In an exciting new discovery, scientists have found a promising way to stop breast cancer before it can spread, offering hope for more effective treatments.
Understanding Tumor Spikes and Their Role
Researchers have uncovered that aggressive breast tumors have a distinct look, often covered in many spikes, resembling the spiky outer shell of a conker.
In contrast, less aggressive tumors tend to have a smooth, round shape with little to no spikes.
These spiky formations could play a key role in how cancer cells travel to other parts of the body, like the lungs, liver, and brain, leading to terminal cancer stages.
It is believed that the spikes act like roads, providing shortcuts for cancer cells to reach blood vessels, from where they can spread through the body.
Insights from Tumor Analysis
The breakthrough came from analyzing tumors from 30 breast cancer patients and 65 melanoma patients.
Professor Victoria Sanz Moreno, senior author of the study at The Institute of Cancer Research in London, emphasized the potential for targeting these spiky tumors with existing drugs.
By doing so, doctors could potentially slow the spread of cancer, particularly for patients already facing terminal stages, and improve survival rates.
How Tumor Spikes Change Cancer Cells
The outer spikes, composed of fibers from the extracellular matrix, influence how cancer cells behave.
Within these spikes, cancer cells become rounder and more resilient, which helps them move through the body more efficiently.
In laboratory tests, scientists were able to show that these spike-like structures allowed cancer cells to spread into the lungs of mice.
Further research revealed that patients with cancers like breast, pancreatic, and melanoma, whose cells exhibited similar spike characteristics, had shorter survival times.
This was linked to heightened gene activity controlling cell shape and size, triggered by the spikes.
Potential for New Cancer Treatments
The key to this discovery lies in the fact that the gene activity linked to these spikes can be controlled.
Existing drugs could potentially halt this gene activity, preventing the cancer cells from spreading.
In cases where the tumor is successfully removed or treated, cancer cells that remain confined within the tumor can be targeted by other drugs, offering more effective treatments.
Why Tumor Spikes Are So Important
While cancer cells can spread through fatty tissue or lymph nodes, the most efficient route is through the bloodstream, which acts as a highway to organs like the lungs and brain.
The spikes on tumors may provide a direct route to blood vessels, facilitating the spread of cancer cells.
Although the scientists can’t yet confirm that the spikes actually link up to blood vessels, they do appear to enhance the cancer cells’ ability to move faster and more efficiently throughout the body.
Improving Early Detection and Treatment
This discovery could significantly improve early detection methods, allowing doctors to identify aggressive tumors based on the spiky collagen structures around them.
More importantly, it could lead to the development of drugs that prevent tumors from becoming spiky in the first place, effectively stopping cancer cells from preparing to spread.
With this knowledge, doctors may be able to keep the cancer contained within the tumor, where treatments can destroy the cells before they have a chance to travel.
A Decade of Research Leading to a New Hope
This breakthrough, published in the journal Nature Communications, marks the culmination of nearly a decade of research.
Dr. Oscar Maiques, who led the study at Barts Cancer Institute, stressed that the exterior of tumors, often overlooked in the past, holds vital clues.
The findings offer valuable insights into how cancer behaves and could lead to a major shift in how we approach treatment, potentially transforming the way we fight the disease.
With this new knowledge, doctors are closer than ever to finding ways to stop cancer in its tracks before it can spread, offering new hope for patients battling this devastating disease.
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