Pub Date : 2021-05-27DOI: 10.36255/EXONPUBLICATIONS.PROSTATECANCER.STEAP.2021
S. M. Rocha, J. Barroca-Ferreira, L. Passarinha, S. Socorro, Cláudio J. Maia
ABSTRACT Prostate cancer is a multifactorial disease and the second most common cancer diagnosed in men worldwide. The six transmembrane epithelial antigen of prostate (STEAP) proteins seem to be involved in prostate tumorigenesis. The STEAP proteins are differentially expressed in prostate cancer cells, and survival analysis reveal that prostate cancer patients with high levels of STEAP1 have poor survival outcomes. In contrast, high expression of STEAP4 offers a better prognosis. This chapter provides an overview of the role of STEAP proteins in prostate cancer. The structure, biological functions, and the potential prognostic significance of each of the four members of the STEAP family in prostate cancer are discussed.
{"title":"The Usefulness of STEAP Proteins in Prostate Cancer Clinical Practice","authors":"S. M. Rocha, J. Barroca-Ferreira, L. Passarinha, S. Socorro, Cláudio J. Maia","doi":"10.36255/EXONPUBLICATIONS.PROSTATECANCER.STEAP.2021","DOIUrl":"https://doi.org/10.36255/EXONPUBLICATIONS.PROSTATECANCER.STEAP.2021","url":null,"abstract":"ABSTRACT \u0000Prostate cancer is a multifactorial disease and the second most common cancer diagnosed in men worldwide. The six transmembrane epithelial antigen of prostate (STEAP) proteins seem to be involved in prostate tumorigenesis. The STEAP proteins are differentially expressed in prostate cancer cells, and survival analysis reveal that prostate cancer patients with high levels of STEAP1 have poor survival outcomes. In contrast, high expression of STEAP4 offers a better prognosis. This chapter provides an overview of the role of STEAP proteins in prostate cancer. The structure, biological functions, and the potential prognostic significance of each of the four members of the STEAP family in prostate cancer are discussed.","PeriodicalId":87076,"journal":{"name":"Clinical prostate cancer","volume":"67 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-05-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"88427188","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
A. Kazama, Toshihiro Saito, Keisuke Takeda, Kazuhiro Kobayashi, T. Tanikawa, Ayae Kanemoto, Fumio Ayukawa, Y. Matsumoto, T. Sugita, N. Hara, Y. Tomita
Background To predict long-term treatment outcome of radiation therapy (RT) plus androgen deprivation therapy (ADT) for high-risk locally advanced prostate cancer. Methods In total, 204 patients with the National Comprehensive Cancer Network (NCCN) high risk locally advanced prostate cancer (PSA > 20 ng/ml, Gleason score ≧ 8, clinical T stage ≧ 3a) were treated with definitive RT with ADT. Median follow up period was 113 months (IQR: 95–128). Median neoadjuvant ADT and total ADT duration were 7 months (IQR: 6–10) and 27 months (IQR: 14–38), respectively. Results PSA recurrence-free survival (PSA-RFS), cancer specific survival (CSS), and overall survival (OS) rates at 5 years were 84.1%, 98.5%, and 93.6%, respectively, and 67.9%, 91.2%, and 78.1%, respectively, at 10 years. Pre-RT PSA less than 0.2 ng/ml was associated with superior outcomes of PSA-RFS (HR = 0.42, 95% CI: 0.25–0.70, p = 0.001), CSS (HR = 0.27, 95% CI: 0.09–0.82, p = 0.013), and OS (HR = 0.48, 95% CI: 0.26–0.91, p = 0.021). On multivariate analysis, age (≥70 y.o.) and pre-RT PSA (≥0.2 ng/ml) were factors predictive of poorer OS (p = 0.032) , but iPSA, T stage, Gleason score, number of NCCN high-risk criteria, a combination with anti-androgen therapy and neoadjuvant ADT duration were not predictive of treatment outcome. Conclusion In patient with high-risk prostate cancer, RT plus ADT achieved good oncologic outcomes. PSA < 0.2 ng/ml before radiation therapy is a strong independent predictor for long overall survival.
{"title":"Achieving PSA < 0.2 ng/ml before Radiation Therapy Is a Strong Predictor of Treatment Success in Patients with High-Risk Locally Advanced Prostate Cancer","authors":"A. Kazama, Toshihiro Saito, Keisuke Takeda, Kazuhiro Kobayashi, T. Tanikawa, Ayae Kanemoto, Fumio Ayukawa, Y. Matsumoto, T. Sugita, N. Hara, Y. Tomita","doi":"10.1155/2019/4050352","DOIUrl":"https://doi.org/10.1155/2019/4050352","url":null,"abstract":"Background To predict long-term treatment outcome of radiation therapy (RT) plus androgen deprivation therapy (ADT) for high-risk locally advanced prostate cancer. Methods In total, 204 patients with the National Comprehensive Cancer Network (NCCN) high risk locally advanced prostate cancer (PSA > 20 ng/ml, Gleason score ≧ 8, clinical T stage ≧ 3a) were treated with definitive RT with ADT. Median follow up period was 113 months (IQR: 95–128). Median neoadjuvant ADT and total ADT duration were 7 months (IQR: 6–10) and 27 months (IQR: 14–38), respectively. Results PSA recurrence-free survival (PSA-RFS), cancer specific survival (CSS), and overall survival (OS) rates at 5 years were 84.1%, 98.5%, and 93.6%, respectively, and 67.9%, 91.2%, and 78.1%, respectively, at 10 years. Pre-RT PSA less than 0.2 ng/ml was associated with superior outcomes of PSA-RFS (HR = 0.42, 95% CI: 0.25–0.70, p = 0.001), CSS (HR = 0.27, 95% CI: 0.09–0.82, p = 0.013), and OS (HR = 0.48, 95% CI: 0.26–0.91, p = 0.021). On multivariate analysis, age (≥70 y.o.) and pre-RT PSA (≥0.2 ng/ml) were factors predictive of poorer OS (p = 0.032) , but iPSA, T stage, Gleason score, number of NCCN high-risk criteria, a combination with anti-androgen therapy and neoadjuvant ADT duration were not predictive of treatment outcome. Conclusion In patient with high-risk prostate cancer, RT plus ADT achieved good oncologic outcomes. PSA < 0.2 ng/ml before radiation therapy is a strong independent predictor for long overall survival.","PeriodicalId":87076,"journal":{"name":"Clinical prostate cancer","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-10-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"76902970","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
A. Kawai, David Martinez, Catherine W Saltus, Z. Vassilev, M. Soriano-Gabarró, J. Kaye
Background and Objective Skeletal-related events (SREs) are common in men with bone metastases and have negative consequences for patients with castration-resistant prostate cancer (CRPC), including pain, reduced quality of life, and increased mortality. We estimated incidence rates of first SREs in a cohort of men with CRPC in the Surveillance, Epidemiology, and End Results-Medicare database. Methods We included men aged ≥ 65 years with a prostate cancer diagnosis in 2000-2011 if they had no prior malignancy (other than nonmelanoma skin cancer) and had surgical or medical castration with subsequent second-line systemic therapy, which was used to infer castration resistance. The first occurrence of an SRE (fracture, bone surgery, radiation therapy, or spinal cord compression) in Medicare claims was identified. Incidence rates of SREs were estimated in all eligible person-time and, in secondary analyses, stratified by any use of bone-targeted agents (BTAs) and history of SRE. Results Of 2,234 men with CRPC (84% white, mean age = 76.6 years), 896 (40%) had an SRE during follow-up, with 74% occurring within a year after cohort entry. Overall, the incidence rate of SREs was 3.78 (95% CI, 3.53-4.03) per 100 person-months. The incidence rate of SREs before any BTA use was 4.16 (95% CI, 3.71-4.65) per 100 person-months, and after any BTA use was 3.60 (95% CI, 3.32-3.91) per 100 person-months. The incidence rate in patients with no history of SRE was 3.33 (95% CI 3.01-3.68) per 100 person-months, and in patients who had such a history, it was 4.20 (95% CI 3.84-4.58) per 100 person-months. Conclusions In this large cohort of elderly men with CRPC in the US, SREs were common. A decrease in incidence of SREs after starting BTA is suggested, but the magnitude of the effect may be confounded by indication and other factors such as age and prior SRE.
{"title":"Incidence of Skeletal-Related Events in Patients with Castration-Resistant Prostate Cancer: An Observational Retrospective Cohort Study in the US","authors":"A. Kawai, David Martinez, Catherine W Saltus, Z. Vassilev, M. Soriano-Gabarró, J. Kaye","doi":"10.1155/2019/5971615","DOIUrl":"https://doi.org/10.1155/2019/5971615","url":null,"abstract":"Background and Objective Skeletal-related events (SREs) are common in men with bone metastases and have negative consequences for patients with castration-resistant prostate cancer (CRPC), including pain, reduced quality of life, and increased mortality. We estimated incidence rates of first SREs in a cohort of men with CRPC in the Surveillance, Epidemiology, and End Results-Medicare database. Methods We included men aged ≥ 65 years with a prostate cancer diagnosis in 2000-2011 if they had no prior malignancy (other than nonmelanoma skin cancer) and had surgical or medical castration with subsequent second-line systemic therapy, which was used to infer castration resistance. The first occurrence of an SRE (fracture, bone surgery, radiation therapy, or spinal cord compression) in Medicare claims was identified. Incidence rates of SREs were estimated in all eligible person-time and, in secondary analyses, stratified by any use of bone-targeted agents (BTAs) and history of SRE. Results Of 2,234 men with CRPC (84% white, mean age = 76.6 years), 896 (40%) had an SRE during follow-up, with 74% occurring within a year after cohort entry. Overall, the incidence rate of SREs was 3.78 (95% CI, 3.53-4.03) per 100 person-months. The incidence rate of SREs before any BTA use was 4.16 (95% CI, 3.71-4.65) per 100 person-months, and after any BTA use was 3.60 (95% CI, 3.32-3.91) per 100 person-months. The incidence rate in patients with no history of SRE was 3.33 (95% CI 3.01-3.68) per 100 person-months, and in patients who had such a history, it was 4.20 (95% CI 3.84-4.58) per 100 person-months. Conclusions In this large cohort of elderly men with CRPC in the US, SREs were common. A decrease in incidence of SREs after starting BTA is suggested, but the magnitude of the effect may be confounded by indication and other factors such as age and prior SRE.","PeriodicalId":87076,"journal":{"name":"Clinical prostate cancer","volume":"32 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-07-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"75237622","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Catherine W Saltus, Z. Vassilev, J. Zong, B. Calingaert, E. Andrews, M. Soriano-Gabarró, J. Kaye
[This corrects the article DOI: 10.1155/2019/4387415.].
[这更正了文章DOI: 10.1155/2019/4387415.]。
{"title":"Corrigendum to “Incidence of Second Primary Malignancies in Patients with Castration-Resistant Prostate Cancer: An Observational Retrospective Cohort Study in the United States”","authors":"Catherine W Saltus, Z. Vassilev, J. Zong, B. Calingaert, E. Andrews, M. Soriano-Gabarró, J. Kaye","doi":"10.1155/2019/3425982","DOIUrl":"https://doi.org/10.1155/2019/3425982","url":null,"abstract":"[This corrects the article DOI: 10.1155/2019/4387415.].","PeriodicalId":87076,"journal":{"name":"Clinical prostate cancer","volume":"146 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-07-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"74492820","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Alexandra Lindsey Zune Djomkam, Theodore Beyeme Sala, Clarisse Baari Memba, D. L. Njimoh
Background. HPC2/ELAC2 has been identified as a prostate cancer (PC) susceptibility gene. Ser- Leu changes at amino acid 217 have been one of the most studied variants of this gene. Several reports have shown association of this variant with PC in samples of men drawn from families with hereditary PC and even sporadic cases. Aim. This study aimed at assessing this association and the prevalence of the Ser217Leu variant of ELAC2 in populations of the Littoral Region of Cameroon. Method. 103 PC case subjects and 80 randomly selected controls identified from the study population participated in the study. 2 milliliters of blood samples was collected from each of the consented participants and used for human genomic DNA extraction and genotyping of the ELAC2 gene by the nonenzymatic salting out and PCR-RFLP methods, respectively. Results. The frequencies of the wild type (SS), heterozygous mutant (SL), and homozygous mutant (LL) genotypes were, respectively, 28.2%, 49.5%, and 22.3% in prostate cancer patients and 28.8%, 67.5%, and 3.7% in controls. Comparing the LL with SS and (SL+LL) with SS showed that the presence of two copies of the L allele confers a high risk of prostate cancer as compared to the presence of only one L allele which presents no risk of prostate cancer (OR = 6.080 and 1.030, respectively). Analysis of our results also suggested an association (P = 0.0012) of the Ser217Leu variant with increased risk of prostate cancer. Conclusion. Alterations in the ELAC2 gene contribute to prostate cancer susceptibility in men living in the Littoral Region of Cameroon.
{"title":"Prevalence of the Ser217Leu Variant of the ELAC2 Gene and Its Association with Prostate Cancer in Population of the Littoral Region of Cameroon","authors":"Alexandra Lindsey Zune Djomkam, Theodore Beyeme Sala, Clarisse Baari Memba, D. L. Njimoh","doi":"10.1155/2019/5974928","DOIUrl":"https://doi.org/10.1155/2019/5974928","url":null,"abstract":"Background. HPC2/ELAC2 has been identified as a prostate cancer (PC) susceptibility gene. Ser- Leu changes at amino acid 217 have been one of the most studied variants of this gene. Several reports have shown association of this variant with PC in samples of men drawn from families with hereditary PC and even sporadic cases. Aim. This study aimed at assessing this association and the prevalence of the Ser217Leu variant of ELAC2 in populations of the Littoral Region of Cameroon. Method. 103 PC case subjects and 80 randomly selected controls identified from the study population participated in the study. 2 milliliters of blood samples was collected from each of the consented participants and used for human genomic DNA extraction and genotyping of the ELAC2 gene by the nonenzymatic salting out and PCR-RFLP methods, respectively. Results. The frequencies of the wild type (SS), heterozygous mutant (SL), and homozygous mutant (LL) genotypes were, respectively, 28.2%, 49.5%, and 22.3% in prostate cancer patients and 28.8%, 67.5%, and 3.7% in controls. Comparing the LL with SS and (SL+LL) with SS showed that the presence of two copies of the L allele confers a high risk of prostate cancer as compared to the presence of only one L allele which presents no risk of prostate cancer (OR = 6.080 and 1.030, respectively). Analysis of our results also suggested an association (P = 0.0012) of the Ser217Leu variant with increased risk of prostate cancer. Conclusion. Alterations in the ELAC2 gene contribute to prostate cancer susceptibility in men living in the Littoral Region of Cameroon.","PeriodicalId":87076,"journal":{"name":"Clinical prostate cancer","volume":"37 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-06-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"83130866","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2019-01-01DOI: 10.1007/978-3-030-32656-2
S. Dehm, D. Tindall
{"title":"Prostate Cancer: Cellular and Genetic Mechanisms of Disease Development and Progression","authors":"S. Dehm, D. Tindall","doi":"10.1007/978-3-030-32656-2","DOIUrl":"https://doi.org/10.1007/978-3-030-32656-2","url":null,"abstract":"","PeriodicalId":87076,"journal":{"name":"Clinical prostate cancer","volume":"2 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"90390743","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2018-09-26DOI: 10.5772/INTECHOPEN.77327
A. Ziaei
Prostate cancer (PCa) is the most frequently diagnosed non-cutaneous male malignancy and one of the leading causes of cancer-related mortality in the United States. Biologic heterogeneity of PCa results is different presentations ranging from indolent to highly aggressive tumors with high morbidity and mortality. Due to this broad range of clinical behavior, it is required to differentiate clinically significant PCa (csPCa) tumors and reduce detection of indolent cancers. PCa is generally diagnosed with non-targeted systematic trans-rectal ultrasound (TRUS)-guided biopsy in patients with elevated prostate serum antigen (PSA) or abnormal digital rectal examination (DRE). Non-targeted systematic TRUS as the typical imaging modality for assessing the prostate, samples only a small part of the gland with a high possibly that the biopsy results may not catch the most aggressive tumor in the gland accurately. Multi-parametric (MP) magnetic resonance imaging (MRI), as the most specific and sensitive imaging modality in PCa management, has been reported to be the reference standard for prostate imaging endorsed. However, there are a variety of interpretive pitfalls, which have been reported to be encountered at mpMRI of the prostate. The purpose of this chapter is to provide a summary of the cur - rent advances in accurate detection of PCa.
{"title":"Advances in Medical Imaging Technology for Accurate Detection of Prostate Cancer","authors":"A. Ziaei","doi":"10.5772/INTECHOPEN.77327","DOIUrl":"https://doi.org/10.5772/INTECHOPEN.77327","url":null,"abstract":"Prostate cancer (PCa) is the most frequently diagnosed non-cutaneous male malignancy and one of the leading causes of cancer-related mortality in the United States. Biologic heterogeneity of PCa results is different presentations ranging from indolent to highly aggressive tumors with high morbidity and mortality. Due to this broad range of clinical behavior, it is required to differentiate clinically significant PCa (csPCa) tumors and reduce detection of indolent cancers. PCa is generally diagnosed with non-targeted systematic trans-rectal ultrasound (TRUS)-guided biopsy in patients with elevated prostate serum antigen (PSA) or abnormal digital rectal examination (DRE). Non-targeted systematic TRUS as the typical imaging modality for assessing the prostate, samples only a small part of the gland with a high possibly that the biopsy results may not catch the most aggressive tumor in the gland accurately. Multi-parametric (MP) magnetic resonance imaging (MRI), as the most specific and sensitive imaging modality in PCa management, has been reported to be the reference standard for prostate imaging endorsed. However, there are a variety of interpretive pitfalls, which have been reported to be encountered at mpMRI of the prostate. The purpose of this chapter is to provide a summary of the cur - rent advances in accurate detection of PCa.","PeriodicalId":87076,"journal":{"name":"Clinical prostate cancer","volume":"13 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2018-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"74881584","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2018-09-26DOI: 10.5772/INTECHOPEN.76372
S. Ayub
The biggest challenge in prostate cancer treatment is to understand the signaling mecha- nisms controlling disease progression. In this context, microRNAs assume huge importance and have recently become an attractive area of research. MicroRNAs are naturally occurring, single-stranded, small non-coding RNAs of 19–25 nucleotides that regulate gene expression. MicroRNAs function as oncogenes or tumor-suppressor genes, and their deregulation is a common feature of human cancers including prostate cancer. Among deregulated microRNAs in prostate cancer, some microRNAs are directly under androgen receptor signaling control and function as the effectors of androgen signaling. Recent findings have shown that apoptosis antagonizing transcription factor (AATF) gene encodes a microRNA designated as miR-2909 that plays an important role in prostate cancer progression. miR-2909 is identified as an androgen-regulated microRNA acting as a novel effector of androgen/androgen receptor signaling. It enhances the proliferation potential of prostate cancer cells and assists in prostate cancer survival under reduced androgen levels by maintaining a positive feedback loop with AR. miR-2909 exerts its oncogenic effects via multiple mechanisms including attenuation of tumor-suppressive effects of TGFβ signaling by directly targeting TGFBR2 and via STAT1 pathway and upregulation of ISGylation pathway through SOCS3/STAT1 pathway.
{"title":"Role of miR-2909 in Prostate Carcinogenesis","authors":"S. Ayub","doi":"10.5772/INTECHOPEN.76372","DOIUrl":"https://doi.org/10.5772/INTECHOPEN.76372","url":null,"abstract":"The biggest challenge in prostate cancer treatment is to understand the signaling mecha- nisms controlling disease progression. In this context, microRNAs assume huge importance and have recently become an attractive area of research. MicroRNAs are naturally occurring, single-stranded, small non-coding RNAs of 19–25 nucleotides that regulate gene expression. MicroRNAs function as oncogenes or tumor-suppressor genes, and their deregulation is a common feature of human cancers including prostate cancer. Among deregulated microRNAs in prostate cancer, some microRNAs are directly under androgen receptor signaling control and function as the effectors of androgen signaling. Recent findings have shown that apoptosis antagonizing transcription factor (AATF) gene encodes a microRNA designated as miR-2909 that plays an important role in prostate cancer progression. miR-2909 is identified as an androgen-regulated microRNA acting as a novel effector of androgen/androgen receptor signaling. It enhances the proliferation potential of prostate cancer cells and assists in prostate cancer survival under reduced androgen levels by maintaining a positive feedback loop with AR. miR-2909 exerts its oncogenic effects via multiple mechanisms including attenuation of tumor-suppressive effects of TGFβ signaling by directly targeting TGFBR2 and via STAT1 pathway and upregulation of ISGylation pathway through SOCS3/STAT1 pathway.","PeriodicalId":87076,"journal":{"name":"Clinical prostate cancer","volume":"53 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2018-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"91248363","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2018-09-26DOI: 10.5772/INTECHOPEN.73515
A. Ali, G. Halldén
Prostate cancer (PCa) is the fifth most common cause of cancer-related deaths in men globally. Androgen receptor (AR) signalling plays a vital role in initiation and progression and antiandrogens are standard of care first-line therapeutics. However, resistance frequently develops resulting in metastatic castration-resistant prostate cancer (mCRPC). Management of CRPC is currently chemotherapy and/or radiotherapy but is mostly palliative due to rapid development of resistance. The need for novel approaches to eliminate mCRPC is compelling; a promising option is replication-selective (oncolytic) adenoviruses with demonstrated efficacy in preclinical models of multidrug-resistant PCa. The safety of various viral mutants has been confirmed in numerous clinical trials with minimal toxicity in patients. Importantly, oncolytic adenoviruses synergise with the current standard of care for mCRPC even in treatment-resistant cells. In early phase I–II clinical trials, promising efficacy in patients with localised PCa was reported after intratumoural administration, and phase III trials are underway. To enable systemic delivery, for targeting of mCRPC, further developments are necessary because of the short half-life of the adenoviral mutants in human blood. Current progress in preventing the high- affinity binding of adenovirus to erythrocytes, hepatocyte uptake, and elimination by hepatic Kupffer cells will be described.
{"title":"Development of Oncolytic Adenoviruses for the Management of Prostate Cancer","authors":"A. Ali, G. Halldén","doi":"10.5772/INTECHOPEN.73515","DOIUrl":"https://doi.org/10.5772/INTECHOPEN.73515","url":null,"abstract":"Prostate cancer (PCa) is the fifth most common cause of cancer-related deaths in men globally. Androgen receptor (AR) signalling plays a vital role in initiation and progression and antiandrogens are standard of care first-line therapeutics. However, resistance frequently develops resulting in metastatic castration-resistant prostate cancer (mCRPC). Management of CRPC is currently chemotherapy and/or radiotherapy but is mostly palliative due to rapid development of resistance. The need for novel approaches to eliminate mCRPC is compelling; a promising option is replication-selective (oncolytic) adenoviruses with demonstrated efficacy in preclinical models of multidrug-resistant PCa. The safety of various viral mutants has been confirmed in numerous clinical trials with minimal toxicity in patients. Importantly, oncolytic adenoviruses synergise with the current standard of care for mCRPC even in treatment-resistant cells. In early phase I–II clinical trials, promising efficacy in patients with localised PCa was reported after intratumoural administration, and phase III trials are underway. To enable systemic delivery, for targeting of mCRPC, further developments are necessary because of the short half-life of the adenoviral mutants in human blood. Current progress in preventing the high- affinity binding of adenovirus to erythrocytes, hepatocyte uptake, and elimination by hepatic Kupffer cells will be described.","PeriodicalId":87076,"journal":{"name":"Clinical prostate cancer","volume":"19 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2018-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"86045245","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2018-09-26DOI: 10.5772/INTECHOPEN.77259
H. Köseoğlu
Any disruption in the intracellular functions ranging from DNA transcription to protein ligand binding as well as intercellular communication may cause cellular transformation to malignant cell in the proper microenvironment when it could escape from the immune system. In this chapter, specifically, genetic alterations playing role in the prostate cancer are intended to be reviewed briefly under the subheadings of genomic instability and the hallmarks of cancer which are sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling the replicative immortality, inducing angiogenesis, activating invasion and progression to metastatic disease, reprogramming of the energy metabolism and evading immune destruction.
{"title":"Genetics in the Prostate Cancer","authors":"H. Köseoğlu","doi":"10.5772/INTECHOPEN.77259","DOIUrl":"https://doi.org/10.5772/INTECHOPEN.77259","url":null,"abstract":"Any disruption in the intracellular functions ranging from DNA transcription to protein ligand binding as well as intercellular communication may cause cellular transformation to malignant cell in the proper microenvironment when it could escape from the immune system. In this chapter, specifically, genetic alterations playing role in the prostate cancer are intended to be reviewed briefly under the subheadings of genomic instability and the hallmarks of cancer which are sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling the replicative immortality, inducing angiogenesis, activating invasion and progression to metastatic disease, reprogramming of the energy metabolism and evading immune destruction.","PeriodicalId":87076,"journal":{"name":"Clinical prostate cancer","volume":"28 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2018-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"85004974","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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