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  • Open Access

    ARTICLE

    Normalization of Elevated Tumor Marker CA27-29 After Bilateral Lung Transplantation in a Patient With Breast Cancer and Idiopathic Pulmonary Fibrosis

    Mehmet Sitki Copur*†, Julie Marie Wurdeman, Debra Nelson*, Ryan Ramaekers*, Dron Gauchan*, David Crockett*

    Oncology Research, Vol.26, No.3, pp. 515-518, 2018, DOI:10.3727/096504017X15128550060375

    Abstract Solid tumors involving glandular organs express mucin glycoprotein that is eventually shed into the circulation. As a result, these proteins can easily be measured in the serum and be used as potential tumor markers. The most commonly used tumor markers for breast cancer are CA27-29 and CA15-3, which both measure the glycoprotein product of the mucin-1 (MUC1) gene. CA27-29 has been approved by the US Food and Drug Administration for monitoring disease activity in breast cancer patients. Most oncology clinical practice guidelines do not recommend the use of tumor markers for routine surveillance of early… More >

  • Open Access

    REVIEW

    Transcriptional factor RUNX1: A potential therapeutic target for fibrotic pulmonary disease

    JIA LIU1,2,#, FAPING WANG1,2,#, BO YUAN3, FENGMING LUO1,2,*

    BIOCELL, Vol.47, No.4, pp. 697-705, 2023, DOI:10.32604/biocell.2023.026148

    Abstract Runt-related transcription factor-1 (RUNX1), also known as the core-binding factor alpha 2 subunit, is closely related to human leukemia. The functions of RUNX1 in modulating cell proliferation, differentiation, and survival in multiple systems have been gradually discovered with the emergence of transgenic mice. RUNX1 is a powerful transcription factor implicated in diverse signaling pathways and cellular mechanisms that participate in lung development and pulmonary diseases. RUNX1 has recently been identified as a target regulator of fibrotic remodeling diseases, particularly in the kidney. However, the role of RUNX1 in pulmonary fibrosis is unclear. Pulmonary fibrosis is More >

  • Open Access

    VIEWPOINT

    Preventive approach against drug-induced pulmonary fibrosis through the suppression of epithelial-mesenchymal transition

    MASASHI KAWAMI*, RYOKO YUMOTO, MIKIHISA TAKANO

    BIOCELL, Vol.46, No.8, pp. 1861-1865, 2022, DOI:10.32604/biocell.2022.019667

    Abstract A number of drugs induce pulmonary injury and subsequently lead to serious lung diseases such as pulmonary fibrosis as the adverse drug reactions. However, an effective preventive approach against drug-induced pulmonary fibrosis has not been established due to poor understanding of common preventive targets in a variety of drugs showing pulmonary toxicity. Epithelial-mesenchymal transition (EMT), a cellular phenotypic change of the epithelial to mesenchymal state, contributes to the development of pulmonary fibrosis through the conversion of damaged alveolar epithelium into myofibroblasts. As several drugs with pulmonary toxicity have been reported to induce EMT, EMT serves… More >

  • Open Access

    ARTICLE

    Different sources of MSCs on pulmonary fibrosis in C57BL/6 mice

    SHUCAI WU1,#, DENGRUI LI1,#, SUMIN GUO1, LI GAO2, YONGHUI YANG1,*

    BIOCELL, Vol.45, No.2, pp. 339-344, 2021, DOI:10.32604/biocell.2021.011379

    Abstract Since stem cell therapy is the most effective treatment in the field of tissue reparation and reconstitution, the present study aimed to explore the different sources of mesenchymal stem cells (MSCs) on the different effects of pulmonary fibrosis-related cytokines in C57BL/6 mice. For reaching this goal, we isolated MSCs from umbilical cord blood and placenta and used for stem cell therapy in a mouse model of pulmonary fibrosis model. The pulmonary fibrosis model was done by injecting bleomycin into the trachea of C57BL/6 mice. Then we assessed the degree of pulmonary fibrosis in each mouse… More >

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