Tumor-growth protein plays a big role in pancreatic cancer

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In cancer research, discoveries often lead to new insights and potential therapies. Dr. Nancy Klauber-DeMore, initially a breast cancer researcher and surgeon, delved into the study of secreted frizzled-related protein 2 (SFRP2).

Her journey began in 2008 when she unveiled SFRP2’s involvement in tumor growth and angiogenesis—the formation of new blood vessels to nourish tumors.

Over time, she expanded her research to include osteosarcoma, a bone cancer that primarily affects children and young adults.

Her latest findings, published in Cancer Biomarkers, shed light on the abundance of SFRP2 in pancreatic cancer and its potential implications.

SFRP2 in Pancreatic Cancer

Dr. Klauber-DeMore’s research highlights that SFRP2 is notably prevalent in pancreatic cancer, with higher levels of this protein correlating with worse patient outcomes.

However, this concentration of SFRP2 within the tumor, while concerning for prognosis, also presents an opportunity for therapeutic intervention.

By targeting SFRP2, researchers may potentially impact various aspects of pancreatic cancer, including tumor fibrosis, angiogenesis, tumor cell destruction, and even immunotherapy. This makes SFRP2 a prospective biomarker and therapeutic target for pancreatic cancer.

The Challenge of Pancreatic Cancer

Pancreatic cancer poses significant challenges in terms of diagnosis and treatment. It is frequently detected at advanced stages when it has already spread beyond the pancreas.

Additionally, pancreatic tumors are surrounded by a dense connective tissue known as stroma, which hinders effective chemotherapy delivery and fosters tumor growth.

Pancreatic cancer currently ranks as the third leading cause of cancer-related deaths, with projections indicating it may become the second leading cause by 2030.

Exploring the Tumor Microenvironment

Efforts to combat pancreatic cancer by targeting the stroma have yielded mixed results. This underscores the need for a deeper understanding of how various elements within the tumor microenvironment interact and influence each other.

SFRP2, given its role in stroma production and its ability to suppress immune responses, holds promise as a multifaceted target for modifying the tumor microenvironment.

Discovery Process

Dr. Klauber-DeMore’s journey into pancreatic cancer research began by examining SFRP2 in the Cancer Genome Atlas—a comprehensive database of 33 different cancers characterized at the molecular level. Notably, pancreatic cancer exhibited the highest expression of SFRP2 among all cancers.

Subsequent investigations revealed that patients with elevated SFRP2 levels faced lower survival odds. Moreover, her team uncovered the connection between SFRP2 and KRAS, a gene significantly implicated in pancreatic cancer when mutated.

Silencing KRAS led to a notable reduction in SFRP2 expression, demonstrating that KRAS, a primary driver of pancreatic cancer, regulates SFRP2 expression.

Conclusion

Dr. Nancy Klauber-DeMore’s research has illuminated the pivotal role of SFRP2 in pancreatic cancer. While its presence is associated with poorer outcomes for patients, it also presents a promising target for therapeutic interventions.

The multifaceted effects of targeting SFRP2 within the complex tumor microenvironment open new avenues for advancing our understanding and treatment of pancreatic cancer.

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The research findings can be found in Cancer Biomarkers.

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