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ditemukan untuk menghentikan pertumbuhan sel tumor dengan menginduksi dormansi
Umumnya obat antikanker yang digunakan dapat membantu untuk membuat sel-sel tumor dorman, para ilmuwan melaporkan . " Hasil penelitian kami menjelaskan mengapa beberapa sel tumor tersebar melalui tubuh berkomitmen untuk tetap berbahaya selama bertahun-tahun , sementara yang lain menyebabkan penyakit aktif, " kata seorang penyidik . " Dalam mencari switch master ini kami menemukan cara untuk menganalisis sel tumor sebelum pengobatan untuk menentukan risiko kambuhnya kanker atau metastasis . "...read more
Master switch
found to stop tumor cell growth by inducing dormancy
Date:
January 31, 2015
Source:
Mount Sinai Medical
Center
Summary:
Commonly used
anticancer drugs may help to make tumor cells dormant, scientists report.
"Our results explain why some tumor cells scattered through the body are
committed to remaining harmless for years, while others cause active
disease," said one investigator. "In finding this master switch we
found a way to analyze tumor cells before treatment to determine the risk of a
cancer recurrence or metastasis."
..........................
two existing cancer
drugs turn on a gene that tells tumor cells to remain inactive, according to a
study led by researchers at the Icahn School of Medicine at Mount Sinai and
published today in Nature Communications.
Researchers discovered that the gene NR2F1, when switched on, programs
tumor cells to stay dormant. When the gene is switched off, tumor cells divide
and multiply as part of abnormal growth, potentially allowing dormant cells to
grow into tumors throughout the body (metastasis). Combining the anticancer
drugs azacytidine and retinoic acid significantly increased the amount of
active NR2F1 in tumor cells. These patterns were found in mouse models of
several cancers, and confirmed in prostate cancer cells from human patients.
Results suggest that NR2F1 is a "master regulator" of tumor cell
growth, influencing several genes that determine whether cells remain inactive,
or quiescent in medical terms. According to the study, NR2F1 exerts control
over long lasting programs in stem cells in the human embryo, where it directs
cells to stop growing and become specialized cells (neurons) for life. This
function suggests that NR2F1 may exert a long-lasting effect on tumor cells,
keeping them dormant after they have broken off from an original tumor.
"Our results explain why some tumor cells scattered through the body
are committed to remaining harmless for years, while others cause active
disease," said Julio A. Aguirre-Ghiso, PhD, Professor of Medicine,
Hematology and Medical Oncology, and Otolaryngology at the Icahn School of
Medicine. "In finding this master switch we found a way to analyze tumor
cells before treatment to determine the risk of a cancer recurrence or
metastasis."
"Azacytidine and retinoic acid, the latter a form of vitamin A,
prevented tumor cells from rapidly multiplying, restored normal cell function,
and activated several tumor suppressor genes that are often turned off in
tumors," said study co-leader Maria Soledad Sosa, PhD, a postdoctoral
fellow in Hematology at the Icahn School of Medicine. "We now have strong
evidence that combining these well-known drugs may have a profound,
long-lasting therapeutic effect."
The current study builds on the research team's earlier finding that
lowering amounts of tumor suppressor genes TGFβ2 and p38 awakened dormant tumor
cells, fueling metastatic tumor growth. Azacytidine and retinoic acid restored
TGFβ2 expression and p38 activation to drive tumor cell dormancy.
Story Source:
The above story is based on materials provided by Mount Sinai Medical Center.Note: Materials may be edited for
content and length.
Journal Reference:
1. Maria Soledad Sosa, Falguni Parikh,
Alexandre Gaspar Maia, Yeriel Estrada, Almudena Bosch, Paloma Bragado, Esther
Ekpin, Ajish George, Yang Zheng, Hung-Ming Lam, Colm Morrissey, Chi-Yeh Chung,
Eduardo F. Farias, Emily Bernstein, Julio A. Aguirre-Ghiso. NR2F1
controls tumour cell dormancy via SOX9- and RARβ-driven quiescence programmes. Nature
Communications, 2015; 6: 6170 DOI: 10.1038/ncomms7170
