scholarly journals Manganese-enhanced MRI (MEMRI) in breast and prostate cancers: exploring the potential role of calcium receptors

2019 ◽  
Author(s):  
Gabriella Baio ◽  
Marina Fabbi ◽  
Michele Cilli ◽  
Francesca Rosa ◽  
Simona Boccardo ◽  
...  

ABSTRACTProceduresTo assess the relationship between Manganese Enhanced Magnetic Resonance Imaging (MEMRI) and the expression of calcium receptors in human prostate and breast cancer animal models.MethodsNOD/SCID mice were inoculated with MDA-MB-231 breast cancer cells and prostate PC3 cancer cells to develop orthotopic or pseudometastatic cancer animal models. Mice were studied on a clinical 3T scanner by using a prototype birdcage coil before and after intravenous injection of MnCl2. Assessment of receptor’s status was carried out after the MR images acquisition by immunohistochemistry on excised tumours.ResultsManganese contrast enhancement in breast or prostate cancer animal models well correlated with CaSR expression (p<0.01), whereas TRPV6 expression levels appeared not relevant to the Mn uptake.ConclusionMEMRI appears an efficient tool to characterize human breast and prostate cancer animal models in the presence of different expression level of CaSR.

2006 ◽  
Vol 25 (7) ◽  
pp. 395-404 ◽  
Author(s):  
P W Harvey ◽  
D J Everett ◽  
C J Springall

Historically, hyperprolactinaemia has been considered of low toxicological relevance when detected in toxicity studies, and even mammary carcinogenesis induced in the rat by prolactin excess has been considered of no relevance to humans. However, recent findings from human epidemiology and molecular biology suggests that prolactin is a risk factor for human breast cancer, and probably prostate cancer. Therefore, this new evidence should be considered in the various decisions to develop and license a new drug or chemical if the compound causes hyperprolactinaemia. This emerging evidence suggests that prolactin can also be produced locally from human breast cancer cells, and that, regardless of source (ie, pituitary or autocrine/paracrine production from cancer cells), prolactin is mitogenic, stimulates proliferation and suppresses apoptosis in breast and prostate cancer cells. This review outlines the evidence that hyperprolactinaemia should be considered a toxicological adverse effect and concludes that prolactin-induced rodent mammary carcinogenesis is relevant to humans and is not species-specific. The effects of prolactin on the prostate gland are also discussed; hyperprolactinaemia may be an additional risk factor for prostate cancer and this also requires consideration in toxicological risk assessments. The implications of increased prolactin secretion as an adverse effect for regulatory toxicology of drugs and chemicals, and in high risk patients receiving therapeutic drugs with hyperprolactinaemic side effects, is discussed. Alteration of prolactin level is also a novel mechanism that requires consideration in endocrine disruption research, since both endogenous oestrogens and also xenoestrogens stimulate prolactin secretion or affect prolactin receptors.


PLoS ONE ◽  
2020 ◽  
Vol 15 (9) ◽  
pp. e0224414
Author(s):  
Gabriella Baio ◽  
Marina Fabbi ◽  
Michele Cilli ◽  
Francesca Rosa ◽  
Simona Boccardo ◽  
...  

2020 ◽  
Author(s):  
Mahdieh Montazeri ◽  
Benyamin Hoseini ◽  
Neda Firouraghi ◽  
Fatemeh Kiani ◽  
Hosein Raouf-Mobini ◽  
...  

Abstract Background: Breast and prostate cancers are the most common gender-specific malignancies. In developing countries, screening of all population at risk of cancers is impractical because of the healthcare resource limitations. Thus, determining the high-risk areas of Cancers might be an important step to conduct a screening program at high-risk areas. This study explores potential high-risk clusters in the incidence pattern of breast and prostate cancers in southern Iran. Methods: This cross-sectional study was conducted in the province of Kerman, South Iran. Patient data were aggregated at the county and district levels and the incidence rate per 100,000 people for both breast and prostate cancer were calculated. We used the natural break classification with five classes to produce descriptive maps. A spatial clustering analysis ( Anselin Local Moran’s I ) was used to identify potential clusters and outliers in the pattern of these cancers from 2014 to 2017. Results: The Age-Standardised Incidence Rate of breast cancer showed an increase from 29.93 to 32.27 cases per 100,000 people and prostate cancer from 13.93 to 15.47 cases per 100,000 during 2014–2017. Cluster analysis at the county level identified high-high clusters of breast cancer in the North-West of the province for all years, but the analysis at the district level showed high-high clusters for only two of the years. Furthermore, cluster analysis at the county and district levels of prostate cancer also identified high-high clusters in the North-West of the province for two years. Conclusions: North-West Kerman had a significantly higher incidence rate of both breast and prostate cancer. These findings may help to design tailored screening and surveillance systems. Furthermore, this study generates new hypotheses to test potential relationships between environmental risk factors and incidence of cancers in areas with higher cancer risk.


Cancers ◽  
2020 ◽  
Vol 12 (7) ◽  
pp. 1812
Author(s):  
Paola Maroni ◽  
Paola Bendinelli

Bone is the primarily preferred site for breast and prostate cancer to metastasize. Bone metastases are responsible for most deaths related to breast and prostate cancer. The bone’s particular microenvironment makes it conducive for the growth of cancer cells. Studies on bone metastasis have focused on the interaction between cancer cells and the bone microenvironment. Osteocytes, the most common cell type of bone tissue, have received little attention in bone metastasis, although they are master signal sensors, integrators, and skeleton transducers. They play an important role in regulating bone mass by acting on both osteoblasts and osteoclasts, through the release of proteins such as sclerostin, Dickkopf-1 (DKK-1), and fibroblast growth factor 23 (FGF23). Osteocytes have been extensively re-evaluated, in light of their multiple functions: with different experimental approaches, it has been shown that, indeed, osteocytes are actively involved in the colonization of bone tissue by cancer cells. The present review focuses on recent research on the role that osteocytes play in bone metastasis of breast and prostate cancers. Moreover, the studies here summarized open up perspectives for new therapeutic approaches focused on modulating the activity of osteocytes to improve the condition of the bone metastatic patients. A better understanding of the complex interactions between cancer cells and bone-resident cells is indispensable for identifying potential therapeutic targets to stop tumor progression and prevent bone metastases.


2004 ◽  
Vol 11 (4) ◽  
pp. 793-814 ◽  
Author(s):  
H E Jones ◽  
L Goddard ◽  
J M W Gee ◽  
S Hiscox ◽  
M Rubini ◽  
...  

De novo and acquired resistance to the anti-tumour drug gefitinib (ZD1839; Iressa), a specific epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI) has been reported. We have determined whether signalling through the IGF-I receptor (IGF-1R) pathway plays a role in the gefitinib-acquired resistance phenotype. Continuous exposure of EGFR-positive MCF-7-derived tamoxifen resistant breast cancer cells (TAM-R) to 1 μM gefitinib resulted in a sustained growth inhibition (90%) for 4 months before the surviving cells resumed proliferation. A stable gefitinib-resistant subline (TAM/TKI-R) was established after a further 2 months and this showed no detectable basal phosphorylated EGFR activity. Compared with the parental TAM-R cells, the TAM/ TKI-R cells demonstrated (a) elevated levels of activated IGF-1R, AKT and protein kinase C (PKC)δ, (b) an increased sensitivity to growth inhibition by the IGF-1R TKI AG1024 and (c) an increased migratory capacity that was reduced by AG1024 treatment. Similarly, the EGFR-positive androgen-independent human prostate cancer cell line DU145 was also continuously challenged with 1 μM gefitinib and, although substantial growth inhibition (60%) was seen initially, a gefitinib-resistant variant (DU145/TKI-R) developed after 3 months. Like their breast cancer counterparts, the DU145/TKI-R cells showed increases in the levels of components of the IGF-1R signalling pathway and an elevated sensitivity to growth inhibition by AG1024 compared with the parent DU145 cell line. Additionally, DU145/TKI-R cell migration was also decreased by this inhibitor. We have therefore concluded that in breast and prostate cancer cells acquired resistance to gefitinib is associated with increased signalling via the IGF-1R pathway, which also plays a role in the invasive capacity of the gefitinib-resistant phenotype.


2020 ◽  
Vol 28 (3) ◽  
pp. 399-405
Author(s):  
Fabrizio Fontana ◽  
Olga A. Babenko

Aim of this letter is to attract the attention of journal readers to the study of exosomes as an important direction in the development of Oncology, in particular, in the diagnosis and treatment of prostate cancer. Exosomes are produced by tumor cells and regulate proliferation, metastasis, and the development of chemoresistance. Their extraction from biological fluids allows further use of these vesicles as potential biomarkers of prostate cancer. In the future, exosomes can be successfully used in the delivery of drugs and other anti-tumor substances to cancer cells.


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