2011
DOI: 10.1186/1471-2164-12-549
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HMGA1 drives stem cell, inflammatory pathway, and cell cycle progression genes during lymphoid tumorigenesis

Abstract: BackgroundAlthough the high mobility group A1 (HMGA1) gene is widely overexpressed in diverse cancers and portends a poor prognosis in some tumors, the molecular mechanisms that mediate its role in transformation have remained elusive. HMGA1 functions as a potent oncogene in cultured cells and induces aggressive lymphoid tumors in transgenic mice. Because HMGA1 chromatin remodeling proteins regulate transcription, HMGA1 is thought to drive malignant transformation by modulating expression of specific genes. Ge… Show more

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Cited by 76 publications
(97 citation statements)
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References 76 publications
(116 reference statements)
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“…3 Emerging evidence suggests that master regulators, such as the high mobility group A1 (HMGA1) chromatin remodeling protein, orchestrates the assembly of Nuclear-factor kappa B (NF-kB) and transcription factor complexes to induce stem cell transcriptional networks and downstream signaling pathways that maintain CSCs. [3][4][5][6] Prior studies also suggest that Nuclear-factor kappa B (NF-kB) is hyperactive in MM and leukemic stem cells (Fig. 1).…”
Section: -2mentioning
confidence: 90%
“…3 Emerging evidence suggests that master regulators, such as the high mobility group A1 (HMGA1) chromatin remodeling protein, orchestrates the assembly of Nuclear-factor kappa B (NF-kB) and transcription factor complexes to induce stem cell transcriptional networks and downstream signaling pathways that maintain CSCs. [3][4][5][6] Prior studies also suggest that Nuclear-factor kappa B (NF-kB) is hyperactive in MM and leukemic stem cells (Fig. 1).…”
Section: -2mentioning
confidence: 90%
“…Gene expression profile analyses demonstrate that HMGA1 drives tumor progression and stem cell properties through transcriptional networks expressed in pluripotent stem cells and developing embryos. 18,[21][22][23] Recently, the metabolic profiles of primary CR tumors and adjacent, nonmalignant tissue have been examined using several techniques, including: magic angle spinning -nuclear magnetic resonance (MAS-NMR), gas chromatography -mass spectrometry (GC-MS), ultra-performance liquid chromatography -quadrupole time-of-flight mass spectrometry (UPLC-QToF-MS) and capillary electrophoresis -MS (CE-MS). [24][25][26][27][28][29][30][31][32][33][34] Other platforms used to investigate metabolomes from urine or serum of patients with CRC include GC-MS, UPLC-QToF-MS (MS/MS), Fourier transform ion-cyclotron-MS (FTICR-MS) and proton NMR ( 1 H-NMR).…”
Section: Introductionmentioning
confidence: 99%
“…This finding suggests that uterine tumors induced by HMGA1 in this model are dependent on MMP-2 for growth at the stage in which we measured tumor size, in contrast to the lymphoid tumors, which may depend on other HMGA1 pathways [10, 12, 21-22]. In primary human carcinosarcomas, we also found a positive correlation between HMGA1 and MMP -2, but only in a subset of these tumors.…”
Section: Discussionmentioning
confidence: 56%