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Cancer-Critical Genes I: Proto-oncogenes01:33

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Genes usually encode proteins necessary for the proper functioning of a healthy cell. Mutations can often cause changes to the gene expression pattern, thereby altering the phenotype.
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Stem cells are undifferentiated cells that divide and produce different cell types. Ordinarily, cells that have differentiated into a specific cell type are terminally differentiated; however, scientists have found a way to reprogram these mature cells so that they dedifferentiate and return to an unspecialized, proliferative state. These cells are pluripotent like embryonic stem cells—able to produce all cell types—and are called induced pluripotent stem cells (iPSCs).
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When a ligand binds to a cell-surface receptor, the receptor's intracellular domain changes shape, which may either activate its enzyme function or allow its binding to other molecules. The initial signal is amplified by most signal transduction pathways. This means that a single ligand molecule can activate multiple molecules of a downstream target. Proteins that relay a signal are most commonly phosphorylated at one or more sites, activating or inactivating the protein. Kinases catalyze...
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Mitogens and their receptors play a crucial role in controlling the progression of the cell cycle. However, the loss of mitogenic control over cell division leads to tumor formation. Therefore, mitogens and mitogen receptors play an important role in cancer research. For instance, the epidermal growth factor (EGF) - a type of mitogen and its transmembrane receptor (EGFR), decides the fate of the cell's proliferation. When EGF binds to EGFR, a member of the ErbB family of tyrosine kinase...
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The Ras-gene-encoded proteins are regulators of signaling pathways controlling cell proliferation, differentiation, or cell survival. The Ras-gene family in humans constitutes three primary members—the HRas, NRas, and KRas. These genes code for four functionally distinct yet closely related proteins—the HRas, NRas, KRas4A, and KRas4B. The involvement of mutant Ras genes in human cancer was first discovered in 1982 and is among the most common causes of human tumorigenesis.
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Epigenetic changes alter the physical structure of the DNA without changing the genetic sequence and often regulate whether genes are turned on or off. This regulation ensures that each cell produces only proteins necessary for its function. For example, proteins that promote bone growth are not produced in muscle cells. Epigenetic mechanisms play an essential role in healthy development. Conversely, precisely regulated epigenetic mechanisms are disrupted in diseases like cancer.
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Mapping the Structure-Function Relationships of Disordered Oncogenic Transcription Factors Using Transcriptomic Analysis
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機能強化剤 形状 染色体外腫瘍遺伝子の増幅

Andrew R Morton1, Nergiz Dogan-Artun2, Zachary J Faber1

  • 1Department of Genetics and Genome Sciences, Case Western Reserve University School of Medicine, Case Comprehensive Cancer Center, Cleveland, OH 44106, USA.

Cell
|November 26, 2019
PubMed
まとめ

ガン遺伝子の増幅はしばしば,非コーディングDNA,特にEGFRのような腫瘍遺伝子の近くの増強剤を含みます. 細胞の健康に不可欠なこれらの領域は,グリオブラストーマの染色体外DNAで維持されます.

キーワード:
EGFRMYC についてMYCN についてダブル・ミニット強化剤エピジェネティック染色体外DNAグリオブラストーマ腫瘍遺伝子の増幅

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科学分野:

  • ゲノミクス
  • 癌 生物学
  • エピジェネティクス

背景:

  • 増幅された腫瘍遺伝子の隣接する非コーディングDNA領域はしばしば見過ごされます.
  • 癌の進行におけるこれらの非コーディング要素の役割を理解することは極めて重要です.

研究 の 目的:

  • 様々な癌のタイプにおける腫瘍遺伝子の非コーディングDNAの共増幅パターンを調査する.
  • グリオブラストーマにおける共同増強された非コーディングの規制要素,特に増強剤の機能的重要性を調査する.

主な方法:

  • 非コーディングDNAの共増幅シグネチャーを特定するための計算分析.
  • CRISPRの干渉スクリーニングは,細胞の適性に対する規制要素の影響を評価します.
  • 染色体トポロジと染色体外DNA増幅の分析

主要な成果:

  • 腫瘍遺伝子の境界を越えた非コーディングDNAの有意な共増幅が5つの癌タイプで観察されました.
  • グリオブラストーマでは,EGFRが細胞型特異の増強剤と共増強され,それらは染色体外DNAに保存された.
  • CRISPRスクリーニングでは,細胞の適性,ミラーリング再配置,およびアンプリカンのクロマチンの再配線に影響を与える様々な要素が特定されました.

結論:

  • 腫瘍遺伝子の増幅は,非コーディングゲノム内の規制依存関係によって影響を受けます.
  • 増強剤を含む共増強された非コーディング要素は,がん細胞の適性において重要な役割を果たします.
  • エクストラクロモソーム増幅は,これらの調節要素とそれに関連するクロマチンのトポロジーの機能的整合性を維持します.