Ca of prostate
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Summary
10 papers analyzed
These studies suggest that calcium signaling and homeostasis play critical roles in prostate cancer progression, metastasis, and treatment response, with implications for genomic instability, androgen receptor regulation, and potential therapeutic targets.
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Prostate Cancer: Insights into Pathophysiology, Treatment, and Molecular Mechanisms
Genomic Instability and SChLAP1 Dysregulation in Prostate Cancer
Intraductal carcinoma (IDC) and cribriform architecture (CA) are subpathologies in localized prostate cancer that are associated with poor outcomes. Research has shown that these subpathologies share a clonal ancestry with adjacent glandular adenocarcinoma and are linked to increased risks of biochemical relapse and metastasis. IDC/CA+ cancers exhibit higher genomic instability, as indicated by a greater percentage of genome alteration, and are often characterized by hypoxia. Notably, the long noncoding RNA SChLAP1 is expressed at significantly higher levels in IDC/CA+ tumors, suggesting its role in the aggressive nature of these cancers.
Calcium Signaling and Prostate Cancer Cell Viability
Calcium (Ca2+) signaling plays a crucial role in the regulation of prostate cancer cell functions, including proliferation and apoptosis. In prostate cancer cells, reactive oxygen species (ROS) are elevated, leading to impaired Ca2+ signaling. This impairment is linked to the formation of heteromeric Orai1/Orai3 channels, which are more sensitive to redox changes in cancer cells compared to normal prostate epithelial cells. Elevated intracellular Ca2+ levels can down-regulate androgen receptor (AR) expression, which is critical for prostate cancer cell growth and differentiation. Additionally, the Ca2+-sensing receptor (CaR) in prostate cancer cells can stimulate parathyroid hormone-related protein (PTHrP) secretion, potentially promoting bone resorption and further cancer progression.
Treatment Modalities and Associated Complications
Prostate cancer treatment typically involves surgical removal of the prostate or radiotherapy for early-stage disease, while hormone therapy or chemotherapy is used for advanced cases. However, these treatments can lead to significant complications such as urinary incontinence and erectile dysfunction, which can severely impact the patient's quality of life. The prevalence of these complications highlights the need for careful consideration of treatment options and the development of strategies to mitigate these adverse effects.
Role of Inflammation and Prostatic Calculi
Prostatic corpora amylacea (CA) and calculi are common findings in prostate cancer patients and are often associated with inflammation. These structures are primarily composed of calcium phosphate and proteins such as lactoferrin, calprotectin, and myeloperoxidase, which are indicative of neutrophil activity. The presence of these inflammatory proteins suggests that acute inflammation may play a role in the biogenesis of CA and calculi, potentially contributing to prostate carcinogenesis.
Ex Vivo Models for Prostate Cancer Research
To better understand prostate cancer and develop effective treatments, researchers have developed ex vivo tissue culture models that preserve the tumor's sensitivity to microenvironmental signals such as hypoxia and extracellular calcium concentration. These models maintain tissue morphology and function, making them valuable tools for studying drug responses and the effects of androgen deprivation.
Conclusion
Prostate cancer is a complex disease influenced by genomic instability, calcium signaling, and inflammation. Understanding these molecular mechanisms is crucial for developing targeted therapies and improving patient outcomes. While current treatments can be effective, they often come with significant complications, underscoring the need for ongoing research and innovation in prostate cancer management.
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