scholarly journals The mechanisms and managements of hormone-therapy resistance in breast and prostate cancers

2005 ◽  
Vol 12 (3) ◽  
pp. 511-532 ◽  
Author(s):  
K-M Rau ◽  
H-Y Kang ◽  
T-L Cha ◽  
S A Miller ◽  
M-C Hung
Keyword(s):  
Hormone Receptors ◽  
Locally Advanced ◽  
Endocrine System ◽  
Therapy Resistance ◽  
The United States ◽  
Breast And Prostate Cancer ◽  
Prostate Cancers ◽  
Locally Advanced Tumors ◽  
Underlying Mechanisms ◽  
Clinical Potential

Breast and prostate cancer are the most well-characterized cancers of the type that have their development and growth controlled by the endocrine system. These cancers are the leading causes of cancer death in women and men, respectively, in the United States. Being hormone-dependent tumors, antihormone therapies usually are effective in prevention and treatment. However, the emergence of resistance is common, especially for locally advanced tumors and metastatic tumors, in which case resistance is predictable. The phenotypes of these resistant tumors include receptorpositive, ligand-dependent; receptor-positive, ligand-independent; and receptor-negative, ligand-independent. The underlying mechanisms of these phenotypes are complicated, involving not only sex hormones and sex hormone receptors, but also several growth factors and growth factor receptors, with different signaling pathways existing alone or together, and with each pathway possibly linking to one another. In this review, we will discuss the potential mechanisms of antihormonetherapy resistance in breast and prostate cancers, especially focusing on the similarities and differences of these two cancers. We will also discuss novel agents that have been applied in clinical practice or with clinical potential in the future.

scholarly journals Calcium cytotoxicity sensitizes prostate cancer cells to standard-of-care treatments for locally advanced tumors

2020 ◽  
Vol 11 (12) ◽  
Author(s):  
Alessandro Alaimo ◽  
Marco Lorenzoni ◽  
Paolo Ambrosino ◽  
Arianna Bertossi ◽  
Alessandra Bisio ◽  
...  
Keyword(s):  
Cancer Cells ◽  
Transient Receptor Potential ◽  
Locally Advanced ◽  
Hormonal Treatment ◽  
Receptor Potential ◽  
Standard Of Care ◽  
Therapy Resistance ◽  
Cation Channel ◽  
Transient Receptor ◽  
Locally Advanced Tumors

AbstractTherapy resistance is a major roadblock in oncology. Exacerbation of molecular dysfunctions typical of cancer cells have proven effective in twisting oncogenic mechanisms to lethal conditions, thus offering new therapeutic avenues for cancer treatment. Here, we demonstrate that selective agonists of Transient Receptor Potential cation channel subfamily M member 8 (TRPM8), a cation channel characteristic of the prostate epithelium frequently overexpressed in advanced stage III/IV prostate cancers (PCa), sensitize therapy refractory models of PCa to radio, chemo or hormonal treatment. Overall, our study demonstrates that pharmacological-induced Ca2+ cytotoxicity is an actionable strategy to sensitize cancer cells to standard therapies.

Female sex steroid induced gallbladder epithelium changes and gallstone deposits in female hamsters: TEM and SEM aspects

1993 ◽  
Vol 51 ◽  
pp. 354-355
Author(s):  
S. Karkare ◽  
J. Gilloteaux ◽  
T. R. Kelly
Keyword(s):  
Hormone Receptors ◽  
Corn Oil ◽  
Estrogen Therapy ◽  
Gallstone Formation ◽  
The United States ◽  
Sex Steroid ◽  
Estradiol Valerate ◽  
Surface Epithelium ◽  
Female Sex ◽  
Purina Chow

Approximately 1 million people in the United States alone develop gallstones each year. The incidence is higher in women than in men and the ratio being 4 ≥ 1. A correlation has also been suggested between oral contraceptives and cholelithiasis. In addition, postmenopausal or cancer estrogen therapy has been reported to be a factor responsible for gallstone formation. Female sex hormone receptors have been detected not only in the gallbladder musculature, but also in its epithelium. As a follow up to experiments effectuated in the male and the ovariectomized Syrian hamster, this report shows that, a combination of a low cholesterol diet with female sex steroid treatment contributes to the formation of gallstone-like deposits, while modifying the surface epithelium morphology. Syrian hamsters (F1B strain, BioBreeders, Watertown MA) were housed under 12h light: 12 h dark cycle, at 20 °C, fed Purina chow and water ad libitum. Several duration/treatment groups were studied, but this report will focus on data obtained with the group injected weekly with estradiol valerate (E weekly, s.c. 8-10 μg/100 g.b.w., in corn oil) and with i.m. medroxyprogesterone acetate (DepoProvera Upjohn Co., Kalamazoo, MI; 8-10 mg/100 g.b.w.) for a 3-month period. Other parameters (blood and bile) were also studied but not reported here.

scholarly journals CBP/p300: Critical Co-Activators for Nuclear Steroid Hormone Receptors and Emerging Therapeutic Targets in Prostate and Breast Cancers

Cancers ◽  
2021 ◽  
Vol 13 (12) ◽  
pp. 2872
Author(s):  
Aaron R. Waddell ◽  
Haojie Huang ◽  
Daiqing Liao
Keyword(s):  
Breast Cancer ◽  
Prostate Cancer ◽  
Tumor Growth ◽  
Signaling Pathways ◽  
Cell Cycle Progression ◽  
Hormone Receptors ◽  
Steroid Hormone Receptors ◽  
Breast Cancers ◽  
Creb Binding Protein ◽  
Breast And Prostate Cancer

The CREB-binding protein (CBP) and p300 are two paralogous lysine acetyltransferases (KATs) that were discovered in the 1980s–1990s. Since their discovery, CBP/p300 have emerged as important regulatory proteins due to their ability to acetylate histone and non-histone proteins to modulate transcription. Work in the last 20 years has firmly established CBP/p300 as critical regulators for nuclear hormone signaling pathways, which drive tumor growth in several cancer types. Indeed, CBP/p300 are critical co-activators for the androgen receptor (AR) and estrogen receptor (ER) signaling in prostate and breast cancer, respectively. The AR and ER are stimulated by sex hormones and function as transcription factors to regulate genes involved in cell cycle progression, metabolism, and other cellular functions that contribute to oncogenesis. Recent structural studies of the AR/p300 and ER/p300 complexes have provided critical insights into the mechanism by which p300 interacts with and activates AR- and ER-mediated transcription. Breast and prostate cancer rank the first and forth respectively in cancer diagnoses worldwide and effective treatments are urgently needed. Recent efforts have identified specific and potent CBP/p300 inhibitors that target the acetyltransferase activity and the acetytllysine-binding bromodomain (BD) of CBP/p300. These compounds inhibit AR signaling and tumor growth in prostate cancer. CBP/p300 inhibitors may also be applicable for treating breast and other hormone-dependent cancers. Here we provide an in-depth account of the critical roles of CBP/p300 in regulating the AR and ER signaling pathways and discuss the potential of CBP/p300 inhibitors for treating prostate and breast cancer.

scholarly journals Regulation of mRNA Translation by Hormone Receptors in Breast and Prostate Cancer

Cancers ◽  
2021 ◽  
Vol 13 (13) ◽  
pp. 3254
Author(s):  
Jianling Xie ◽  
Eric P. Kusnadi ◽  
Luc Furic ◽  
Luke A. Selth
Keyword(s):  
Prostate Cancer ◽  
Protein Synthesis ◽  
Causes Of Death ◽  
Hormone Receptors ◽  
Mrna Translation ◽  
Estrogen Receptor Α ◽  
Growth And Survival ◽  
Cancer Types ◽  
Breast And Prostate Cancer ◽  
Hormone Signalling

Breast and prostate cancer are the second and third leading causes of death amongst all cancer types, respectively. Pathogenesis of these malignancies is characterised by dysregulation of sex hormone signalling pathways, mediated by the estrogen receptor-α (ER) in breast cancer and androgen receptor (AR) in prostate cancer. ER and AR are transcription factors whose aberrant function drives oncogenic transcriptional programs to promote cancer growth and progression. While ER/AR are known to stimulate cell growth and survival by modulating gene transcription, emerging findings indicate that their effects in neoplasia are also mediated by dysregulation of protein synthesis (i.e., mRNA translation). This suggests that ER/AR can coordinately perturb both transcriptional and translational programs, resulting in the establishment of proteomes that promote malignancy. In this review, we will discuss relatively understudied aspects of ER and AR activity in regulating protein synthesis as well as the potential of targeting mRNA translation in breast and prostate cancer.

scholarly journals Magnetic Resonance–Guided Prostate Ablation

2019 ◽  
Vol 36 (05) ◽  
pp. 351-366
Author(s):  
David A. Woodrum ◽  
Akira Kawashima ◽  
Krzysztof R. Gorny ◽  
Lance A. Mynderse
Keyword(s):  
Prostate Cancer ◽  
Prediction Models ◽  
Focal Therapy ◽  
The United States ◽  
Management Approach ◽  
Low Grade ◽  
Intermediate Risk ◽  
Screening Programs ◽  
Risk Prostate Cancer ◽  
Prostate Cancers

AbstractIn 2019, the American Cancer Society (ACS) estimates that 174,650 new cases of prostate cancer will be diagnosed and 31,620 will die due to the prostate cancer in the United States. Prostate cancer is often managed with aggressive curative intent standard therapies including radiotherapy or surgery. Regardless of how expertly done, these standard therapies often bring significant risk and morbidity to the patient's quality of life with potential impact on sexual, urinary, and bowel functions. Additionally, improved screening programs, using prostatic-specific antigen and transrectal ultrasound-guided systematic biopsy, have identified increasing numbers of low-risk, low-grade “localized” prostate cancer. The potential, localized, and indolent nature of many prostate cancers presents a difficult decision of when to intervene, especially within the context of the possible comorbidities of aggressive standard treatments. Active surveillance has been increasingly instituted to balance cancer control versus treatment side effects; however, many patients are not comfortable with this option. Although active debate continues on the suitability of either focal or regional therapy for the low- or intermediate-risk prostate cancer patients, no large consensus has been achieved on the adequate management approach. Some of the largest unresolved issues are prostate cancer multifocality, limitations of current biopsy strategies, suboptimal staging by accepted imaging modalities, less than robust prediction models for indolent prostate cancers, and safety and efficiency of the established curative therapies following focal therapy for prostate cancer. In spite of these restrictions, focal therapy continues to confront the current paradigm of therapy for low- and even intermediate-risk disease. It has been proposed that early detection and proper characterization may play a role in preventing the development of metastatic disease. There is level-1 evidence supporting detection and subsequent aggressive treatment of intermediate- and high-risk prostate cancer. Therefore, accurate assessment of cancer risk (i.e., grade and stage) using imaging and targeted biopsy is critical. Advances in prostate imaging with MRI and PET are changing the workup for these patients, and advances in MR-guided biopsy and therapy are propelling prostate treatment solutions forward faster than ever.

Hyperfractionated-Accelerated Radiotherapy Followed by Radical Surgery in Locally Advanced Tumors of the Oral Cavity

2006 ◽  
Vol 182 (3) ◽  
pp. 157-163 ◽  
Author(s):  
Ulrike Hoeller ◽  
Iris Biertz ◽  
Sebastian Flinzberg ◽  
Silke Tribius ◽  
Reiner Schmelzle ◽  
...  
Keyword(s):  
Oral Cavity ◽  
Radical Surgery ◽  
Locally Advanced ◽  
Accelerated Radiotherapy ◽  
Locally Advanced Tumors ◽  
Advanced Tumors
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