A study has found that pp32, a tumour-blocking protein in prostate and breast cancer development, may play a vital role in the growth of pancreatic cancer.
Researchers at the Kimmel Cancer Centre at Jefferson in Philadelphia have claimed that pp32 could be the key factor behind the most aggressive type of pancreatic cancer.
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The scientists revealed that in experimental models without the protein, mutations in the cancer-causing gene K-ras took over, turning cells cancerous.
Adding pp32 to pancreatic cancer cells that have K-ras mutations and lack the protein, could slow the growth of these fast-growing cells, leading the scientists to contemplate that losing pp32 might be a critical event in determining how aggressively a pancreatic cancer behaves.
According to lead reseracher Jonathan Brody, Ph.D., assistant professor of Surgery, earlierlaboratory and animal studies have shown that pp32 inhibits K-ras-activating gene mutations found in more than 90 percent of all pancreatic cancers and in some early pre-cancerous lesions as well.
However, in a subset of fast-moving, "poorly differentiated" pancreatic cancers, the researchers found that "pp32 is either reduced or lost."
"Losing the protein in pre-cancerous lesions could be a marker for an aggressive form of pancreatic cancer," Prof Brody said.
"Connecting a protein that can inhibit a critical mutation found in almost every pancreatic cancer to the pathology is powerful information. These types of studies can help us understand more about the early development of pancreatic cancer on a molecular level," he added.
Although the study is at its initial stages, the researchers say the absent protein could become a marker for the disease and a potential drug target.
The study is published in the journal Modern Pathology.
Source: ANI
LIN/C
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According to lead reseracher Jonathan Brody, Ph.D., assistant professor of Surgery, earlierlaboratory and animal studies have shown that pp32 inhibits K-ras-activating gene mutations found in more than 90 percent of all pancreatic cancers and in some early pre-cancerous lesions as well.
However, in a subset of fast-moving, "poorly differentiated" pancreatic cancers, the researchers found that "pp32 is either reduced or lost."
"Losing the protein in pre-cancerous lesions could be a marker for an aggressive form of pancreatic cancer," Prof Brody said.
"Connecting a protein that can inhibit a critical mutation found in almost every pancreatic cancer to the pathology is powerful information. These types of studies can help us understand more about the early development of pancreatic cancer on a molecular level," he added.
Although the study is at its initial stages, the researchers say the absent protein could become a marker for the disease and a potential drug target.
The study is published in the journal Modern Pathology.
Source: ANI
LIN/C
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