Scientists untangle the biology of an 'undruggable' cancer gene
🇬🇧 English
One of the most elusive and tantalizing targets in cancer is so common that scientists have a nickname for it: Mc Gene. In 70 percent of cancers, this gene — whose proper name is MYC — is too active and fuels the aggressive growth, spread and survival of tumors. A study published in the journal Molecular Cell reveals details about the control circuit that triggers cells to churn out extra copies of MYC — offering a new and potentially more tractable target for drugs.
The new study examined the buildup of extra gene copies. Scientists at Fox Chase Cancer Center in Philadelphia focused on the molecular machinery that orchestrates which genes are active. They found that two switches can tweak MYC activity, causing extra copies to accumulate or not. One switch is an enzyme called KDM4C, which prompts the copying machinery to make duplicates of MYC. When an experimental drug blocked KDM4C in cells and in mice, the extra copies decreased. Another switch, SET D2, keeps MYC in check; shutting it off caused extra copies to accumulate.
"The idea for a very long time has been these extra copies of MYC observed in tumors were just a random result of chaos in cancer cells," said Laura Soucek, a molecular biologist at Vall d'Hebron Institute of Oncology. The new study shows that extra MYC is controlled by a specific molecular process. Dr. Soucek and other scientists cautioned that this was a laboratory study, far from suggesting an immediate therapeutic strategy for patients.
🇸🇦 العربية
العلماء يستهدفون جين السرطان MYC الذي لا يمكن استهدافه بالأدوية
One of the most elusive and tantalizing targets in cancer is so common that scientists have a nickname for it: Mc Gene. In 70 percent of cancers, this gene — whose proper name is MYC — is too active and fuels the aggressive growth, spread and survival of tumors. A study published in the journal Molecular Cell reveals details about the control circuit that triggers cells to churn out extra copies of MYC — offering a new and potentially more tractable target for drugs.
The new study examined the buildup of extra gene copies. Scientists at Fox Chase Cancer Center in Philadelphia focused on the molecular machinery that orchestrates which genes are active. They found that two switches can tweak MYC activity, causing extra copies to accumulate or not. One switch is an enzyme called KDM4C, which prompts the copying machinery to make duplicates of MYC. When an experimental drug blocked KDM4C in cells and in mice, the extra copies decreased. Another switch, SET D2, keeps MYC in check; shutting it off caused extra copies to accumulate.
"The idea for a very long time has been these extra copies of MYC observed in tumors were just a random result of chaos in cancer cells," said Laura Soucek, a molecular biologist at Vall d'Hebron Institute of Oncology. The new study shows that extra MYC is controlled by a specific molecular process. Dr. Soucek and other scientists cautioned that this was a laboratory study, far from suggesting an immediate therapeutic strategy for patients.
ما هو جين MYC ولماذا يسمى 'غير قابل للاستهداف بالأدوية'؟
MYC هو جين طبيعي يكون نشطًا بشكل مفرط في 70% من السرطانات، مما يغذي نمو الورم. يسمى 'غير قابل للاستهداف بالأدوية' لأنه يفتقر إلى جيوب لربط الأدوية، مما يجعل استهدافه مباشرة بالأدوية التقليدية صعبًا.
🇧🇩 বাংলা
বিজ্ঞানীরা অপ্রতিরোধ্য ক্যান্সার জিন MYC-কে লক্ষ্য করছেন
One of the most elusive and tantalizing targets in cancer is so common that scientists have a nickname for it: Mc Gene. In 70 percent of cancers, this gene — whose proper name is MYC — is too active and fuels the aggressive growth, spread and survival of tumors. A study published in the journal Molecular Cell reveals details about the control circuit that triggers cells to churn out extra copies of MYC — offering a new and potentially more tractable target for drugs.
The new study examined the buildup of extra gene copies. Scientists at Fox Chase Cancer Center in Philadelphia focused on the molecular machinery that orchestrates which genes are active. They found that two switches can tweak MYC activity, causing extra copies to accumulate or not. One switch is an enzyme called KDM4C, which prompts the copying machinery to make duplicates of MYC. When an experimental drug blocked KDM4C in cells and in mice, the extra copies decreased. Another switch, SET D2, keeps MYC in check; shutting it off caused extra copies to accumulate.
"The idea for a very long time has been these extra copies of MYC observed in tumors were just a random result of chaos in cancer cells," said Laura Soucek, a molecular biologist at Vall d'Hebron Institute of Oncology. The new study shows that extra MYC is controlled by a specific molecular process. Dr. Soucek and other scientists cautioned that this was a laboratory study, far from suggesting an immediate therapeutic strategy for patients.
MYC জিন কী এবং কেন একে 'অপ্রতিরোধ্য' বলা হয়?
MYC একটি সাধারণ জিন যা 70% ক্যান্সারে অতিসক্রিয় থাকে, টিউমার বৃদ্ধি ত্বরান্বিত করে। একে 'অপ্রতিরোধ্য' বলা হয় কারণ এতে ওষুধ বাঁধাইয়ের জন্য পকেটের অভাব রয়েছে, যা ঐতিহ্যগত ওষুধ দিয়ে সরাসরি লক্ষ্য করা কঠিন করে তোলে।
🇩🇪 Deutsch
Wissenschaftler zielen auf das nicht-medikamentöse Krebsgen MYC
One of the most elusive and tantalizing targets in cancer is so common that scientists have a nickname for it: Mc Gene. In 70 percent of cancers, this gene — whose proper name is MYC — is too active and fuels the aggressive growth, spread and survival of tumors. A study published in the journal Molecular Cell reveals details about the control circuit that triggers cells to churn out extra copies of MYC — offering a new and potentially more tractable target for drugs.
The new study examined the buildup of extra gene copies. Scientists at Fox Chase Cancer Center in Philadelphia focused on the molecular machinery that orchestrates which genes are active. They found that two switches can tweak MYC activity, causing extra copies to accumulate or not. One switch is an enzyme called KDM4C, which prompts the copying machinery to make duplicates of MYC. When an experimental drug blocked KDM4C in cells and in mice, the extra copies decreased. Another switch, SET D2, keeps MYC in check; shutting it off caused extra copies to accumulate.
"The idea for a very long time has been these extra copies of MYC observed in tumors were just a random result of chaos in cancer cells," said Laura Soucek, a molecular biologist at Vall d'Hebron Institute of Oncology. The new study shows that extra MYC is controlled by a specific molecular process. Dr. Soucek and other scientists cautioned that this was a laboratory study, far from suggesting an immediate therapeutic strategy for patients.
Was ist das MYC-Gen und warum wird es als 'nicht-medikamentös' bezeichnet?
MYC ist ein normales Gen, das in 70% der Krebserkrankungen überaktiv ist und das Tumorwachstum fördert. Es wird als 'nicht-medikamentös' bezeichnet, weil ihm Taschen für die Arzneimittelbindung fehlen, was eine direkte Bekämpfung mit herkömmlichen Medikamenten erschwert.
🇪🇸 Español
Científicos apuntan al gen cancerígeno no farmacable MYC
One of the most elusive and tantalizing targets in cancer is so common that scientists have a nickname for it: Mc Gene. In 70 percent of cancers, this gene — whose proper name is MYC — is too active and fuels the aggressive growth, spread and survival of tumors. A study published in the journal Molecular Cell reveals details about the control circuit that triggers cells to churn out extra copies of MYC — offering a new and potentially more tractable target for drugs.
The new study examined the buildup of extra gene copies. Scientists at Fox Chase Cancer Center in Philadelphia focused on the molecular machinery that orchestrates which genes are active. They found that two switches can tweak MYC activity, causing extra copies to accumulate or not. One switch is an enzyme called KDM4C, which prompts the copying machinery to make duplicates of MYC. When an experimental drug blocked KDM4C in cells and in mice, the extra copies decreased. Another switch, SET D2, keeps MYC in check; shutting it off caused extra copies to accumulate.
"The idea for a very long time has been these extra copies of MYC observed in tumors were just a random result of chaos in cancer cells," said Laura Soucek, a molecular biologist at Vall d'Hebron Institute of Oncology. The new study shows that extra MYC is controlled by a specific molecular process. Dr. Soucek and other scientists cautioned that this was a laboratory study, far from suggesting an immediate therapeutic strategy for patients.
¿Qué es el gen MYC y por qué se llama 'no farmacable'?
MYC es un gen normal que está hiperactivo en el 70% de los cánceres, impulsando el crecimiento tumoral. Se llama 'no farmacable' porque carece de bolsillos para la unión de fármacos, lo que dificulta atacarlo directamente con medicamentos tradicionales.
🇫🇷 Français
Les scientifiques ciblent le gène du cancer MYC, réputé non médicamentable
One of the most elusive and tantalizing targets in cancer is so common that scientists have a nickname for it: Mc Gene. In 70 percent of cancers, this gene — whose proper name is MYC — is too active and fuels the aggressive growth, spread and survival of tumors. A study published in the journal Molecular Cell reveals details about the control circuit that triggers cells to churn out extra copies of MYC — offering a new and potentially more tractable target for drugs.
The new study examined the buildup of extra gene copies. Scientists at Fox Chase Cancer Center in Philadelphia focused on the molecular machinery that orchestrates which genes are active. They found that two switches can tweak MYC activity, causing extra copies to accumulate or not. One switch is an enzyme called KDM4C, which prompts the copying machinery to make duplicates of MYC. When an experimental drug blocked KDM4C in cells and in mice, the extra copies decreased. Another switch, SET D2, keeps MYC in check; shutting it off caused extra copies to accumulate.
"The idea for a very long time has been these extra copies of MYC observed in tumors were just a random result of chaos in cancer cells," said Laura Soucek, a molecular biologist at Vall d'Hebron Institute of Oncology. The new study shows that extra MYC is controlled by a specific molecular process. Dr. Soucek and other scientists cautioned that this was a laboratory study, far from suggesting an immediate therapeutic strategy for patients.
Qu'est-ce que le gène MYC et pourquoi est-il appelé 'non médicamentable' ?
MYC est un gène normal hyperactif dans 70% des cancers, favorisant la croissance tumorale. Il est dit 'non médicamentable' car il manque de poches de liaison aux médicaments, ce qui le rend difficile à cibler directement avec les médicaments traditionnels.
🇮🇳 हिन्दी
वैज्ञानिकों ने अघुलनशील कैंसर जीन MYC को लक्षित किया
One of the most elusive and tantalizing targets in cancer is so common that scientists have a nickname for it: Mc Gene. In 70 percent of cancers, this gene — whose proper name is MYC — is too active and fuels the aggressive growth, spread and survival of tumors. A study published in the journal Molecular Cell reveals details about the control circuit that triggers cells to churn out extra copies of MYC — offering a new and potentially more tractable target for drugs.
The new study examined the buildup of extra gene copies. Scientists at Fox Chase Cancer Center in Philadelphia focused on the molecular machinery that orchestrates which genes are active. They found that two switches can tweak MYC activity, causing extra copies to accumulate or not. One switch is an enzyme called KDM4C, which prompts the copying machinery to make duplicates of MYC. When an experimental drug blocked KDM4C in cells and in mice, the extra copies decreased. Another switch, SET D2, keeps MYC in check; shutting it off caused extra copies to accumulate.
"The idea for a very long time has been these extra copies of MYC observed in tumors were just a random result of chaos in cancer cells," said Laura Soucek, a molecular biologist at Vall d'Hebron Institute of Oncology. The new study shows that extra MYC is controlled by a specific molecular process. Dr. Soucek and other scientists cautioned that this was a laboratory study, far from suggesting an immediate therapeutic strategy for patients.
MYC जीन क्या है और इसे 'अघुलनशील' क्यों कहा जाता है?
MYC एक सामान्य जीन है जो 70% कैंसर में अति सक्रिय होता है, ट्यूमर के विकास को बढ़ावा देता है। इसे 'अघुलनशील' कहा जाता है क्योंकि इसमें दवा बंधन के लिए पॉकेट की कमी होती है, जिससे पारंपरिक दवाओं से सीधे लक्षित करना मुश्किल हो जाता है।
🇮🇩 Bahasa Indonesia
Ilmuwan Menargetkan Gen Kanker MYC yang Tidak Dapat Diobati
One of the most elusive and tantalizing targets in cancer is so common that scientists have a nickname for it: Mc Gene. In 70 percent of cancers, this gene — whose proper name is MYC — is too active and fuels the aggressive growth, spread and survival of tumors. A study published in the journal Molecular Cell reveals details about the control circuit that triggers cells to churn out extra copies of MYC — offering a new and potentially more tractable target for drugs.
The new study examined the buildup of extra gene copies. Scientists at Fox Chase Cancer Center in Philadelphia focused on the molecular machinery that orchestrates which genes are active. They found that two switches can tweak MYC activity, causing extra copies to accumulate or not. One switch is an enzyme called KDM4C, which prompts the copying machinery to make duplicates of MYC. When an experimental drug blocked KDM4C in cells and in mice, the extra copies decreased. Another switch, SET D2, keeps MYC in check; shutting it off caused extra copies to accumulate.
"The idea for a very long time has been these extra copies of MYC observed in tumors were just a random result of chaos in cancer cells," said Laura Soucek, a molecular biologist at Vall d'Hebron Institute of Oncology. The new study shows that extra MYC is controlled by a specific molecular process. Dr. Soucek and other scientists cautioned that this was a laboratory study, far from suggesting an immediate therapeutic strategy for patients.
Apa itu gen MYC dan mengapa disebut 'tidak dapat diobati'?
MYC adalah gen normal yang terlalu aktif pada 70% kanker, mendorong pertumbuhan tumor. Disebut 'tidak dapat diobati' karena tidak memiliki kantong untuk pengikatan obat, sehingga sulit ditargetkan langsung dengan obat tradisional.
🇯🇵 日本語
科学者たちが「薬剤耐性」がん遺伝子MYCを標的に
One of the most elusive and tantalizing targets in cancer is so common that scientists have a nickname for it: Mc Gene. In 70 percent of cancers, this gene — whose proper name is MYC — is too active and fuels the aggressive growth, spread and survival of tumors. A study published in the journal Molecular Cell reveals details about the control circuit that triggers cells to churn out extra copies of MYC — offering a new and potentially more tractable target for drugs.
The new study examined the buildup of extra gene copies. Scientists at Fox Chase Cancer Center in Philadelphia focused on the molecular machinery that orchestrates which genes are active. They found that two switches can tweak MYC activity, causing extra copies to accumulate or not. One switch is an enzyme called KDM4C, which prompts the copying machinery to make duplicates of MYC. When an experimental drug blocked KDM4C in cells and in mice, the extra copies decreased. Another switch, SET D2, keeps MYC in check; shutting it off caused extra copies to accumulate.
"The idea for a very long time has been these extra copies of MYC observed in tumors were just a random result of chaos in cancer cells," said Laura Soucek, a molecular biologist at Vall d'Hebron Institute of Oncology. The new study shows that extra MYC is controlled by a specific molecular process. Dr. Soucek and other scientists cautioned that this was a laboratory study, far from suggesting an immediate therapeutic strategy for patients.
MYC遺伝子とは何ですか？なぜ「薬剤耐性」と呼ばれるのですか？
MYCは正常な遺伝子で、70%のがんで過剰に活性化し、腫瘍の増殖を促進します。薬剤結合のためのポケットがないため、従来の薬剤で直接標的にすることが難しく、「薬剤耐性」と呼ばれています。
🇧🇷 Português
Cientistas miram o gene do câncer MYC, considerado não medicável
One of the most elusive and tantalizing targets in cancer is so common that scientists have a nickname for it: Mc Gene. In 70 percent of cancers, this gene — whose proper name is MYC — is too active and fuels the aggressive growth, spread and survival of tumors. A study published in the journal Molecular Cell reveals details about the control circuit that triggers cells to churn out extra copies of MYC — offering a new and potentially more tractable target for drugs.
The new study examined the buildup of extra gene copies. Scientists at Fox Chase Cancer Center in Philadelphia focused on the molecular machinery that orchestrates which genes are active. They found that two switches can tweak MYC activity, causing extra copies to accumulate or not. One switch is an enzyme called KDM4C, which prompts the copying machinery to make duplicates of MYC. When an experimental drug blocked KDM4C in cells and in mice, the extra copies decreased. Another switch, SET D2, keeps MYC in check; shutting it off caused extra copies to accumulate.
"The idea for a very long time has been these extra copies of MYC observed in tumors were just a random result of chaos in cancer cells," said Laura Soucek, a molecular biologist at Vall d'Hebron Institute of Oncology. The new study shows that extra MYC is controlled by a specific molecular process. Dr. Soucek and other scientists cautioned that this was a laboratory study, far from suggesting an immediate therapeutic strategy for patients.
O que é o gene MYC e por que é chamado de 'não medicável'?
MYC é um gene normal que está hiperativo em 70% dos cânceres, impulsionando o crescimento tumoral. É chamado de 'não medicável' porque carece de bolsos para ligação de medicamentos, dificultando o ataque direto com drogas tradicionais.
🇷🇺 Русский
Ученые нацелились на неподдающийся лекарствам раковый ген MYC
One of the most elusive and tantalizing targets in cancer is so common that scientists have a nickname for it: Mc Gene. In 70 percent of cancers, this gene — whose proper name is MYC — is too active and fuels the aggressive growth, spread and survival of tumors. A study published in the journal Molecular Cell reveals details about the control circuit that triggers cells to churn out extra copies of MYC — offering a new and potentially more tractable target for drugs.
The new study examined the buildup of extra gene copies. Scientists at Fox Chase Cancer Center in Philadelphia focused on the molecular machinery that orchestrates which genes are active. They found that two switches can tweak MYC activity, causing extra copies to accumulate or not. One switch is an enzyme called KDM4C, which prompts the copying machinery to make duplicates of MYC. When an experimental drug blocked KDM4C in cells and in mice, the extra copies decreased. Another switch, SET D2, keeps MYC in check; shutting it off caused extra copies to accumulate.
"The idea for a very long time has been these extra copies of MYC observed in tumors were just a random result of chaos in cancer cells," said Laura Soucek, a molecular biologist at Vall d'Hebron Institute of Oncology. The new study shows that extra MYC is controlled by a specific molecular process. Dr. Soucek and other scientists cautioned that this was a laboratory study, far from suggesting an immediate therapeutic strategy for patients.
Что такое ген MYC и почему его называют 'неподдающимся лекарствам'?
MYC — это нормальный ген, который гиперактивен в 70% раковых заболеваний, стимулируя рост опухоли. Его называют 'неподдающимся лекарствам', потому что ему не хватает карманов для связывания лекарств, что затрудняет прямое воздействие традиционными препаратами.
🇨🇳 简体中文
科学家瞄准不可成药的癌症基因MYC
One of the most elusive and tantalizing targets in cancer is so common that scientists have a nickname for it: Mc Gene. In 70 percent of cancers, this gene — whose proper name is MYC — is too active and fuels the aggressive growth, spread and survival of tumors. A study published in the journal Molecular Cell reveals details about the control circuit that triggers cells to churn out extra copies of MYC — offering a new and potentially more tractable target for drugs.
The new study examined the buildup of extra gene copies. Scientists at Fox Chase Cancer Center in Philadelphia focused on the molecular machinery that orchestrates which genes are active. They found that two switches can tweak MYC activity, causing extra copies to accumulate or not. One switch is an enzyme called KDM4C, which prompts the copying machinery to make duplicates of MYC. When an experimental drug blocked KDM4C in cells and in mice, the extra copies decreased. Another switch, SET D2, keeps MYC in check; shutting it off caused extra copies to accumulate.
"The idea for a very long time has been these extra copies of MYC observed in tumors were just a random result of chaos in cancer cells," said Laura Soucek, a molecular biologist at Vall d'Hebron Institute of Oncology. The new study shows that extra MYC is controlled by a specific molecular process. Dr. Soucek and other scientists cautioned that this was a laboratory study, far from suggesting an immediate therapeutic strategy for patients.
什么是MYC基因，为什么它被称为“不可成药”？
MYC是一种正常基因，在70%的癌症中过度活跃，促进肿瘤生长。它被称为“不可成药”，因为它缺乏药物结合的口袋，使得传统药物难以直接靶向。