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CERI strongly stands behind the importance of cancer patient empowerment and is a worldwide leading source for simplified, multi-language cancer education. Knowledge is power and empowerment is the key for greater treatment success, early diagnosis, as well as cancer prevention.
For any questions or requests, please submit your inquiry at our CERI Personalized Patient Program™ page.
New Research - Pancreatic Cancer
Aygün Sahin, MSc, PhD | CEO, President, and Cancer Lead, Cancer Education and Research Institute (CERI)
CD9 identifies pancreatic cancer stem cells and modulates glutamine metabolism to fuel tumor growth
New Research: CD9 Identifies Pancreatic Cancer Stem Cells and Modulates Glutamine Metabolism to Fuel Tumor Growth.
This groundbreaking study uncovers the role of the CD9 protein on the cell surface in pancreatic cancer and how it affects tumor growth.
Pancreatic cancer is a devastating disease with limited treatment options. Pancreatic ductal adenocarcinoma (PDAC) is the fourth most common cause of cancer-related deaths in the US. Although the tumors are often non-resectable, even with resectable tumors, a five-year survival rate is only 30%.
Cancer cell heterogeneity (meaning, cancer cells within a tumor showing distinct morphological and phenotypic profiles, which include cellular morphology, gene expression, metabolism, motility, proliferation, and metastatic potential) is believed to be one of the main causes of tumor aggressiveness and resistance to therapy; therefore, understanding the sources of intratumoral Pancreatic ductal adenocarcinoma (PDAC) diversity was a key aim in this study.
This article reveals that the CD9 protein is not just a passive tumor marker, but actively promotes pancreatic cancer stem cells to form tumors.
Let’s explain some background information:
What is the CD9 protein?
CD9 is a cell-surface protein and a member of the tetraspanin family which is found in several tissues. It modifies multiple cellular events, including adhesion, migration, proliferation, and survival.
CD9 and cancer:
CD9 has been described as a cancer stem cell marker in several types of cancers, including glioblastoma, B-acute lymphoblastic leukemia (ALL), and AML (Acute Myeloblastic Leukemia), and it actively promotes the growth of AML.
What are cancer stem cells?
Cancer stem cells are a small subset of cells within a tumor that have the ability to self-renew and give rise to new cancer cells. They are often resistant to traditional cancer treatments and contribute to tumor growth and progression.
The researchers discovered that CD9 is highly expressed in pancreatic cancer stem cells, making it a promising biomarker for their identification. This finding has significant implications for developing targeted therapies specifically aimed at eradicating these stem cells, which could potentially lead to more effective treatments for pancreatic cancer.
Additionally, the study uncovered an intriguing connection between CD9 and glutamine metabolism. Glutamine is an essential nutrient that cancer cells utilize to fuel their growth. The researchers found that CD9 influences glutamine metabolism in pancreatic cancer cells, promoting their ability to acquire and utilize glutamine for energy and proliferation.
This newly identified role of CD9 in modulating glutamine metabolism suggests that targeting CD9 could disrupt the metabolic processes that support tumor growth. By inhibiting CD9 or blocking glutamine utilization, it may be possible to impede the growth and survival of pancreatic cancer cells.
These findings open up exciting possibilities for the development of novel therapies and personalized treatment approaches for pancreatic cancer. By understanding the mechanisms that drive tumor growth, researchers can now explore innovative strategies to target cancer stem cells and disrupt their metabolic dependencies.
In conclusion, the article 'CD9 Identifies Pancreatic Cancer Stem Cells and Modulates Glutamine Metabolism to Fuel Tumor Growth' sheds light on the role of CD9 in pancreatic cancer and its potential as a biomarker and therapeutic target. This research provides valuable insights into the complex biology of pancreatic cancer and paves the way for the development of more effective treatments in the future.
We hope you found this information both fascinating and helpful. If you did, please share this page with others and subscribe to our free e-newsletter more exciting content about cancer. Our goal is to empower you with ACCURATE knowledge about cancer. So, thanks for being here!
This groundbreaking study uncovers the role of the CD9 protein on the cell surface in pancreatic cancer and how it affects tumor growth.
Pancreatic cancer is a devastating disease with limited treatment options. Pancreatic ductal adenocarcinoma (PDAC) is the fourth most common cause of cancer-related deaths in the US. Although the tumors are often non-resectable, even with resectable tumors, a five-year survival rate is only 30%.
Cancer cell heterogeneity (meaning, cancer cells within a tumor showing distinct morphological and phenotypic profiles, which include cellular morphology, gene expression, metabolism, motility, proliferation, and metastatic potential) is believed to be one of the main causes of tumor aggressiveness and resistance to therapy; therefore, understanding the sources of intratumoral Pancreatic ductal adenocarcinoma (PDAC) diversity was a key aim in this study.
This article reveals that the CD9 protein is not just a passive tumor marker, but actively promotes pancreatic cancer stem cells to form tumors.
Let’s explain some background information:
What is the CD9 protein?
CD9 is a cell-surface protein and a member of the tetraspanin family which is found in several tissues. It modifies multiple cellular events, including adhesion, migration, proliferation, and survival.
CD9 and cancer:
CD9 has been described as a cancer stem cell marker in several types of cancers, including glioblastoma, B-acute lymphoblastic leukemia (ALL), and AML (Acute Myeloblastic Leukemia), and it actively promotes the growth of AML.
What are cancer stem cells?
Cancer stem cells are a small subset of cells within a tumor that have the ability to self-renew and give rise to new cancer cells. They are often resistant to traditional cancer treatments and contribute to tumor growth and progression.
The researchers discovered that CD9 is highly expressed in pancreatic cancer stem cells, making it a promising biomarker for their identification. This finding has significant implications for developing targeted therapies specifically aimed at eradicating these stem cells, which could potentially lead to more effective treatments for pancreatic cancer.
Additionally, the study uncovered an intriguing connection between CD9 and glutamine metabolism. Glutamine is an essential nutrient that cancer cells utilize to fuel their growth. The researchers found that CD9 influences glutamine metabolism in pancreatic cancer cells, promoting their ability to acquire and utilize glutamine for energy and proliferation.
This newly identified role of CD9 in modulating glutamine metabolism suggests that targeting CD9 could disrupt the metabolic processes that support tumor growth. By inhibiting CD9 or blocking glutamine utilization, it may be possible to impede the growth and survival of pancreatic cancer cells.
These findings open up exciting possibilities for the development of novel therapies and personalized treatment approaches for pancreatic cancer. By understanding the mechanisms that drive tumor growth, researchers can now explore innovative strategies to target cancer stem cells and disrupt their metabolic dependencies.
In conclusion, the article 'CD9 Identifies Pancreatic Cancer Stem Cells and Modulates Glutamine Metabolism to Fuel Tumor Growth' sheds light on the role of CD9 in pancreatic cancer and its potential as a biomarker and therapeutic target. This research provides valuable insights into the complex biology of pancreatic cancer and paves the way for the development of more effective treatments in the future.
We hope you found this information both fascinating and helpful. If you did, please share this page with others and subscribe to our free e-newsletter more exciting content about cancer. Our goal is to empower you with ACCURATE knowledge about cancer. So, thanks for being here!
References:
- CD9 identifies pancreatic cancer stem cells and modulates glutamine metabolism to fuel tumour growth. Nat Cell Biol. 2019 Nov;21(11):1425-1435. https://pubmed.ncbi.nlm.nih.gov/31685994/
- CD9, a potential leukemia stem cell marker, regulates drug resistance and leukemia development in acute myeloid leukemia. Stem Cell Research & Therapy volume 12, Article number: 86 (2021) https://stemcellres.biomedcentral.com/articles/10.1186/s13287-021-02155-6
- CD9. Science Direct. 2012. https://www.sciencedirect.com/topics/neuroscience/cd9
Gene identified necessary for pancreatic cancer development
Researchers from New York University and University of Michigan have identified a gene called Atdc (ataxia-telangiectasiagroup D-complementing) that is necessary for pancreatic cancer development.
Pancreatic ductaladenocarcinoma (PDA) is an aggressive form of pancreatic cancer that is driven by the oncogenic (cancer causing) KRAS. It is diagnosed in late stages and is resistant to therapy.
“We thought the deletion [of the Atdc gene] would slow cancer growth, not completely prevent it,” said Diane Simeone, director of the Pancreatic Cancer Center of NYU LangoneHealth’s PerlmutterCancer Center, and corresponding author of the study
The researchers have shown that deletion of the ataxia-telangiectasia group D-complementing (Atdc) gene, which is up-regulated (found in multiple copies) in the majority of pancreatic adenocarcinoma, completely prevented PDA development in the context of oncogenic KRAS. When the Atdc gene was present, 100% of the mice with KRAS and other mutations (gene abnormalities) developed PDA. Mice lacking ATDC are protected from developing PDA.
As for the mechanism, the researchers showed that ATDC promotes acinar–ductal metaplasia (ADM) to pancreatic intraepithelial neoplasia (PanIN) through the activation of β-catenin signaling and subsequent SOX9 up-regulation (over expression).
This breakthrough study revealed great hope for the development of potential new therapies for pancreatic cancer.
The study has been published today, May 2, 2019 in the scientific journal Genes & Development.
Corresponding author of this study is Dr. Diane Simeone: [email protected]
Pancreatic ductaladenocarcinoma (PDA) is an aggressive form of pancreatic cancer that is driven by the oncogenic (cancer causing) KRAS. It is diagnosed in late stages and is resistant to therapy.
“We thought the deletion [of the Atdc gene] would slow cancer growth, not completely prevent it,” said Diane Simeone, director of the Pancreatic Cancer Center of NYU LangoneHealth’s PerlmutterCancer Center, and corresponding author of the study
The researchers have shown that deletion of the ataxia-telangiectasia group D-complementing (Atdc) gene, which is up-regulated (found in multiple copies) in the majority of pancreatic adenocarcinoma, completely prevented PDA development in the context of oncogenic KRAS. When the Atdc gene was present, 100% of the mice with KRAS and other mutations (gene abnormalities) developed PDA. Mice lacking ATDC are protected from developing PDA.
As for the mechanism, the researchers showed that ATDC promotes acinar–ductal metaplasia (ADM) to pancreatic intraepithelial neoplasia (PanIN) through the activation of β-catenin signaling and subsequent SOX9 up-regulation (over expression).
This breakthrough study revealed great hope for the development of potential new therapies for pancreatic cancer.
The study has been published today, May 2, 2019 in the scientific journal Genes & Development.
Corresponding author of this study is Dr. Diane Simeone: [email protected]
#breakingnews #breakthrough #science #sciencenews #cancerresearch #pancreaticcancer #cancer #cancerresearch #genes #hope #pancreaticcancerawareness
Link between INFLAMMATION and PANCREATIC CANCER development uncovered
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References:
- Nassiri, F., Patil, V., Yefet, L.S. et al. Oncolytic DNX-2401 virotherapy plus pembrolizumab in recurrent glioblastoma: a phase 1/2 trial. Nat Med (2023). https://www.nature.com/articles/s41591-023-02347-y (accessed May 16, 2023)
- Scientists find new way to treat deadly brain cancer effectively. Knowrigde. https://knowridge.com/2023/05/scientists-find-new-way-to-treat-deadly-brain-cancer-effectively (accessed May 16, 2023)
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