Methoxylpoly(ethylene glycol)‐retinoic acid Micelles Loaded with Dimethylcurcumin for Efficient Castration‐Resistant Prostate Cancer Therapy

2019 ◽  
Vol 4 (41) ◽  
pp. 12015-12021
Author(s):  
Hang Hu ◽  
Huan Zhou ◽  
Zihan Zhen ◽  
Zhe Wu ◽  
Rong Zhang ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Retinoic Acid ◽  
Cancer Therapy ◽  
Ethylene Glycol ◽  
Castration Resistant Prostate Cancer ◽  
Castration Resistant ◽  
Prostate Cancer Therapy

scholarly journals Glucocorticoid signaling delays castration-induced regression in murine models of prostate cancer

2021 ◽  
Author(s):  
Aerken Maolake ◽  
Renyuan Zhang ◽  
Kai Sha ◽  
Shalini Singh ◽  
Chunliu Pan ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Human Prostate ◽  
Murine Models ◽  
Castration Resistant Prostate Cancer ◽  
High Frequency Ultrasound ◽  
Over Expression ◽  
Castration Resistant ◽  
Glucocorticoid Signaling ◽  
Prostate Cancer Therapy ◽  
Prostate Cancers

Androgen deprivation therapy (ADT) is the mainstay therapy for recurrent and advanced prostate cancer. While human prostate cancers initially regress following ADT, many tumors fail this therapy and recur. To understand the response of prostate cancers to ADT, we have employed high frequency ultrasound imaging to track the kinetics of tumor volume in murine models of prostate cancer. Previously, we showed that normal (non-tumor) prostate regression begins within two days of castration. Following castration, murine prostate cancers also regress but only after a delay of 3-14 days, dependent on initial tumor size. Delayed regression is observed in two distinct mouse models (MYC over-expression, PTEN-deficient) implying that the genetic lesion which initiates carcinogenesis does not play a role. Intra-tumoral androgen levels are undetectable 16 hours post-castration, arguing that residual androgen signaling is not the cause of delayed regression. Castration induces tumor cell proliferation during this period. There is an increase in the active glucocorticoids, as well as glucocorticoid receptor (GR) mRNA and protein and a set of GR-regulated genes. A selective GR inhibitor eliminates the delayed regression phenotype in both models. Thus, GR signaling is activated following castration and transiently enhances tumor proliferation. This response to ADT resembles the GR-dependent mechanism of escape for prostate cancers that are resistant to anti-androgen therapies and may provide mechanistic insight into the development of castration resistant prostate cancer. If ADT-induced GR signaling is similar in human prostate cancers, simultaneous blockade of GR and androgen receptor signaling could improve prostate cancer therapy.

New Pharmacotherapies in the Treatment of Advanced Prostate Cancer

2010 ◽  
Vol 4 ◽  
pp. CMU.S5075
Author(s):  
Walid El-Ayass ◽  
Joelle El-Amm ◽  
Maneesh Jain ◽  
Jeanny B. Aragon-Ching
Keyword(s):  
Prostate Cancer ◽  
Advanced Prostate Cancer ◽  
Standard Treatment ◽  
Locally Advanced ◽  
Castration Resistant Prostate Cancer ◽  
Clinical Safety ◽  
Treatment Practice ◽  
Castration Resistant ◽  
Prostate Cancer Therapy ◽  
The Right

Recent drug approvals in the field of prostate cancer therapy have brought about a change in the treatment landscape of locally advanced and metastatic castration-resistant prostate cancer. While this improvement offers a welcoming change in the standard treatment practice of prostate cancer, questions remain with regard to the proper sequencing of the right therapy for the appropriate patient. This review highlights the pre-clinical, safety and clinical studies that help bring to the forefront the drugs recently approved for the treatment of advanced prostate cancer and offer some insights to its use.

scholarly journals Targeted Radionuclide Therapy of Prostate Cancer—From Basic Research to Clinical Perspectives

Molecules ◽  
2020 ◽  
Vol 25 (7) ◽  
pp. 1743 ◽  
Author(s):  
Malwina Czerwińska ◽  
Aleksander Bilewicz ◽  
Marcin Kruszewski ◽  
Aneta Wegierek-Ciuk ◽  
Anna Lankoff
Keyword(s):  
Prostate Cancer ◽  
Basic Research ◽  
Morbidity Rate ◽  
Castration Resistant Prostate Cancer ◽  
Mortality And Morbidity ◽  
Castration Resistant ◽  
Prostate Cancer Therapy ◽  
Specific Antigens ◽  
Almost All ◽  
New Generation

Prostate cancer is the most commonly diagnosed malignancy in men and the second leading cause of cancer-related deaths in Western civilization. Although localized prostate cancer can be treated effectively in different ways, almost all patients progress to the incurable metastatic castration-resistant prostate cancer. Due to the significant mortality and morbidity rate associated with the progression of this disease, there is an urgent need for new and targeted treatments. In this review, we summarize the recent advances in research on identification of prostate tissue-specific antigens for targeted therapy, generation of highly specific and selective molecules targeting these antigens, availability of therapeutic radionuclides for widespread medical applications, and recent achievements in the development of new-generation small-molecule inhibitors and antibody-based strategies for targeted prostate cancer therapy with alpha-, beta-, and Auger electron-emitting radionuclides.

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