ArticleProceedings of the National Academy of Sciences of the United States of America1997
Loss of functional cell surface transforming growth factor beta (TGF-beta) type 1 receptor correlates with insensitivity to TGF-beta in chronic lymphocytic leukemia.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 98 citations in OpenAlex.
- Identification of CD105 (endoglin) as novel risk marker in CLL.Annals of hematology · 2022Article
- Transforming Growth Factor-Beta Orchestrates Tumour and Bystander Cells in B-Cell Non-Hodgkin Lymphoma.Cancers · 2022Review
- Wnt, Notch, and TGF-β Pathways Impinge on Hedgehog Signaling Complexity: An Open Window on Cancer.Frontiers in genetics · 2019Review
- Association between Altered Expression and Genetic Variations of Transforming Growth Factor β-Smad Pathway with Chronic Myeloid Leukemia.International journal of hematology-oncology and stem cell research · 2018Article
- Targeting TGF-β signaling in cancer.Expert opinion on therapeutic targets · 2013Review
- Cellular origin and pathophysiology of chronic lymphocytic leukemia.The Journal of experimental medicine · 2012Article
- TGF-β - an excellent servant but a bad master.Journal of translational medicine · 2012Review
- The TEL-AML1 leukemia fusion gene dysregulates the TGF-beta pathway in early B lineage progenitor cells.The Journal of clinical investigation · 2009Article
- Characterization of novel transforming growth factor-beta type I receptors found in malignant pleural effusion tumor cells.BMC molecular biology · 2007Article
- Growth regulation of simian and human AIDS-related non-Hodgkin's lymphoma cell lines by TGF-beta1 and IL-6.BMC cancer · 2007Article
- Review
- TGFbeta/BMP inhibits the bone marrow transformation capability of Hoxa9 by repressing its DNA-binding ability.The EMBO journal · 2006Article
- Beta3 integrin and Src facilitate transforming growth factor-beta mediated induction of epithelial-mesenchymal transition in mammary epithelial cells.Breast cancer research : BCR · 2006Article
- Role of tumor-derived transforming growth factor-beta1 (TGF-beta1) in site-dependent tumorigenicity of murine ascitic lymphosarcoma.Cancer immunology, immunotherapy : CII · 2005Article
- Deregulated TGF-beta signaling in leukemogenesis.Oncogene · 2005Review
- TGFBR1*6A is not associated with prostate cancer in men of European ancestry.Prostate cancer and prostatic diseases · 2005Article
- Circulating proangiogenic cytokines and angiogenesis inhibitor endostatin in untreated patients with chronic lymphocytic leukemia.Mediators of inflammation · 2003Article
- TGF-beta-mediated control of allergen-specific T-cell responses.Current allergy and asthma reports · 2002Review
- Targets of transcriptional regulation by transforming growth factor-beta: expression profile analysis using oligonucleotide arrays.Japanese journal of cancer research : Gann · 2001Article
- Disruption of TGF-beta growth inhibition by oncogenic ras is linked to p27Kip1 mislocalization.Oncogene · 2000Article
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Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
Abstract
Chronic lymphocytic leukemia (CLL) is the most common form of adult leukemia in Western countries, and there is significant variability in survival within CLL clinical stages. Earlier studies showed that CLL cells produce and are usually growth inhibited by transforming growth factor beta type 1 (TGF-beta1), suggesting a mechanism for the clinically indolent course of most CLL. Here we studied the mechanism by which CLL cells from about one-third of the patients are insensitive to TGF-beta1. Of the 13 patients studied, CLL cells isolated from the peripheral blood of 8 patients were sensitive to growth inhibition by TGF-beta1, as determined by incorporation of tritiated thymidine, whereas those from 5 patients were completely resistant to TGF-beta1. As judged by binding of radiolabeled TGF-beta1 followed by cross-linking and immunoprecipitation with anti-receptor antisera, CLL cells sensitive to TGF-beta1 exhibited normal cell surface expression of both types 1 and 2 TGF-beta receptors. In contrast, all CLL cells resistant to TGF-beta1 exhibited no detectable surface type I receptors able to bind TGF-beta1, but normal expression of type II receptors. Both TGF-beta1-sensitive and TGF-beta1-resistant CLL cells contained normal amounts of both type 1 and type 2 receptor mRNAs. Specific loss of type 1 receptor expression represents a new mechanism by which cells acquire resistance to TGF-beta1-mediated growth inhibition in the development and progression of human lymphoproliferative malignancies.
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