Elevated serum progastrin-releasing peptide (31-98) in metastatic and androgen-independent prostate cancer patients

The Prostate ◽  
2002 ◽  
Vol 51 (2) ◽  
pp. 84-97 ◽  
Author(s):  
Masahiro Yashi ◽  
Osamu Muraishi ◽  
Yutaka Kobayashi ◽  
Akihiko Tokue ◽  
Hiroshi Nanjo
Keyword(s):  
Prostate Cancer ◽  
Cancer Patients ◽  
Elevated Serum ◽  
Androgen Independent

scholarly journals Oral low-dose dexamethasone for androgen-independent prostate cancer patients

2010 ◽  
Vol 1 (1) ◽  
pp. 73-79 ◽  
Author(s):  
AKIRA KOMIYA ◽  
MASAKI SHIMBO ◽  
HIROYOSHI SUZUKI ◽  
TAKASHI IMAMOTO ◽  
TOMONORI KATO ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cancer Patients ◽  
Low Dose ◽  
Androgen Independent

Phase II Trial of Oxaliplatin and Capecitabine After Progression to First-Line Chemotherapy in Androgen-Independent Prostate Cancer Patients

2010 ◽  
pp. 1 ◽  
Author(s):  
J. M. Gasent Blesa ◽  
V. Giner Marco ◽  
V. Giner-Bosch ◽  
P. Cerezuela ◽  
V. Alberola Candel
Keyword(s):  
Prostate Cancer ◽  
Cancer Patients ◽  
Phase Ii ◽  
Phase Ii Trial ◽  
First Line ◽  
Line Chemotherapy ◽  
Androgen Independent

scholarly journals MP28-11 ELEVATED SERUM GAMMA-GLUTAMYLTRANSFERASE IS AN ADVERSE PROGNOSTIC FACTOR IN CASTRATION-RESISTANT PROSTATE CANCER PATIENTS TREATED WITH ENZALUTAMIDE

2019 ◽  
Vol 201 (Supplement 4) ◽  
Author(s):  
Kosuke Takemura* ◽  
Masaya Ito ◽  
Yasukazu Nakanishi ◽  
Madoka Kataoka ◽  
Kazumasa Sakamoto ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Prognostic Factor ◽  
Cancer Patients ◽  
Elevated Serum ◽  
Castration Resistant Prostate Cancer ◽  
Gamma Glutamyltransferase ◽  
Adverse Prognostic Factor ◽  
Castration Resistant

Prior estrogen therapy as a predictor of response to subsequent estramustine-based therapy in androgen-independent prostate cancer patients

2004 ◽  
Vol 22 (14_suppl) ◽  
pp. 4595-4595 ◽  
Author(s):  
J. A. Garcia ◽  
V. Weinberg ◽  
B. I. Rini ◽  
J. E. Rosenberg ◽  
C. J. Ryan ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cancer Patients ◽  
Estrogen Therapy ◽  
Androgen Independent

scholarly journals Interleukin-10 Induces Expression of Neuroendocrine Markers and PDL1 in Prostate Cancer Cells

2020 ◽  
Vol 2020 ◽  
pp. 1-12 ◽  
Author(s):  
Abrar Samiea ◽  
Jeff S. J. Yoon ◽  
Christopher J. Ong ◽  
Amina Zoubeidi ◽  
Thomas C. Chamberlain ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Androgen Receptor ◽  
Cancer Cells ◽  
Cancer Patients ◽  
Cancer Cell ◽  
Immune Cells ◽  
Prostate Cancer Cell ◽  
Elevated Serum ◽  
Interleukin 10 ◽  
Prostate Cancer Cells

Interleukin-10 (IL10) is best studied for its inhibitory action on immune cells and ability to suppress an antitumour immune response. But IL10 also exerts direct effects on nonimmune cells such as prostate cancer epithelial cells. Elevated serum levels of IL10 observed in prostate and other cancer patients are associated with poor prognosis. After first-line androgen-deprivation therapy, prostate cancer patients are treated with androgen receptor antagonists such as enzalutamide to inhibit androgen-dependent prostate cancer cell growth. However, development of resistance inevitably occurs and this is associated with tumour differentiation to more aggressive forms such as a neuroendocrine phenotype characterized by expression of neuron specific enolase and synaptophysin. We found that treatment of prostate cancer cell lines in vitro with IL10 or enzalutamide induced markers of neuroendocrine differentiation and inhibited androgen receptor reporter activity. Both also upregulated the levels of PDL1, which could promote tumour survival in vivo through its interaction with the immune cell inhibitory receptor PD1 to suppress antitumour immunity. These findings suggest that IL10’s direct action on prostate cancer cells could contribute to prostate cancer progression independent of IL10’s suppression of host immune cells.

scholarly journals Determination of Reference Values for Total PSA, F/T and PSAD According to Prostatic Volume in Japanese Prostate Cancer Patients with Slightly Elevated Serum PSA Levels

1999 ◽  
Vol 29 (12) ◽  
pp. 617-622 ◽  
Author(s):  
M. Kuriyama ◽  
H. Uno ◽  
H. Watanabe ◽  
H. Yamanaka ◽  
Y. Saito ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cancer Patients ◽  
Reference Values ◽  
Elevated Serum ◽  
Prostatic Volume ◽  
Total Psa

scholarly journals Suppression of TRPM7 Inhibited Hypoxia-Induced Migration and Invasion of Androgen-Independent Prostate Cancer Cells by Enhancing RACK1-Mediated Degradation of HIF-1α

2020 ◽  
Vol 2020 ◽  
pp. 1-15 ◽  
Author(s):  
Fei Yang ◽  
Jiarong Cai ◽  
Hailun Zhan ◽  
Jie Situ ◽  
Wenbiao Li ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cell Migration ◽  
Cancer Cells ◽  
Cancer Patients ◽  
Molecular Mechanisms ◽  
Migration And Invasion ◽  
Annexin A1 ◽  
Prostate Cancer Cells ◽  
Cell Migration And Invasion ◽  
Androgen Independent

Transient receptor potential melastatin subfamily member 7 (TRPM7) was essential in the growth and metastatic ability of prostate cancer cells. However, the effects and the relevant molecular mechanisms of TRPM7 on metastasis of prostate cancer under hypoxic atmosphere remain unclear. This study investigated the role of TRPM7 in the metastatic ability of androgen-independent prostate cancer cells under hypoxia. First, data mining was carried out to disclose the relationship between the TRPM7 gene level and the survival of prostate cancer patients. Specific siRNAs were used to knockdown target genes. Western blotting and qPCR were employed to determine protein and gene expression, respectively. The gene transcription activity was evaluated by luciferase activity assay of promoter gene. The protein interaction was determined by coimmunoprecipitation. Wound healing and transwell assays were employed to evaluated cell migration and invasion, respectively. Open access database results showed that high expression of TRPM7 was closely related to the poor survival of prostate cancer patients. Hypoxia simultaneously increased TRPM7 expression and induced HIF-1α accumulation in androgen-independent prostate cancer cells. Knockdown of TRPM7 significantly promoted HIF-1α degradation through the proteasome and inhibited EMT changes in androgen-independent prostate cancer cells under hypoxic condition. Moreover, TRPM7 knockdown increased the phosphorylation of RACK1 and strengthened the interaction between RACK1 and HIF-1α but attenuated the binding of HSP90 to HIF-1α. Whereas knockdown of RACK1 increased the binding of HSP90 to HIF-1α. Furthermore, both TRPM7 and HIF-1α knockdown significantly suppressed hypoxia-induced Annexin A1 protein expression, and suppression of HIF-1α/Annexin A1 signaling significantly inhibited hypoxia-induced cell migration and invasion of androgen-independent prostate cancer cells. Our findings demonstrate that TRPM7 knockdown promotes HIF-1α degradation via an oxygen-independent mechanism involving increased binding of RAKC1 to HIF-1α, and TRPM7-HIF-1α-Annexin A1 signaling axis plays a crucial role in the EMT, cell migration, and invasion of androgen-independent prostate cancer cells under hypoxic conditions.

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