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関連する概念動画

The Tumor Microenvironment02:17

The Tumor Microenvironment

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Every normal cell or tissue is embedded in a complex local environment called stroma, consisting of different cell types, a basal membrane, and blood vessels. As normal cells mutate and develop into cancer cells, their local environment also changes to allow cancer progression. The tumor microenvironment (TME) consists of a complex cellular matrix of stromal cells and the developing tumor. The cross-talk between cancer cells and surrounding stromal cells is critical to disrupt normal tissue...
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Adaptive Mechanisms in Cancer Cells02:53

Adaptive Mechanisms in Cancer Cells

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Cancer cells accumulate genetic changes at an abnormally rapid rate due to the defects in the DNA repair mechanisms. From an evolutionary perspective, such genetic instability is advantageous for cancer development. Mutant cell lines accumulate a series of beneficial mutations that contribute to their progression into cancer.
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Abnormal Proliferation02:23

Abnormal Proliferation

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Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the...
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mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

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The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
The mTOR pathway or the...
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Cancer Stem Cells and Tumor Maintenance02:40

Cancer Stem Cells and Tumor Maintenance

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Early diagnosis and treatment can often cure cancer. However, even with treatment, residual cells called cancer stem cells (CSC) might remain, often causing tumor recurrence. These cancer stem cells possess the potential for self-renewal and multi-lineage differentiation and are often responsible for the therapeutic resistance displayed in most cancers.
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Cancer02:18

Cancer

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Cancers arise due to mutations in genes involved in the regulation of cell division, which leads to unrestricted cell proliferation. Modern science and medicine have made great strides in the understanding and treatment of cancer, including eradicating cancer in some patients. However, there is still no cure for cancer. This is largely due to the fact that cancer is a large group of many diseases.
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Utilizing Functional Genomics Screening to Identify Potentially Novel Drug Targets in Cancer Cell Spheroid Cultures
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腫瘍の微小環境における細胞プログラムされた栄養分離

Bradley I Reinfeld1,2,3, Matthew Z Madden1,4, Melissa M Wolf2,3

  • 1Medical Scientist Training Program, Vanderbilt University, Nashville, TN, USA.

Nature
|April 8, 2021
PubMed
まとめ
この要約は機械生成です。

免疫細胞と癌細胞は,好ましくは腫瘍の微小環境 (TME) で異なる栄養素を消費する. mTORC1のシグナル伝達によって引き起こされるこの細胞内部の栄養分断は,がん免疫に影響を与え,治療の標的となる可能性があります.

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A Mimic of the Tumor Microenvironment: A Simple Method for Generating Enriched Cell Populations and Investigating Intercellular Communication
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Enrichment and Characterization of the Tumor Immune and Non-immune Microenvironments in Established Subcutaneous Murine Tumors
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A Mimic of the Tumor Microenvironment: A Simple Method for Generating Enriched Cell Populations and Investigating Intercellular Communication
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Enrichment and Characterization of the Tumor Immune and Non-immune Microenvironments in Established Subcutaneous Murine Tumors
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科学分野:

  • 癌 生物学
  • 免疫学
  • メタボリズム

背景:

  • ガン細胞はワーバーグ代謝を通じてグルコースを利用し,ポジトロン放出トモグラフィー (PET) 画像の基礎を形成する.
  • 腫瘍に浸透する免疫細胞もグルコースに依存し,腫瘍の微小環境 (TME) でその代謝の障害は免疫逃避につながる可能性があります.
  • TMEにおける免疫細胞の代謝失調は,内在的なプログラムによるものなのか,それとも癌細胞との栄養競争によるものなのかは不明である.

研究 の 目的:

  • TME内の特定の細胞サブセットによるグルコースとグルタミンの異なる吸収と分割を調査する.
  • 細胞内部のプログラムや 栄養素の利用が 代謝の異常を誘発するかどうかを判断する
  • TMEにおける細胞選択的栄養素獲得を標的とした治療とイメージングの可能性を調査する.

主な方法:

  • TME内の特定の細胞集団におけるグルコースとグルタミン吸収を定量化するために,ポジトロン放出トモグラフィ (PET) トレーサーを使用した.
  • 骨髄細胞,T細胞,がん細胞を含む様々ながんモデルにおける栄養分離を分析した.
  • 細胞内栄養代謝におけるラパミシン複合体1 (mTORC1) 信号伝達と遺伝子発現のメカニズム的標的の役割を調査した.

主要な成果:

  • ミエロイド細胞はTMEで最も高いグルコース吸収を示し,次にT細胞,そしてがん細胞が続いた.
  • がん細胞は免疫細胞に比べて グルタミン摂取量が最も高いことが示されました
  • mTORC1のシグナリングによって調節される細胞内部のプログラムは,それぞれ免疫細胞と癌細胞によるグルコースとグルタミンの大量摂取を制御する.
  • グルタミン摂取の抑制は,グルコース摂取の増加を示し,グルタミン代謝は,グルコース制限とは無関係にグルコース利用を抑制する.

結論:

  • TME内の免疫細胞と癌細胞の間の 異なるグルコースとグルタミン分断を 細胞内プログラムが指示します
  • この選択的な栄養摂取は 免疫細胞の機能と癌の進行に影響します
  • これらの細胞選択的代謝経路をターゲットにすることで 新しいがん治療法や 先進的なイメージング戦略の可能性が生まれます