЭ солидную опухоль иссекали и измеряли ее объем. Эффект введения макрофагов оценивали качественно по визуальной и пальпаторной характеристикам солидной опухоли и количественно по изменению ее объема по сравнению с группой без введения макрофагов (контроль). Результаты. Установлено, что M3 макрофаги при раннем введении от начала развития опухоли оказывают выраженный антиопухолевый эффект in vivo , который был существенно более выражен, чем при позднем введении макрофагов. Заключение. Установлено, что введение репрограммированных макрофагов M3 ограничивает развитие солидной карциномы в экспериментах in vivo . Противоопухолевый эффект более выражен при раннем введении М3 макрофагов. Обнаруженные в работе факты делают перспективным разработку клинической версии биотехнологии ограничения роста опухоли, путем предварительного программирования антиопухолевого врожденного иммунного ответа «в пробирке». Aim. To verify a hypothesis that macrophages reprogrammed in vitro to the M3 phenotype and injected into the body substantially restrict the development of solid carcinoma in vivo . Methods. Growth of a solid tumor was initiated in mice in vivo with a subcutaneous injection of Ehrlich carcinoma (EC) cells. Macrophages with a native M0 phenotype or reprogrammed towards the M3 phenotype were injected into the region of developing solid EC. Reprogramming was performed using low doses of serum, STAT3/6 and SMAD3 transcription factor blockers, and lipopolysaccharide. Two schemes of macrophage administration were used: early and late. With the early administration, macrophages were injected on days 1, 5, 10, and 15 following the injection of EC cells at four sides of the tumor development area. With the late administration, macrophages were injected on days 10, 15, 20, and 25. At 15 and 30 days after the EC cell injection, the solid tumor was excised and its volume was measured. The effect of macrophage administration was assessed both qualitatively by visual and palpation characteristics of solid tumor and quantitatively by changes in the tumor volume compared with the group without the macrophage treatment. Results. M3 macrophages administered early after the onset of tumor development exerted a pronounced antitumor effect in vivo , which was significantly greater than the antitumor effect of the late administration of M3 macrophages. Conclusion. The observed significant inhibition of in vivo growth of solid carcinoma by M3 macrophages makes promising the development of a clinical version of the biotechnology for restriction of tumor growth by in vitro pre-programming of the antitumor, innate immune response.


Pathobiology ◽  
2021 ◽  
pp. 1-6
Author(s):  
Antonio Travaglino ◽  
Antonio Raffone ◽  
Annarita Gencarelli ◽  
Serena Saracinelli ◽  
Fulvio Zullo ◽  
...  

Here, we present a case that highlights the crucial pitfalls related to the presence of morular metaplasia (MM) in endometrioid carcinoma, which are insufficiently recognized in the routine pathology practice. A 45-year-old woman underwent hysterectomy with rectosigmoidectomy due to a 11-cm mass involving uterus, right ovary, and rectosigmoid colon. Histologically, the lesion appeared as a predominantly solid carcinoma with a minor glandular component. Results of the first immunohistochemical analysis suggested a colorectal origin (PAX8-, CK7-, WT1-, hormone receptors-, and CDX2+ in the absence of mucinous features). Subsequent immunohistochemistry (nuclear β-catenin+, CD10+, and low ki67 in the solid areas) supported a diagnosis of endometrioid carcinoma with diffuse MM. This case remarks that morphological and immunohistochemical features of MM may conceal the glandular architecture and the typical immunophenotype of endometrioid carcinomas. Acknowledging the diagnostic issues related to MM appears crucial to avoid misdiagnosis and inappropriate patient management.


Medicine ◽  
1973 ◽  
Vol 52 (2) ◽  
pp. 141-171 ◽  
Author(s):  
C. STRATTON HILL ◽  
MICHAEL L. IBANEZ ◽  
NAGUIB A. SAMAAN ◽  
MICHAEL J. AHEARN ◽  
R. LEE CLARK

2010 ◽  
Vol 2010 ◽  
pp. 1-5 ◽  
Author(s):  
Saravana Kumar Jaganathan ◽  
Dilip Mondhe ◽  
Z. A. Wani ◽  
Harish C. Pal ◽  
Mahitosh Mandal

Ehrlich ascites carcinoma is a spontaneous murine mammary adenocarcinoma adapted to ascites form and carried in outbred mice by serial intraperitoneal (i/p) passages. The previous work from our laboratory showed that honey having higher phenolic content was potent in inhibiting colon cancer cell proliferation. In this work, we extended our research to screen the antitumor activity of two selected honey samples and eugenol (one of the phenolic constituents of honey) against murine Ehrlich ascites and solid carcinoma models. Honey containing higher phenolic content was found to significantly inhibit the growth of Ehrlich ascites carcinoma as compared to other samples. When honey containing higher phenolic content was given at 25% (volume/volume) intraperitoneally (i/p), the maximum tumor growth inhibition was found to be 39.98%. However, honey was found to be less potent in inhibiting the growth of Ehrlich solid carcinoma. On the other hand, eugenol at a dose of 100 mg/kg i/p was able to inhibit the growth of Ehrlich ascites by 28.88%. In case of solid carcinoma, eugenol (100 mg/kg; i/p) showed 24.35% tumor growth inhibition. This work will promote the development of honey and eugenol as promising candidates in cancer chemoprevention.


2003 ◽  
Vol 40 (1) ◽  
pp. 86-91 ◽  
Author(s):  
K. Hirayama ◽  
Y. Honda ◽  
T. Sako ◽  
M. Okamoto ◽  
N. Tsunoda ◽  
...  

A 21-year-old thoroughbred mare had a 35 X 14 X 10 cm mass involving the mammary gland. Metastases were found in the kidneys, lungs, skeletal muscles, and regional lymph nodes. Histopathologic examination of the tumor revealed a ductal solid carcinoma with extensive intraductal and intralobular involvement and focal infiltration of the adjacent stroma. The intralobular neoplasms were divided into irregularly shaped islands and sheets of polygonal and spindle-shaped epithelial cells by thick or thin fibrous connective tissue bundles. The neoplastic cells had a small or moderate amount of cytoplasm that stained faintly with eosin and round or oval hyperchromatic nuclei. Immunohistochemically, the neoplastic cells were strongly positive for Lu-5, weakly positive for AE1/AE3, vimentin, and glial fibrillary acidic protein, and negative for cytokeratin 8, cytokeratin 14, a-smooth muscle actin, calponin, and S100. The neoplasm was diagnosed as an invasive ductal carcinoma of the mammary gland with multiple metastases.


1986 ◽  
Vol 33 (1-10) ◽  
pp. 208-211 ◽  
Author(s):  
J. S. Linde-Sipman ◽  
I. Gaag ◽  
M. A. Velden
Keyword(s):  

2014 ◽  
Vol 150 (1) ◽  
pp. 105
Author(s):  
A. Gulcubuk ◽  
O. Erdogan ◽  
E.R. Bozkurt ◽  
A. Gurel ◽  
M.N. Arikan ◽  
...  

2015 ◽  
Vol 58 ◽  
pp. 129-142
Author(s):  
Sayed K. Areida ◽  
Amira O. Abd El-Azim ◽  
Maggie E. Amer

Sign in / Sign up

Export Citation Format

Share Document