scholarly journals Tumour cell survival mechanisms in lethal metastatic prostate cancer differ between bone and soft tissue metastases

2013 ◽  
Vol 230 (3) ◽  
pp. 291-297 ◽  
Author(s):  
Canan Akfirat ◽  
Xiaotun Zhang ◽  
Aviva Ventura ◽  
Dror Berel ◽  
Mary E Colangelo ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Soft Tissue ◽  
Cell Survival ◽  
Tumour Cell ◽  
Metastatic Prostate Cancer ◽  
Survival Mechanisms

scholarly journals p62/SQSTM1 is required for cell survival of apoptosis-resistant bone metastatic prostate cancer cell lines

The Prostate ◽  
2013 ◽  
Vol 74 (2) ◽  
pp. 149-163 ◽  
Author(s):  
Megan A. Chang ◽  
Micaela Morgado ◽  
Curtis R. Warren ◽  
Cimona V. Hinton ◽  
Mary C. Farach-Carson ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cell Survival ◽  
Cell Lines ◽  
Cancer Cell ◽  
Metastatic Prostate Cancer ◽  
Prostate Cancer Cell ◽  
Cancer Cell Lines ◽  
Prostate Cancer Cell Lines

Metastatic Prostate Cancer Presenting as Lower Extremity Soft Tissue Mass: A Rare Case Presentation

Urology ◽  
2017 ◽  
Vol 99 ◽  
pp. e27-e28
Author(s):  
Paulette Cutruzzula ◽  
Daniel C. Edwards ◽  
David Cahn ◽  
Carmen Tong ◽  
Dana Kivlin ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Soft Tissue ◽  
Lower Extremity ◽  
Rare Case ◽  
Metastatic Prostate Cancer ◽  
Soft Tissue Mass ◽  
Tissue Mass ◽  
Case Presentation

scholarly journals Snail regulates cell survival and inhibits cellular senescence in human metastatic prostate cancer cell lines

2010 ◽  
Vol 26 (6) ◽  
pp. 553-567 ◽  
Author(s):  
Modjtaba Emadi Baygi ◽  
Zahra Soheila Soheili ◽  
Ingo Schmitz ◽  
Shahram Sameie ◽  
Wolfgang A. Schulz
Keyword(s):  
Prostate Cancer ◽  
Cell Survival ◽  
Cell Lines ◽  
Cancer Cell ◽  
Cellular Senescence ◽  
Metastatic Prostate Cancer ◽  
Prostate Cancer Cell ◽  
Cancer Cell Lines ◽  
Prostate Cancer Cell Lines

Imaging metastatic prostate cancer with 18F-DCFBC PET/CT (DCFBC) and 18F-NaF PET/CT (NaF).

2017 ◽  
Vol 35 (6_suppl) ◽  
pp. 231-231
Author(s):  
Farhad Fakhrejahani ◽  
Maria Liza Lindenberg ◽  
Ethan S. Bargvall ◽  
Esther Mena ◽  
Baris Turkbey ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Soft Tissue ◽  
Functional Imaging ◽  
Metastatic Prostate Cancer ◽  
Whole Body ◽  
Inverse Association ◽  
Non Invasive ◽  
Imaging Results ◽  
Pet Ct ◽  
Antiandrogen Therapy

231 Background: Conventional imaging of advanced prostate cancer (computerized tomography and nuclear bone scintigraphy) is limited and indicates a need for a more specific molecular imaging probe. DCFBC is a radiolabeled PET agent that binds with high affinity to prostate specific membrane antigen (PSMA), which is overexpressed in almost all prostate cancers and through whole-body non-invasive functional imaging, may provide new information on the expression of PSMA. We compare the uptake of DCFBC in bone with respect to NaF PET/CT in metastatic prostate cancer patients. DCFBC has added capability to detect soft tissue metastasis whereas NaF is confined to secondary effects of bone disease. Methods: Subjects with known or suspected prostate cancer metastasis underwent DCFBC PET/CT imaging performed at 1 hour and 2 hours after IV bolus injection of 8 mCi of DCFBC. Patients also underwent a whole body NaF PET/CT scan within 3 weeks of DCFBC PET/CT to assess for bone metastases. Patients received 3 mCi of NaF IV bolus and then were imaged 1hour post injection. PSA levels and antiandrogen therapy status were obtained at the time of DCFBC imaging. Results: Fifteen patients have been preliminarily analyzed. PSA ranged from < .01 to 4379 ng/mL. NaF identified bone lesions in 10 patients but matching focal DCFBC uptake was only seen in 3 patients. DCFBC additionally showed lymph node metastasis in 1of these 3 patient. There were 5 patients without focal abnormal bone uptake on NaF or DCFBC. In this group, 4 of 5 patients had focal DCFBC uptake in lymph nodes or soft tissue lesions. Ten patients were on some form of androgen deprivation therapy (ADT). For those on ADT, 7 of 10 patients had positive findings on NaF, compared to 2 of 10 patients on DCFBC. Conclusions: DCFBC uptake in bone metastasis does not routinely correspond to focal NaF uptake which could be due to distinct mechanisms of tracer uptake and tumor biology. There is an inverse association in focal bone findings when comparing each tracer on antiandrogen therapy. Through whole-body non-invasive functional imaging and further study, DCFBC may prove useful in characterizing prostate cancer based on PSMA expression. Clinical trial information: NCT02190279.

scholarly journals Curcumin downregulates cell survival mechanisms in human prostate cancer cell lines

Oncogene ◽  
2001 ◽  
Vol 20 (52) ◽  
pp. 7597-7609 ◽  
Author(s):  
Asok Mukhopadhyay ◽  
Carlos Bueso-Ramos ◽  
Devasis Chatterjee ◽  
Panayotis Pantazis ◽  
Bharat B Aggarwal
Keyword(s):  
Prostate Cancer ◽  
Cell Survival ◽  
Cell Lines ◽  
Cancer Cell ◽  
Prostate Cancer Cell ◽  
Human Prostate ◽  
Human Prostate Cancer ◽  
Human Prostate Cancer Cell ◽  
Prostate Cancer Cell Lines ◽  
Survival Mechanisms

QUANTITATIVE ANALYSIS OF TUMOUR CELL BURDEN IN METASTATIC PROSTATE CANCER USING LYMPH NODE DISINTEGRATES

2008 ◽  
Vol 7 (3) ◽  
pp. 285
Author(s):  
D. Schilling ◽  
J. Hennenlotter ◽  
K. Sotlar ◽  
U. Nagele ◽  
U. Kühs ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Lymph Node ◽  
Quantitative Analysis ◽  
Tumour Cell ◽  
Metastatic Prostate Cancer

scholarly journals Primary multiple synchronous tumors: soft tissue sarcoma of the retroperitoneal space and metastatic prostate cancer

2020 ◽  
Vol 7 (2) ◽  
pp. 171-178
Author(s):  
O. A. Mailyan ◽  
K. Yu. Kanukoev ◽  
P. G. Berezin ◽  
K. M. Nyushko ◽  
V. A. Gorbach
Keyword(s):  
Prostate Cancer ◽  
Soft Tissue ◽  
Soft Tissue Sarcoma ◽  
Metastatic Prostate Cancer ◽  
Malignant Tumors ◽  
Soft Tissue Sarcomas ◽  
Cancer Recurrence ◽  
Relative Survival ◽  
Screening Tests ◽  
Multiple Malignancies

At the present time primary-multiple malignancies are of interest in connection with the frequency of prevalence, which remains at the rather high level and continues to grow up, therefore increasing the relevance of this pathology in clinical oncology and everyday practice. With the exception of the treatment of primary multiple malignancies requiring a multimodal approach, as well as in the case of the use of complex treatment in conjunction with chemotherapists and radiotherapy specialists. In the past three decades, the development of screening tests that prevent and detect some cancers at an early, more treatable stage, and treatment advances have increased the 5‑year relative survival rate for all cancers to 66%. In addition to concerns about cancer recurrence, survivors also worry about their risk of developing a new cancer. Prostate cancer is a leader in terms of morbidity and mortality in the world, just as often are found in combination with other malignant tumors. However, given the high detectability of prostate cancer, primary patients are currently receiving radical treatment, and if metastatic prostate cancer is detected, they are receiving drug treatment, which improves the survival and quality of life of patients. Soft tissue sarcomas are rare malignant tumors that develop in the connective tissues and remain poorly understood due to the fact that they make up less than 1% of all malignant diseases. One of the main methods for treating soft tissue sarcomas is the surgical method. Soft tissue sarcomas are difficult to treat and therefore it is imperative that surgeons and other specialists have experience in treating this disease. Studies show that patients with this pathology show better results if they receive treatment in specialized cancer centers that have experience in treating soft tissue sarcoma. This article demonstrates the clinical case of surgical treatment of a patient with primary multiple retroperitoneal tumors and metastatic prostate cancer.

Circulating tumor cells in patients with castration-resistant metastatic prostate cancer

2007 ◽  
Vol 25 (18_suppl) ◽  
pp. 5076-5076
Author(s):  
D. C. Danila ◽  
M. A. Leversha ◽  
R. Gonzalez-Espinoza ◽  
A. Anand ◽  
B. Gu ◽  
...  
Keyword(s):  
Gene Expression ◽  
Prostate Cancer ◽  
Bone Metastasis ◽  
Soft Tissue ◽  
Tumor Cells ◽  
Circulating Tumor Cells ◽  
Metastatic Prostate Cancer ◽  
Cellular Adhesion ◽  
Cellular Adhesion Molecule ◽  
Number Of Patients

5076 Background: Blood-based assays are urgently needed to provide molecular information on the specific targets expressed in tumor cells to optimize treatment selection. Antibody-capture technologies have been applied to isolate circulating tumor cells (CTC) from small volumes of peripheral blood from patients with progressive castrate metastatic prostate cancer. It has been demonstrated previously that CTC isolated from these patients represent authentic prostate cancer cells. Methods: CTC, positive for EpCAM (epithelial cellular adhesion molecule) and nuclear DAPI, and CD45 negative, were isolated from 120 patients with clinical castrate metastatic disease. All patients had rising PSA levels and were on stable treatment regimens at the time of CTC sampling. We tested the association between CTC counts and PSA levels, and the extent of disease to bone, and soft tissue metastasis by Wilcoxon rank sum. Fluorescence in situ hybridization was performed for AR and ERBB2 genes by an adapted method in CTC. Results: The average age in this patient cohort was 69 years, and median PSA at the time when CTC were drawn was 111 ng/mL (range 0.86–12147 ng/mL). The patterns of metastatic spread included disease in soft tissue only in 12 patients (10%), in bone and soft tissue in 67 (56%), and in bone only in 41 patients (34%). CTC counts ranged from 0 to 1958 cells per 7.5 mL of blood. A large number of patients (54, 45%) had 10 or more circulating tumor cells, while only 33 patients (27.5%) had 1 or less CTC per sample of blood. Significantly higher numbers of CTC were detected in patients with bone metastasis compared to those without bone metastasis (11 vs. 2.5, p<0.01). In patients with marked amplification of AR locus (five patients), tetraploidy was noted in the majority of cases (four cases). Two patients without AR amplification showed apparent tetraploidy, while no analyzed samples (nine) had amplification of ERBB2. Conclusions: The analysis of cancer-related gene alterations in CTC is feasible in a hospital-based laboratory. Further gene expression studies focused on the patients with higher numbers of CTC in correlation with clinical outcomes, as well as the investigation of CTC gene expression during specific treatments are under way. No significant financial relationships to disclose.

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