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Department of Pathology, Yonsei University College of Medicine, Seoul, South Korea
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Department of Pathology, Yonsei University College of Medicine, Seoul, South Korea
Severance Biomedical Science Institute (SBSI), Yonsei University College of Medicine, Seoul, South Korea
Global 5-5-10 System Biology, Yonsei University, Seoul, South Korea
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et al . 2005 , Janni et al . 2011 ). Recurrence after long period of dormancy is especially common in estrogen receptor-positive (ER+) breast cancer ( Han et al . 2016 , Zhang et al . 2013 ). While estrogen receptor-negative (ER−) cancer rarely
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stepwise model, influenced by the concepts of metastatic dormancy and cancer stem cells (CSC). Metastatic dormancy is defined as the ability of individual or small clusters of cancer cells to migrate to a distant site and then survive in a quiescent state
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. The process involves four stages: (1) migration/recruitment to the ovaries; (2) seeding and establishment in the ovaries; (3) induction of a dormant cancer stage; and (4) expansion and tumor progression. Stages 1 to 3 occur during the reproductive age
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metastatic breast cancer. Tumour cells arriving in bone undergo dormancy. Osteoclasts and osteoblasts secrete factors to maintain bone homeostasis (factors released by osteoblasts and osteoclasts are indicated in orange and purple, respectively). Bone
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subsequent invasion of organs in patients. The low proliferative activity or dormancy of individual DTC in BM of patients with non-metastatic cancer at the time of primary surgery ( Pantel et al. 1993 ), might explain the relative resistance of
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Department of Medicine (Oncology), Albert Einstein College of Medicine, Bronx, New York, USA
Montefiore-Einstein Comprehensive Cancer Research Center, Albert Einstein College of Medicine, Bronx, New York, USA
Cancer Dormancy Tumor Microenvironment Institute, Albert Einstein College of Medicine, Bronx, New York, USA
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Montefiore-Einstein Comprehensive Cancer Research Center, Albert Einstein College of Medicine, Bronx, New York, USA
Cancer Dormancy Tumor Microenvironment Institute, Albert Einstein College of Medicine, Bronx, New York, USA
Department of Medicine (Hepatology), Albert Einstein College of Medicine, Bronx, New York, USA
Marion Bessin Liver Research Center, Albert Einstein College of Medicine and Montefiore Medical Center, Bronx, New York, USA
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Introduction Anaplastic thyroid cancer (ATC) is a rare, undifferentiated, and highly aggressive form of thyroid cancer associated with a poor prognosis. Although its incidence is low (i.e. ~3% of all thyroid cancer cases), it accounts for
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Uro-Oncology Research, Surgery, Biomedical Sciences, Biostatistics and Bioinformatics Center, Department of Pathology, Department of Pathology, Department of Biochemistry and Cell Biology, Department of Medicine, Samuel Oschin Comprehensive Cancer Center, Cedars-Sinai Medical Center, 8750 Beverly Blvd., Atrium 103, Los Angeles, California 90048, USA Departments of
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Uro-Oncology Research, Surgery, Biomedical Sciences, Biostatistics and Bioinformatics Center, Department of Pathology, Department of Pathology, Department of Biochemistry and Cell Biology, Department of Medicine, Samuel Oschin Comprehensive Cancer Center, Cedars-Sinai Medical Center, 8750 Beverly Blvd., Atrium 103, Los Angeles, California 90048, USA Departments of
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Uro-Oncology Research, Surgery, Biomedical Sciences, Biostatistics and Bioinformatics Center, Department of Pathology, Department of Pathology, Department of Biochemistry and Cell Biology, Department of Medicine, Samuel Oschin Comprehensive Cancer Center, Cedars-Sinai Medical Center, 8750 Beverly Blvd., Atrium 103, Los Angeles, California 90048, USA Departments of
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Uro-Oncology Research, Surgery, Biomedical Sciences, Biostatistics and Bioinformatics Center, Department of Pathology, Department of Pathology, Department of Biochemistry and Cell Biology, Department of Medicine, Samuel Oschin Comprehensive Cancer Center, Cedars-Sinai Medical Center, 8750 Beverly Blvd., Atrium 103, Los Angeles, California 90048, USA Departments of
Uro-Oncology Research, Surgery, Biomedical Sciences, Biostatistics and Bioinformatics Center, Department of Pathology, Department of Pathology, Department of Biochemistry and Cell Biology, Department of Medicine, Samuel Oschin Comprehensive Cancer Center, Cedars-Sinai Medical Center, 8750 Beverly Blvd., Atrium 103, Los Angeles, California 90048, USA Departments of
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Uro-Oncology Research, Surgery, Biomedical Sciences, Biostatistics and Bioinformatics Center, Department of Pathology, Department of Pathology, Department of Biochemistry and Cell Biology, Department of Medicine, Samuel Oschin Comprehensive Cancer Center, Cedars-Sinai Medical Center, 8750 Beverly Blvd., Atrium 103, Los Angeles, California 90048, USA Departments of
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a new paradigm beyond the clonal expansion and evolution of cancer cells, where a population of metastasis-initiating PCa cells recruits and activates bystander cells, including ‘dormant’ cancer cells, through RANK-mediated signal amplification
Cancer Biology Laboratory, The Kinghorn Cancer Centre, Garvan Institute of Medical Research, Darlinghurst, New South Wales, Australia
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St. Vincent’s Clinical School, Faculty of Medicine, University of New South Wales Australia, Sydney, New South Wales, Australia
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St. Vincent’s Clinical School, Faculty of Medicine, University of New South Wales Australia, Sydney, New South Wales, Australia
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St. Vincent’s Clinical School, Faculty of Medicine, University of New South Wales Australia, Sydney, New South Wales, Australia
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Introduction In 1863 Rudolf Virchow, ‘the father of modern cellular pathology’, hypothesised a link between microinflammation and subsequent cancer development ( Balkwill & Mantovani 2001 ). The concept of harnessing the power of the immune
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The interaction between cell death and cell proliferation determines the growth dynamics of all tissues. Studies are described here which relate the changes in proliferation and apoptosis that occur in human breast cancer during medical therapeutic manoeuvres. Xenograft studies strongly support the involvement of increased apoptosis as well as decreased proliferation after oestrogen withdrawal, and limited studies in clinical samples confirm the involvement of both processes. Cytotoxic chemotherapy induces increases in apoptosis within 24 h of starting treatment. However, after 3 months therapy the residual cell population shows apoptotic and proliferation indices much below pretreatment levels. Further molecular studies of this "dormant" population are important to characterise the mechanism of their resistance to drug therapy. The early changes in proliferation and apoptosis may provide useful intermediate response indices.
Department of Epigenetics and Molecular Carcinogenesis, Cancer Stem Cell Institute, The University of Texas MD Anderson Cancer Center, Science Park, Park Road 1C, Smithville, Texas 78957, USA
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, estrogen may either promote or diminish BCSC activity. Nevertheless, anti-estrogen therapies seem to primarily target ER + breast cancer cells leading to enrichment of dormant ER − BCSCs, which could become ‘reactivated’ to mediate endocrine therapy