
A new study has answered a question that has puzzled doctors for many years about one of the most dangerous forms of ovarian cancer. Researchers have discovered that this cancer does not actually begin in the ovaries as once believed.
Instead, it starts in the fallopian tubes, the narrow passages that connect the ovaries to the uterus. This finding could help doctors detect the disease earlier and develop better treatments for a cancer that is often diagnosed too late.
The cancer is called high‑grade serous carcinoma. It is the most common and deadly form of ovarian cancer.
Many patients do not notice symptoms until the disease has already spread, making treatment difficult. Because of this, survival rates have remained low. Understanding where the cancer begins is an important step toward finding it sooner and saving more lives.
The research was led by Professor Alexander Nikitin from Cornell University and published in the journal Nature Communications. For decades, scientists assumed that this cancer started in ovarian tissue because tumors were usually found there. However, careful study has now shown that the earliest changes happen in certain cells inside the fallopian tubes.
The team identified a special group of cells called pre‑ciliated tubal epithelial cells as the likely starting point. These cells are in a transitional stage between simple stem cells and mature cells that have tiny hair‑like structures known as cilia.
The cilia help move eggs through the fallopian tube. Because these transitional cells are still developing, they appear to be more vulnerable to harmful genetic changes that can lead to cancer.
To investigate further, the scientists conducted experiments using mice, whose uterine tubes function similarly to human fallopian tubes. They examined different cell types and studied what happened when important protective genes were damaged.
Two key genes were involved: TP53 and RB1. These genes normally help control cell growth and prevent tumors from forming. In many human cases of this cancer, both genes are disrupted.
When the researchers switched off these genes in stem cells of the fallopian tube, the cells simply died and did not form tumors. But when the same genes were turned off in the transitional pre‑ciliated cells, cancer developed quickly. This showed that these cells are especially sensitive to genetic damage and are likely the true origin of the disease.
The scientists also used a powerful method called single‑cell sequencing to study each cell’s activity in detail.
This technique allowed them to see which genes were active inside the cells. They found markers such as Pax8 and Krt5 that helped identify the dangerous cell type. These markers may one day help doctors detect early changes before cancer fully develops.
This discovery is important because it gives researchers a clear target for early diagnosis and prevention. If doctors know exactly where the cancer starts and which cells are involved, they may be able to screen high‑risk patients more effectively. It could also lead to new treatments that stop the disease before it spreads.
Although more research is needed before this knowledge can be turned into routine medical tests or therapies, the findings offer new hope. Ovarian cancer has long been difficult to detect early, and many lives have been lost because of late diagnosis. Understanding the true starting point of the disease is a major step forward.
This study shows how advances in science can change our understanding of serious illnesses. By learning how and where cancers begin, doctors may one day prevent them or catch them at a stage when they are easier to treat. For patients and families affected by ovarian cancer, this research brings a message of hope for the future.
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