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Study shows that recessive dystrophic epidermolysis bullosa- squamous cell carcinoma (SCC) tumors harbor genetic alterations similar to those in UV-related SCCs. Mutations in NOTCH1/2/4 and TP53 and copy number alterations in MYC, together with the activation of the TGFbeta receptor signaling pathway, seem to play a major role in this malignancy.
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propose that under conditions of oxidative stress given by the internalization of oxLDL, macrophages employ the formation of the amphiphysin 2(Bin1)/c-Myc complex as a control mechanism to initially avoid the process of cell death
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DPT regulates CDK4, CDK6 and p21, through MEK-ERK-MYC signaling to repress papillary thyroid cancer proliferation.
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MYC protein interactome profiling reveals functionally distinct regions that cooperate to drive tumorigenesis.
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MTOR2/C-MYC/GFAT1 axis is responsible for the modulation on the crosstalk between glycolysis and glutaminolysis in glioblastoma cells.
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In cisplatin-resistant ovarian cancer cells c-Myc enhances the expression of EZH2 by directly suppressing miR-137 that targets EZH2 mRNA. Inhibition of c-Myc-miR-137-EZH2 pathway re-sensitizes resistant cells to cisplatin. Clinical studies further confirm the activated c-Myc-miR-137-EZH2 pathway in platinum drug-resistant or recurrent ovarian cancer patients.
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c-Myc transactivates miR-141 expression and that BRD7, a direct target of c-Myc, serves as a cofactor of c-Myc and forms a negative feedback loop with c-Myc in miR-141 transcription in NPC.
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Study demonstrates that the plasmacytoid dendritic cells (pDCs)-specific RUNX2 super-enhancer is hijacked to activate expression of MYC via t(6;8) in blastic plasmacytoid dendritic cell neoplasm (BPDCN) cells, and unveil the molecular mechanisms underlying the pathogenesis of BPDCN, which originates from a precursor of pDCs.
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PHF10 expression in cells of different lines is activated by the c-MYC oncogene. Since PHF10 stimulates cell proliferation, its c-MYC-dependent activation in cancer cells should lead to an increase in their proliferation rate.
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C-Myc transcriptionally enhances MTDH (metadherin) expression and subsequently activates Twist1 expression to induce EMT.
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Mitochondrial AKAP1 supports mTOR pathway and tumor growth.
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MYC protein is expressed in variable degrees among pediatric small round blue cell tumors (SRBCT), and expression of this protein can be upregulated/deregulated in many ways. Findings provide a baseline for MYC expression in pediatric SRBCT and suggest that there may be multiple mechanisms of MYC upregulation in these different neoplasms.
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Our study highlighted the high colorectal cancer risk of people carrying MYC rs6983267 G and KBTBD11 rs11777210 C alleles
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miR-105 promotes MYC-mediated metabolic reprogramming of breast cancer stromal cells, contributing to sustained tumour growth by conditioning the shared metabolic environment.
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The high expression of c-myc may promote the invasion and metastasis of cervical cancer, and the high expression of bcat1 may promote the proliferation, invasion and metastasis of cervical cancer, which may have a synergistic effect in the pathogenesis of cervical cancer.
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MYC activity underlies intrinsic resistance to ibrutinib in MCL. As a client protein of HSP90, MYC can be inhibited via PU-H71 to overcome primary ibrutinib resistance.
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RMRP functions as a miR-34a-5p sponge to promote cell proliferation and repress cell apoptosis through upregulation of c-Myc in MM
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Authors show that loss of the tumor suppressor p53 increased MYC mRNA levels even in the absence of estrogen stimulation. However, in cells with wild-type p53, SRC acted to overcome p53-mediated inhibition of estrogen-stimulated cell cycle entry and progression.
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Study reports a high-resolution crystal structure (2.35 A) of the major quadruplex formed in the NHE III1 region of the c-MYC promoter. The crystal structure is in general agreement with the solution NMR structure, however, key differences are observed in the position of nucleotides outside the G-quartet core.
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Findings suggested that KPNA2, a potential tumor oncogene, performs its function in part via regulating cellular metabolism through c-myc signaling axis. It would provide a possible explanation for Warburg effect and thus offer a new perspective to the roles of KPNA2 in gliomagenesis.
