Jove
Visualize
お問い合わせ
JoVE
x logofacebook logolinkedin logoyoutube logo
JoVEについて
概要リーダーシップブログJoVEヘルプセンター
著者向け
出版プロセス編集委員会範囲と方針査読よくある質問投稿
図書館員向け
推薦の声購読アクセスリソース図書館諮問委員会よくある質問
研究
JoVE JournalMethods CollectionsJoVE Encyclopedia of Experimentsアーカイブ
教育
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab Manual教員リソースセンター教員サイト
利用規約
プライバシーポリシー
ポリシー

関連する概念動画

Adaptive Mechanisms in Cancer Cells02:53

Adaptive Mechanisms in Cancer Cells

5.7K
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.
Some of the advantages that cancer cells have on normal cells include - enhanced ability to divide without terminally differentiating, induce new blood vessel formation,...
5.7K
Targeted Cancer Therapies02:57

Targeted Cancer Therapies

7.6K
The targeted cancer therapies, also known as “molecular targeted therapies,” take advantage of the molecular and genetic differences between the cancer cells and the normal cells. It needs a thorough understanding of the cancer cells to develop drugs that can target specific molecular aspects that drive the growth, progression, and spread of cancer cells without affecting the growth and survival of other normal cells in the body.
There are several types of targeted therapies against...
7.6K
Treatment Resistant Cancers02:56

Treatment Resistant Cancers

3.3K
Cancer is the second leading cause of death in the United States. A cancer cell is genetically unstable and hence can mutate faster. They can also modify their microenvironment and escape immune surveillance. The difficulties in treating cancer are further compounded by the emergence of rapid resistance to anticancer drugs. The most common ways to attain resistance in cancer cells include alteration in drug transport and metabolism, modification of drug target, elevated DNA damage response, or...
3.3K
Abnormal Proliferation02:23

Abnormal Proliferation

4.5K
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...
4.5K
Cancer-Critical Genes II: Tumor Suppressor Genes01:05

Cancer-Critical Genes II: Tumor Suppressor Genes

7.4K
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.
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...
7.4K
Combination Therapies and Personalized Medicine02:50

Combination Therapies and Personalized Medicine

4.9K
Combining two or more treatment methods increases the life span of cancer patients while reducing damage to vital organs or tissue from the overuse of a single treatment. Combination therapy also targets different cancer-inducing pathways, thus reducing the chances of developing resistance to treatment.
The combination of the drug acetazolamide and sulforaphane is a good example of combination therapy to treat cancer. The cells in the interior of a large tumor often die due to the hypoxic and...
4.9K
このページは機械翻訳されています。他のページは英語で表示される場合があります。View in English
  1. ホーム
  3. 研究分野
  5. 生物医学と臨床科学
  7. 腫瘍学とがん発生
  9. 分子標的
  11. 糖分解性代謝物は,brca2による"二重ヒット"腫瘍抑制をバイパスする

糖分解性代謝物は,BRCA2による"二重ヒット"腫瘍抑制をバイパスする

Li Ren Kong1, Komal Gupta2, Andy Jialun Wu3

  • 1Cancer Science Institute of Singapore, Singapore 117599, Singapore; NUS Centre for Cancer Research (N2CR), National University of Singapore, Singapore 117599, Singapore; MRC Cancer Unit, University of Cambridge, Cambridge CB2 0XZ, UK; Department of Pharmacology, National University of Singapore, Singapore 117600, Singapore.

Cell
|April 12, 2024

関連する実験動画

Silencing of BRCA2 to Identify Novel BRCA2-regulated Biological Functions in Cultured Human Cells
09:24

Silencing of BRCA2 to Identify Novel BRCA2-regulated Biological Functions in Cultured Human Cells

Published on: August 12, 2015

9.1K
Evaluating the Effectiveness of Cancer Drug Sensitization In Vitro and In Vivo
09:19

Evaluating the Effectiveness of Cancer Drug Sensitization In Vitro and In Vivo

Published on: February 6, 2015

8.7K
Author Spotlight: Transmitochondrial Cybrid Generation Using Cancer Cell Lines
07:49

Author Spotlight: Transmitochondrial Cybrid Generation Using Cancer Cell Lines

Published on: March 17, 2023

2.4K

PubMed で要約を見る

まとめ
この要約は機械生成です。

メチルグリオキサル (MGO) は一時的にBRCA2を不活性化させ,2つのヒットがんモデルをバイパスします. この代謝メカニズムは,MGOと癌の発生における特定の変異シグネチャーを結びつける.

キーワード:
DNA 修復と複製乳がん遺伝子BRCA2ガンゲノム癌の代謝

関連する実験動画

Silencing of BRCA2 to Identify Novel BRCA2-regulated Biological Functions in Cultured Human Cells
09:24

Silencing of BRCA2 to Identify Novel BRCA2-regulated Biological Functions in Cultured Human Cells

Published on: August 12, 2015

9.1K
Evaluating the Effectiveness of Cancer Drug Sensitization In Vitro and In Vivo
09:19

Evaluating the Effectiveness of Cancer Drug Sensitization In Vitro and In Vivo

Published on: February 6, 2015

8.7K
Author Spotlight: Transmitochondrial Cybrid Generation Using Cancer Cell Lines
07:49

Author Spotlight: Transmitochondrial Cybrid Generation Using Cancer Cell Lines

Published on: March 17, 2023

2.4K

科学分野:

  • 生物化学
  • 遺伝学
  • 腫瘍学

背景:

  • Knudsonの"二重ヒット"パラダイムは,腫瘍抑制遺伝子の両方のコピーが不活性化されることが必要であると説明しています.
  • BRCA2はDNA修復に関与する重要な乳がん抑制タンパク質です.

研究 の 目的:

  • メチルグリオキサール (MGO) の癌発症における役割を"二重打撃"のパラダイムを超えて調査する.
  • MGOによるBRCA2の一時的な無活性化とその変異シグネチャーとの関連を調べる.

主な方法:

  • 非悪性乳腺細胞と患者からのオーガノイドの分析
  • クラス駆動型のマウンの臓がんとヒトの乳がんにおけるMGO蓄積とDNA損傷の調査.
  • BRCA2タンパク質分解と機能的ハプロイン不全の評価

主要な成果:

  • MGOはBRCA2を一時的に不活性化させ,バイアレル不活性化なしに単基置換 (SBS) シグネチャーを引き起こします.
  • ゲルムライン単型BRCA2変異は,MGO誘発SBSシグネチャーを誘発する.
  • 断続的なMGO被曝は,永久的なBRCA2損失なしにエピソード的な変異をもたらす.

結論:

  • MGO誘発のBRCA2ハプロイン欠乏症は,Knudsonの2回ヒット要求を回避する代謝メカニズムを提供します.
  • この経路は,代謝不調 (例えば,糖分解の活性化) を癌に関連した変異シグネチャーと結びつける.
  • 発見は,一時的な腫瘍抑制器の不活性化による代謝と癌の進化の間の新しい関連を示唆しています.
環境発がん
遺伝子と環境の相互作用
グリコリス
メチルグリオキサール
変異シグネチャー
腫瘍抑制