Related Experiment Videos
Cross-cancer transcriptomic integration identifies a core immune-signaling network in hormone-driven malignancies
Prasanna Kumar Selvam1, Supraja Mohan1, Karthick Vasudevan1
1Manipal Academy of Higher Education (MAHE), Manipal, India; Institute of Bioinformatics, International Technology Park, Bangalore, India.
Advances in Protein Chemistry and Structural Biology
|July 14, 2026
Summary
This study found a shared immune-signaling transcriptional program in breast, ovarian, and thyroid cancers. Prostate cancer showed less overlap, suggesting distinct molecular drivers in hormone-driven malignancies.
Area of Science:
- Genomics and Molecular Biology
- Cancer Research
- Endocrinology
Background:
- Hormone-dependent cancers (breast, ovarian, thyroid, prostate) are driven by endocrine signaling but show molecular heterogeneity.
- Understanding shared transcriptional programs across these cancers is crucial for developing targeted therapies.
- Existing research has not fully elucidated conserved gene expression signatures in hormone-driven malignancies.
Purpose of the Study:
- To identify conserved gene expression signatures across hormone-driven cancers using a systematic transcriptomic framework.
- To investigate the degree of transcriptional overlap and directionality of gene dysregulation among breast, ovarian, thyroid, and prostate cancers.
- To define a core pan-hormone transcriptional signature and analyze its functional characteristics.
Main Methods:
- Applied a direction-aware transcriptomic framework to RNA-sequencing data from hormone-driven cancers and matched controls.
- Performed differential gene expression analysis using DESeq2 for each cancer type.
- Integrated differentially expressed genes (DEGs) across cancers using a presence-direction matrix and conducted leave-one-out sensitivity analysis.
Main Results:
- Identified 15,648 significant DEGs across the four cancer types, with limited universal overlap (only one gene shared across all four).
- Prostate cancer exhibited lower transcriptional concordance; excluding it revealed 10,948 shared DEGs across breast, ovarian, and thyroid cancers.
- A core pan-hormone signature of 270 genes was defined for breast, ovarian, and thyroid cancers, enriched for immune signaling and cytokine-related functions.
Conclusions:
- A conserved, immune-signaling-centric transcriptional program is shared among breast, ovarian, and thyroid cancers.
- Prostate cancer displays distinct transcriptional patterns compared to the other hormone-dependent malignancies studied.
- These findings highlight potential common therapeutic targets and underscore the importance of considering cancer-specific molecular profiles.
Related Concept Videos
Adaptive Mechanisms in Cancer Cells
Cancer cells accumulate genetic changes at an abnormally rapid rate due to the defects in the DNA repair mechanisms. From an evolutionary perspective, such genetic instability is advantageous for cancer development. Mutant cell lines accumulate a series of beneficial mutations that contribute to their progression into cancer.
Some of the advantages that cancer cells have on normal cells include - enhanced ability to divide without terminally differentiating, induce new blood vessel formation,...
Some of the advantages that cancer cells have on normal cells include - enhanced ability to divide without terminally differentiating, induce new blood vessel formation,...
Adaptive Mechanisms in Cancer Cells
Cancer cells accumulate genetic changes at an abnormally rapid rate due to the defects in the DNA repair mechanisms. From an evolutionary perspective, such genetic instability is advantageous for cancer development. Mutant cell lines accumulate a series of beneficial mutations that contribute to their progression into cancer.
Some of the advantages that cancer cells have on normal cells include - enhanced ability to divide without terminally differentiating, induce new blood vessel formation,...
Some of the advantages that cancer cells have on normal cells include - enhanced ability to divide without terminally differentiating, induce new blood vessel formation,...
mTOR Signaling and Cancer Progression
The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
The mTOR pathway or the...
The mTOR pathway or the...
mTOR Signaling and Cancer Progression
The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
The mTOR pathway or the...
The mTOR pathway or the...
Cancer-Critical Genes II: Tumor Suppressor Genes
Genes usually encode proteins necessary for the proper functioning of a healthy cell. Mutations can often cause changes to the gene expression pattern, thereby altering the phenotype.
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...
Cancer-Critical Genes II: Tumor Suppressor Genes
Genes usually encode proteins necessary for the proper functioning of a healthy cell. Mutations can often cause changes to the gene expression pattern, thereby altering the phenotype.
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...