Given a passage, construct a question on the basis of the information present in the passage. Construct the question in such a way that (i) it is unambiguous, (ii) it is answerable from the passage, (iii) its answer is unique (iv) it answer uses text phrases from the passage. Avoid creating questions that (i) can't be answered correctly without actually understanding the passage and (ii) uses the same words or phrases given in the passage.

Ex Input:
Potent antitumor responses can be induced through cytokine immunotherapy. Interleukin (IL)-2 and granulocyte-macrophage colony-stimulating factor (GM-CSF) are among the most effective cytokines to induce tumor-specific systemic immune responses and can act synergistically. To overcome the limitations of combined use of these two cytokines, we have constructed an IL2-GMCSF fusion protein and characterized its antitumor effects in this study.', 'The expression of IL-2 receptor and GM-CSF receptor of cell lines were detected with quantitative real-time PCR. On this basis, the bioactivities of IL2-GMCSF, especially effects on DC2.4 cells were assayed. Another function of IL2-GMCSF-bridge two types of cells-was assessed by cell contact counting and cytotoxicity assays. The anti-tumor activity in vivo of IL2-GMCSF was evaluated in the melanoma model. The statistical significance among treatment groups were determined by One-Way ANOVA.', 'The fusion protein IL2-GMCSF maintained the activities of IL-2 and GM-CSF, and could significantly promote DC2.4 cell activities, including phagocytosis, proliferation and cytokine secretion. In addition to the inherent cytokine activity, IL2-GMCSF bridges direct cell-cell interactions and enhances splenocyte killing efficacy against multiple tumor cell lines in vitro. Co-injection of IL2-GMCSF and inactivated B16F10 mouse melanoma cells induced complete immunoprotective responses in about 30 % of mice.

Ex Output:
Does fusion cytokine IL-2-GMCSF enhance anticancer immune responses through promoting cell-cell interactions?


Ex Input:
A fundamental prerequisite for using degradable synthetic biopolymers as composite skin substitutes is the ability to establish vascular tissue. PEGT/PBT block-copolymer matrices have previously been shown as a favorable dermal substitute. In this study, quantitative data on neovascularization of PEGT/PBT block-copolymer matrices are presented.', 'PEGT/PBT-block-copolymer discs of three different pore diameters (1: < 75 microm, 2: 75-212 microm, 3: 250-300 microm) were implanted into dorsal skinfold chambers of balb/c mice. Histological sections were evaluated 7, 14, and 21 days post implantation by light and scanning electron microscopy. Blood vessel analysis was performed by means of digital image analysis (n = 288) of hematoxylin/eosin stained sections within apical (AOF) and basal (BOF) observation fields of the matrices.', 'Twenty-one days after implantation the density of blood vessels within the BOF of the scaffolds with a pore size of 75-212 and 250-300 microm were 4.6 +/- 0.45 and 5.8 +/- 0.62 (mean +/- S.E.M.; blood vessel profiles (BVF)), respectively. In <75 microm scaffolds, smaller numbers of BVF were found (4.2 +/- 0.39). In contrast, the evaluation within the AOF revealed significantly higher numbers of BVF in 75-212 microm group (3.5 +/- 0.49) and 250-300 microm group (4.5 +/- 0.66) as compared to the < 75 microm group (2.3 +/- 0.48).

Ex Output:
Does analysis of neovascularization of PEGT/PBT-copolymer dermis substitute in balb/c-mice?


Ex Input:
MicroRNA-26b (miR-26b) has been reported to be down-regulated in a wide range of malignant tumors, However, the mechanism by which miR-26b is implicated in breast cancer tumorigenesis is incompletely understood. This study was undertaken to evaluate the expression pattern of miR-26b and characterize its biological role in human breast cancer.', 'Reverse transcription-polymerase chain reaction (RT-PCR) was used to quantify the expression levels of miR-26b in breast cancer and adjacent non-cancerous breast tissues. MTT, colony formation assay and cell cycle assay were carried out to characterize the miR-26b function. Finally, to validate the target gene of miR-26b, luciferase reporter assay was employed, followed by RT-PCR and Western blot confirmation.', "Here, we found that miR-26b expression was relatively downregulated in breast cancer specimens (P<0.01). Overexpression of miR-26b dramatically suppressed cell proliferation, colony formation and induced G0/G1 cell cycle arrest of MDA-MB-231 and Mcf-7 cells. Luciferase assays revealed that miR-26b directly targeted the 3'UTR of CDK8. Overexpression of miR-26b led to the downregulation of CDK8 and β-catenin expression. Similarly, CDK8 knockdown by siRNA suppressed cell growth and subsequent β-catenin expression.

Ex Output:

Does miRNA-26b inhibit cellular proliferation by targeting CDK8 in breast cancer?