Cancer / Oncology/Androgen-sensitive prostate cancer
Genitourinary · subtype
Androgen-sensitive prostate cancer
Subtype of Prostate cancer
Clinical / Scientific
AR-dependent disease responds to androgen deprivation. and metabolic programmes still operate. Adjunctive metabolic ideas must not be framed as alternatives to androgen deprivation where that is indicated.
Core Biological Drivers
AR ligand dependence
Canonical AR .
Key Pathways
Scientific explanation
AR is a nuclear factor required for most prostate adenocarcinoma growth. Resistance can occur through AR amplification, splice variants, or lineage plasticity.
Scientific explanation
phosphorylates PIP2 to PIP3, recruiting . supports growth, survival, glucose uptake and mTORC1 input. Pathway activation is common via PIK3CA mutation, PTEN loss or -tyrosine- signalling.
Scientific explanation
mTORC1 integrates growth-factor and nutrient signals to drive protein synthesis, lipid synthesis and suppression. It sits downstream of PI3K/AKT and amino-acid sensing.
Scientific explanation
De novo lipogenesis, fatty-acid oxidation and lipid uptake are rewired in a tumour-type-specific way, especially in hypoxic, obese-host, or OXPHOS-dependent subsets.
Pathway Convergence
Target → pathway → downstream effect → biological consequence. Shared intersections are mechanistic maps, not protocols.
Growth-factor signalling
Ligand or mutation-driven RTK input feeds PI3K/AKT and mTORC1, supporting anabolic growth. This is a map of signalling, not a treatment protocol.
Energy stress
Energetic stress activates AMPK, which can restrain mTORC1. Biguanides and related tools map onto this axis in models.
Metabolic Vulnerabilities
Aerobic supports ATP, biomass and acidification even when oxygen is available. Extent varies by tumour and remains a vulnerability hypothesis rather than a uniform target.
Tumor Microenvironment
Disordered vasculature creates , HIF-1α stabilization, induction and immune-suppressive adenosine/lactate milieus.
Metastasis Module
Bone tropism already possible in sensitive disease.
Resistance Biology
Clonal selection toward AR-independent programmes under deprivation.
Cancer Stemness
Wnt, Notch, Hedgehog, ALDH and CD44-associated programmes can mark stem-like fractions with quiescence and therapy tolerance. These markers are not interchangeable across tumour types.
Mechanism-Based Adjunctive Strategies
Compounds appear only where a mechanistic overlap exists for this cancer. Evidence tiers are not equivalent. Nothing here is a treatment recommendation.
Target / Mechanism
Modest complex I inhibition raises AMP:ATP, activating and restraining hepatic and -linked anabolism. Direct antineoplastic efficacy is not established from that pharmacology alone.
Cancer relevance
activation and restraint provide a metabolic rationale in - and -linked tumours. Human data are mixed and do not establish metformin as cancer therapy.
Metabolic adjunctive research context. Convergence: AMPK, mTOR, Glycolysis.
Statins (HMG-CoA reductase inhibitors)
Target / Mechanism
Inhibit HMG-CoA reductase, depleting mevalonate-pathway isoprenoids needed for RAS/RHO prenylation and some sterol-dependent growth programmes. Observational oncology signals are mixed and not a licence to treat cancer with statins.
Cancer relevance
Mevalonate-pathway blockade can affect prenylation of RAS-family GTPases. Observational human signals are mixed and confounding is substantial.
Mevalonate / prenylation mechanistic overlap. Convergence: RAS/RAF, Fatty-acid metabolism.
Research Context
- Hallmarks. Hanahan D, Weinberg RA. Hallmarks of cancer: the next generation. Cell. 2011;144(5):646-674. https://doi.org/10.1016/j.cell.2011.02.013
- Metformin oncology. Pollak MN. Investigating metformin for cancer prevention and treatment: the end of the beginning. Cancer Discov. 2012;2(9):778-790. https://doi.org/10.1158/2159-8290.CD-12-0263
This oncology atlas is educational. Pathway maps, adjunctive strategies, and compound listings describe mechanistic relevance. They do not establish clinical efficacy, do not recommend treatment, and are not a substitute for oncology care. Evidence tiers are not equivalent.