Case: Growth on pancreas shows estrogen link to pancreatic cancer
Treatments to block changes in estrogen signaling may help some patients
Changes in how cells respond to the hormone estrogen may underlie the development of certain forms of pancreatic cancer.
That’s according to findings from testing done on a growth removed from the pancreas of a woman in Japan who had given birth several months before. While analyses showed the abnormal growth — identified as a mucinous cystic neoplasm, or MCN — had telltale signs of cancer, the woman six months later showed no signs of recurrence or additional health issues.
Meanwhile, the testing revealed hallmarks of MCN that had turned cancerous. Specifically, in some areas, the cells looked relatively healthy, but in other parts, there was a lot of dysplasia or abnormal cell growth that’s a sign of cancer. In areas with extensive dysplasia, the cells showed high amounts of the estrogen receptor protein.
As such, these findings suggest that therapies aimed at blocking estrogen signaling, or how cells respond to estrogen, may be beneficial for treating some pancreatic cancers, according to the researchers.
Their study, “Progressive Estrogen Receptor Acquisition During Malignant Transformation: Insights From MCN-Derived Anaplastic Pancreatic Carcinoma,” was published in the journal Pathology International.
Mucinous cystic neoplasm, or MCN for short, is a type of abnormal growth that can sometimes form on the pancreas. It’s most common in middle-aged women. MCN itself is considered benign, but in some people, the growth progresses to form a type of pancreatic cancer called anaplastic pancreatic carcinoma.
Findings from case involving pregnant woman hold cancer clues
It’s not clear why MCN turns into cancer in some individuals but not others, but researchers think the findings of this new research may hold a clue.
In their study, a team from Toranomon Hospital in Tokyo reported the case of a 34-year-old woman who sought medical attention due to persistent abdominal pain that had lasted several months after giving birth. Imaging of the woman’s abdomen revealed a growth on her pancreas that looked very much like a tumor.
After the growth was discovered, the woman underwent surgery to remove it. The surgery itself was completed without any complications, and six months later, the woman was reported to be in good health.
Once the growth was removed, researchers took it to a lab to conduct tissue analyses. These tests revealed hallmarks of MCN that had turned cancerous, with areas of dysplasia or abnormal cell growth, which is a telltale sign of cancer.
The researchers also observed differences in protein expression across the various regions. Specifically, healthy-looking cells had relatively low levels of the estrogen receptor protein; however, in areas with extensive dysplasia, the cells expressed high amounts of the estrogen receptor.
The estrogen receptor protein is how the body’s cells respond to estrogen, a hormone that plays important roles in controlling sexual development and other bodily processes. It’s well-established that increased levels of estrogen receptor can drive cancer growth — this is a hallmark of many forms of breast cancer, for example.
Increased estrogen during pregnancy may have led growth to turn cancerous
Because estrogen levels become very high during pregnancy, the researchers speculated that this woman likely had benign MCN prior to getting pregnant. Then, during pregnancy, some cells in the MCN started responding to increased estrogen levels, and that led the benign growth to turn cancerous.
If that’s indeed the case, then it follows that treatments to block estrogen may offer therapeutic value for these cancers, the scientists said, noting that “hormone production [seen in pregant people] may help sustain tumor growth beyond pregnancy.”
The research team emphasized a need for additional studies to further investigate this idea, but concluded that “the correlation between hormone receptor expression and tumor cell proliferation suggests a reason for exploring targeted therapeutic strategies.”
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