हमारा समूह 1000 से अधिक वैज्ञानिक सोसायटी के सहयोग से हर साल संयुक्त राज्य अमेरिका, यूरोप और एशिया में 3000+ वैश्विक सम्मेलन श्रृंखला कार्यक्रम आयोजित करता है और 700+ ओपन एक्सेस जर्नल प्रकाशित करता है जिसमें 50000 से अधिक प्रतिष्ठित व्यक्तित्व, प्रतिष्ठित वैज्ञानिक संपादकीय बोर्ड के सदस्यों के रूप में शामिल होते हैं।
ओपन एक्सेस जर्नल्स को अधिक पाठक और उद्धरण मिल रहे हैं
700 जर्नल और 15,000,000 पाठक प्रत्येक जर्नल को 25,000+ पाठक मिल रहे हैं
Hinrich P Hansen, Katrin S Reiners and Elke Pogge von Strandmann
In most cases, cancer cells cannot proliferate alone. They receive support form stromal cells and recruit and reprogram non-malignant immune cells not to damage the cancer cells but to support the tumor growth. Classical Hodgkin lymphoma (cHL) is a good example, as its growth critically depends on tumor-supporting immune cells. The affected lymphoid tissue contains very few disseminated malignant Hodgkin- and Reed-Sternberg (H-RS) cells, which are outnumbered by a massive infiltrate of lymphocytes, fibroblasts and innate immune cells. [1]. The H-RS cells need this environment to survive and proliferate because they are usually not detectable in the peripheral blood and they have difficulties to grow in immune-deficient mice [2]. H-RS cells manipulate the bystander cells for better development of their malignant phenotype and evasion of the host defense [3]. Among the infiltrated immune cells, the eosinophils and mast cells play an important role and their cell count indicates a negative prognostic feature [4,5]. In vitro, the direct interaction with cancer cells communicates survival in cancer cells and the production of cancersupporting factors in immune cells. In the last years, extracellular vesicles (EVs) emerged as important vehicles to shuttle between different the cell types and communicate as a surrogate cellular crosstalk in trans [6,7].