The secret hideouts of ovarian cancer revealed
Date:
February 11, 2022
Source:
University of Helsinki
Summary:
Researchers discovered how ovarian cancer hides from the body's
immune system. The findings will help develop novel precision
therapies for ovarian cancer, a common and aggressive cancer type.
FULL STORY ========================================================================== Every year, roughly 550 women develop ovarian cancer in Finland. Ovarian
cancer is difficult to treat and it is commonly fatal, with 320 women
dying of ovarian cancer annually in Finland.
========================================================================== Cancer can only develop and progress when the tumour cells are
able to hide from the body's immune system. Cancer immunotherapies,
which boost the body's immune defence against cancer, have emerged as
promising therapies in multiple tumor types. However, the effectiveness
of immunotherapies against ovarian cancer has remained modest. This
is mainly since the mechanisms how ovarian cancer cells hide from the
immune system have been unknown.
Now, researchers at the University of Helsinki have uncovered how tumour
cells interact with the immune system in ovarian cancer. Utilising a
novel imaging technology, the researchers characterized more than 110,000 individual cells from clinical ovarian cancer samples. The researchers investigated how the genetic characteristics of ovarian cancer the shape
human immune system, and how tumour and immune cells communicate with
each other.
"With the help of this revolutionary imaging technology and advanced data analysis, we were able to study individual tumour cells, their functional properties and interactions with unprecedented precision," says Associate professor Anniina Fa"rkkila", the corresponding author of the study.
Tumour genes trick the immune system "By studying individual cells
directly in the tissue, we demonstrated how cancer cells hide in different ways, depending on the specific gene mutation.
We found that the body's immune system is more effective against tumors
with a mutation in BRCA1/2 genes. By contrast, tumours without such
mutations have a connective tissue barrier prohibiting the interaction
between the cancer and immune cells," says doctoral researcher Inga-Maria Launonen, BM.
BRCA1/2 mutations occur in approximately 20% of poorly differentiated
serous carcinomas, the most common form of ovarian cancer. The killer
T-cells closely guarded the aggressive tumour cells particularly in
tumours with BRCA1/ 2 mutations, which is why these patients had a
markedly better prognosis.
"By increasing our understanding of how tumour genes trick the immune
system, we will be able to develop more effective ways to activate the
body's own immune defences to kill the cancer cells," Inga-Maria says.
Results will promote the tailoring of precision therapies The results
of the study confirm the significance of the interaction between tumour
and immune cells in identifying new and more effective therapies as well
as in choosing the right therapy for each patient.
"Our findings will enable us to tailor precision immuno- and combination therapies that have the potential to even cure ovarian cancer in the
future," Fa"rkkila" says.
========================================================================== Story Source: Materials provided by University_of_Helsinki. Note:
Content may be edited for style and length.
========================================================================== Journal Reference:
1. I.-M. Launonen, N. Lyytika"inen, J. Casado, E. A. Anttila,
A. Szabo', U.-
M. Haltia, C. A. Jacobson, J. R. Lin, Z. Maliga, B. E. Howitt, K. C.
Strickland, S. Santagata, K. Elias, A. D. D'Andrea, P. A.
Konstantinopoulos, P. K. Sorger, A. Fa"rkkila". Single-cell
tumor-immune microenvironment of BRCA1/2 mutated high-grade serous
ovarian cancer.
Nature Communications, 2022; 13 (1) DOI: 10.1038/s41467-022-28389-3 ==========================================================================
Link to news story:
https://www.sciencedaily.com/releases/2022/02/220211102631.htm
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