Prostate cancer is a major disease for men. In the US for 2023, there will be close to 290,000 new cases and nearly 35,000 deaths. These numbers will rise with an aging population. It is a slow growing cancer requiring minimal or no treatment, and patient survival is high. In about 10-15% of the cases, however, the cancer is aggressive and can spread quickly. For cancer that has spread, anti-androgen therapy could be effective. In many cases, castration resistance develops, and the cancer can no longer be manageable. Since about half of the patients are now being managed by active surveillance, means to preventing the cancer from becoming more aggressive is of clinical need. Advances have been made in early detection and likely outcome analysis from tumor pathology.
The purpose of this Research Topic is to provide mechanistic explanations for the biology of prostate cancer using principally human specimens. Areas of interest include the following:
(1) What underlies the loss of cancer differentiation from the glandular histology of Gleason pattern 3, aglandular histology of Gleason pattern 4 to no-organized histology of Gleason pattern 5? How are the different cancer types of adenocarcinoma, non-adenocarcinoma and small cell carcinoma related?
(2) Epithelial-stromal cell interaction and intercellular signaling are responsible for proper tissue organization. In what ways are these processes defective in tumors due to gene expression changes in cancer epithelial as well as cancer-associated stromal cells?
(3) How is dissemination of cancer cells facilitated through loss of tissue integrity?
(4) Does local spread differ from distant spread? The first involves penetration of the prostatic capsule, the second dissemination by the circulatory systems. Many distant metastases in bone and soft tissues display an adenocarcinoma phenotype with glandular differentiation being positive for PSA synthesis, whereas PSA expression is down-regulated from Gleason 3 to Gleason 5 in tandem with loss of differentiation. One would not expect that cancer cells in metastases to be differentiated.
(5) What causes the loss of basal epithelial cells in tumors? Is there a subset of cancer cells derived from the transformation of basal cells, in particular, the more aggressive type?
(6) Are there suitable antigens differentially expressed by cancer cells that can be targeted for development of viable therapies?
(7) Is cancer vaccination possible?
To answer these questions, proper research tools and methods such as omics technologies, cell isolation, cell culture, gene transfection are invaluable. Our hope is that these research findings will go towards benefiting patient care.
Much has been learned about the gene and protein expression of prostate cancer; as well as its impact on patients. Nevertheless, very little has been made clear on the molecular biology of cancer development from the transformation of normal epithelial cells, the loss of cell-cell interaction in tissue organization, the change in cancer cell types over time, the mechanism of cancer spread, to how mutations affect oncogenesis. Solutions to these questions would lead to cancer prevention and more effective treatments. Mechanistic studies that shed light on these processes advance our understanding on the pathobiology of prostate cancer, and are of interest to this research topic.
Contributors, please submit original findings, new methodologies, or concise reviews for consideration on relevance and pertinence to the scope outlined.
Prostate cancer is a major disease for men. In the US for 2023, there will be close to 290,000 new cases and nearly 35,000 deaths. These numbers will rise with an aging population. It is a slow growing cancer requiring minimal or no treatment, and patient survival is high. In about 10-15% of the cases, however, the cancer is aggressive and can spread quickly. For cancer that has spread, anti-androgen therapy could be effective. In many cases, castration resistance develops, and the cancer can no longer be manageable. Since about half of the patients are now being managed by active surveillance, means to preventing the cancer from becoming more aggressive is of clinical need. Advances have been made in early detection and likely outcome analysis from tumor pathology.
The purpose of this Research Topic is to provide mechanistic explanations for the biology of prostate cancer using principally human specimens. Areas of interest include the following:
(1) What underlies the loss of cancer differentiation from the glandular histology of Gleason pattern 3, aglandular histology of Gleason pattern 4 to no-organized histology of Gleason pattern 5? How are the different cancer types of adenocarcinoma, non-adenocarcinoma and small cell carcinoma related?
(2) Epithelial-stromal cell interaction and intercellular signaling are responsible for proper tissue organization. In what ways are these processes defective in tumors due to gene expression changes in cancer epithelial as well as cancer-associated stromal cells?
(3) How is dissemination of cancer cells facilitated through loss of tissue integrity?
(4) Does local spread differ from distant spread? The first involves penetration of the prostatic capsule, the second dissemination by the circulatory systems. Many distant metastases in bone and soft tissues display an adenocarcinoma phenotype with glandular differentiation being positive for PSA synthesis, whereas PSA expression is down-regulated from Gleason 3 to Gleason 5 in tandem with loss of differentiation. One would not expect that cancer cells in metastases to be differentiated.
(5) What causes the loss of basal epithelial cells in tumors? Is there a subset of cancer cells derived from the transformation of basal cells, in particular, the more aggressive type?
(6) Are there suitable antigens differentially expressed by cancer cells that can be targeted for development of viable therapies?
(7) Is cancer vaccination possible?
To answer these questions, proper research tools and methods such as omics technologies, cell isolation, cell culture, gene transfection are invaluable. Our hope is that these research findings will go towards benefiting patient care.
Much has been learned about the gene and protein expression of prostate cancer; as well as its impact on patients. Nevertheless, very little has been made clear on the molecular biology of cancer development from the transformation of normal epithelial cells, the loss of cell-cell interaction in tissue organization, the change in cancer cell types over time, the mechanism of cancer spread, to how mutations affect oncogenesis. Solutions to these questions would lead to cancer prevention and more effective treatments. Mechanistic studies that shed light on these processes advance our understanding on the pathobiology of prostate cancer, and are of interest to this research topic.
Contributors, please submit original findings, new methodologies, or concise reviews for consideration on relevance and pertinence to the scope outlined.
