Signal Transduction in Cancer: Oncogene and Tumor Suppressors in Cancer
A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cell Signaling".
Deadline for manuscript submissions: closed (30 September 2021) | Viewed by 728
Special Issue Editor
Special Issue Information
Dear Colleagues,
Altered signal transduction underpins almost every hallmark of cancer. These alterations stem from genetic and/or epigenetic changes in regulatory networks that are under the control of oncogenes and tumor-suppressor genes. Importantly, aberrant activation of these signal transduction pathways (often associated with oncogenic processes such as increased proliferation, suppressed cell death, tumor angiogenesis, metabolic rewiring, and immune evasion) can provide therapeutic opportunities. In fact, signal transduction inhibitors (STIs) are an important part of the therapeutic armamentarium currently available to treat various cancers. Our evolving understanding of these signaling pathways in normal physiology and of the impact of mutation on both the molecular circuitries and cellular processes they regulate will continue to be a great conduit for improving our understanding of cancer, and provide a source of rational drug targets.
With the impressive success of immuno-oncological drugs in a number of patient populations, knowledge of how signaling pathways deregulated by altered oncogene and/or tumor suppressor function influence the cancer immunity cycle could improve our understanding of how to best deploy these treatments, particularly in combination with STIs.
This Special Issue aims to summarize the current knowledge on oncogene- and tumor-suppressor-regulated signal transduction and its importance in modulating tumorigenesis and treatment response.
Dr. Igor Vivanco
Guest Editor
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Keywords
- cancer
- signal transduction
- oncogene
- tumor suppressor genes
- oncogene addiction
- non-oncogene addiction
- oncogenic metabolism
- cancer immunity cycle
- precision medicine
- kinases
- transcription factors
- epigenetics
- DNA damage
- cell death
- cell proliferation
- cell invasion
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