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Cell Anaplastic Lymphoma - BioProject

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Last Updated: 15 September 2022

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STAT3 cooperates with the core transcriptional regulatory circuitry to drive MYC expression and oncogenesis in anaplastic large cell lymphoma [ChIP-seq]

Anaplastic large cell lymphoma is an acute, CD30+ T-cell lymphoma of infants and adults. In most ALCL tumors, fusion transcripts or mutations in the JAK-STAT pathway are present, but the mechanism underlying tumor formation are not fully understood. The proto-oncogene MYC, which necessitates active STAT3 to promote high amounts of MYC transcription, is one of the network's critical downstream targets of this network in ALCL cells. MYC binding to the enhancer regions associated with STAT3 and each of the key regulatory transcription factors is further strengthened by the existence of this auto-regulatory transcription loop.

Source link: https://www.ncbi.nlm.nih.gov/bioproject/873776


STAT3 cooperates with the core transcriptional regulatory circuitry to drive MYC expression and oncogenesis in anaplastic large cell lymphoma [RNA-seq]

Anaplastic large cell lymphoma is a rare, CD30+ T-cell lymphoma of children and adults. In most ALCL tumors, fusion transcripts or mutations in the JAK-STAT pathway are present, but tumor-related tumor formation are not fully understood. The proto-oncogene MYC, which requires active STAT3 to promote high rates of MYC transcription, is one of this network's critical downstream targets of this network in ALCL cells. MYC binding to the enhancer regions associated with STAT3 and each of the main regulatory transcription factors is complemented by MYC's participation in this auto-regulatory transcription loop.

Source link: https://www.ncbi.nlm.nih.gov/bioproject/873775


STAT3 cooperates with the core transcriptional regulatory circuitry to drive MYC expression and oncogenesis in anaplastic large cell lymphoma [CUT&RUN-seq]

An Anaplastic large cell lymphoma is a deadly, CD30+ T-cell lymphoma of children and adults. In most ALCL tumors, fusion transcripts or mutations in the JAK-STAT pathway are present, but the mechanisms underlying tumor formation are not fully understood. The proto-oncogene MYC, which necessitates active STAT3 to promote high amounts of MYC transcription, is one of the network's ALCL cell's key downstream targets of this network in ALCL cells. MYC binding to the enhancer regions associated with STAT3 and each of the main regulatory transcription factors are confirmed by MYC binding to the main transcription factors. In ALCL cell lines, the overall layout: CUT&RUN-sequencing against transcription regulators is the CUT&RUN-sequencing against transcription regulators.

Source link: https://www.ncbi.nlm.nih.gov/bioproject/873774

* Please keep in mind that all text is summarized by machine, we do not bear any responsibility, and you should always check original source before taking any actions

* Please keep in mind that all text is summarized by machine, we do not bear any responsibility, and you should always check original source before taking any actions