Fiducial markers visibility and artefacts in prostate cancer radiotherapy multi-modality imaging

Abstract Background In this study, a novel pelvic phantom was developed and used to assess the visibility and presence of artefacts from different types of commercial fiducial markers (FMs) on multi-modality imaging relevant to prostate cancer. Methods and materials The phantom was designed with 3D printed hollow cubes in the centre. These cubes were filled with gel to mimic the prostate gland and two parallel PVC rods were used to mimic bones in the pelvic region. Each cube was filled with gelatine and three unique FMs were positioned with a clinically-relevant spatial distribution. The FMs investigated were; Gold Marker (GM) CIVCO, GM RiverPoint, GM Gold Anchor (GA) line and ball shape, and polymer marker (PM) from CIVCO. The phantom was scanned using several imaging modalities typically used to image prostate cancer patients; MRI, CT, CBCT, planar kV-pair, ExacTrac, 6MV, 2.5MV and integrated EPID imaging. The visibility of the markers and any observed artefacts in the phantom were compared to in-vivo scans of prostate cancer patients with FMs. Results All GMs were visible in volumetric scans, however, they also had the most visible artefacts on CT and CBCT scans, with the magnitude of artefacts increasing with FM size. PM FMs had the least visible artefacts in volumetric scans but they were not visible on portal images and had poor visibility on lateral kV images. The smallest diameter GMs (GA) were the most difficult GMs to identify on lateral kV images. Conclusion The choice between different FMs is also dependent on the adopted IGRT strategy. PM was found to be superior to investigated gold markers in the most commonly used modalities in the management of prostate cancer; CT, CBCT and MRI imaging.

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Evaluation of set-up errors and estimation of set-up margin during external beam radiation therapy of prostate cancer using electronic portal imaging device (EPID)

Journal of Radiotherapy in Practice ◽

10.1017/s1460396921000297 ◽

2021 ◽

pp. 1-8

Author(s):

Daryoush Khoramian ◽

Soroush Sistani ◽

Bagher Farhood

Keyword(s):

Prostate Cancer ◽

Radiation Therapy ◽

Target Volume ◽

External Beam Radiation ◽

Beam Radiation ◽

Cancer Radiotherapy ◽

Imaging Device ◽

Portal Images ◽

Set Up ◽

Prostate Cancer Radiotherapy

Abstract Aim: In radiation therapy, accurate dose distribution in target volume requires accurate treatment setup. The set-up errors are unwanted and inherent in the treatment process. By achieving these errors, a set-up margin (SM) of clinical target volume (CTV) to planning target volume (PTV) can be determined. In the current study, systematic and random set-up errors that occurred during prostate cancer radiotherapy were measured by an electronic portal imaging device (EPID). The obtained values were used to propose the optimum CTV-to-PTV margin in prostate cancer radiotherapy. Materials and methods: A total of 21 patients with prostate cancer treated with external beam radiation therapy (EBRT) participated in this study. A total of 280 portal images were acquired during 12 months. Gross, population systematic (Σ) and random (σ) errors were obtained based on the portal images in Anterior–Posterior (AP), Medio-Lateral (ML) and Superior–Inferior (SI) directions. The SM of CTV to PTV were then calculated and compared by using the formulas presented by the International Commission on Radiation Units and Measurements (ICRU) 62, Stroom and Heijmen and Van Herk et al. Results: The findings showed that the population systematic errors during prostate cancer radiotherapy in AP, ML and SI directions were 1·40, 1·95 and 1·94 mm, respectively. The population random errors in AP, ML and SI directions were 2·09, 1·85 and 2·29 mm, respectively. The SM of CTV to PTV calculated in accordance with the formula of ICRU 62 in AP, ML and SI directions were 2·51, 2·68 and 3·00 mm, respectively. And according to Stroom and Heijmen, formula were 4·23, 5·19 and 5·48 mm, respectively. And Van Herk et al. formula were 4·96, 6·17 and 6·45 mm, respectively. Findings: The SM of CTV to PTV in all directions, based on the formulas of ICRU 62, Stroom and Heijmen and van Herk et al., were equal to 2·73, 4·98 and 5·86 mm, respectively; these values were obtained by averaging the margins in all directions.

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Molecular imaging of orthotopic prostate cancer with nanobubble ultrasound contrast agents targeted to PSMA

Scientific Reports ◽

10.1038/s41598-021-84072-5 ◽

2021 ◽

Vol 11 (1) ◽

Author(s):

Yu Wang ◽

Al Christopher De Leon ◽

Reshani Perera ◽

Eric Abenojar ◽

Ramamurthy Gopalakrishnan ◽

...

Keyword(s):

Prostate Cancer ◽

Ultrasound Imaging ◽

Prostate Gland ◽

Ultrasound Contrast Agent ◽

Tumor Model ◽

Focal Therapy ◽

Ultrasound Contrast Agents ◽

Time Intensity Curve ◽

Ultrasound Contrast

AbstractUltrasound imaging is routinely used to guide prostate biopsies, yet delineation of tumors within the prostate gland is extremely challenging, even with microbubble (MB) contrast. A more effective ultrasound protocol is needed that can effectively localize malignancies for targeted biopsy or aid in patient selection and treatment planning for organ-sparing focal therapy. This study focused on evaluating the application of a novel nanobubble ultrasound contrast agent targeted to the prostate specific membrane antigen (PSMA-targeted NBs) in ultrasound imaging of prostate cancer (PCa) in vivo using a clinically relevant orthotopic tumor model in nude mice. Our results demonstrated that PSMA-targeted NBs had increased extravasation and retention in PSMA-expressing orthotopic mouse tumors. These processes are reflected in significantly different time intensity curve (TIC) and several kinetic parameters for targeted versus non-targeted NBs or LUMASON MBs. These, may in turn, lead to improved image-based detection and diagnosis of PCa in the future.

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Computerized estimation of patient setup errors in portal images based on localized pelvic templates for prostate cancer radiotherapy

Journal of Radiation Research ◽

10.1093/jrr/rrs043 ◽

2012 ◽

Vol 53 (6) ◽

pp. 961-972 ◽

Cited By ~ 6

Author(s):

Hidetaka Arimura ◽

Wataru Itano ◽

Yoshiyuki Shioyama ◽

Norimasa Matsushita ◽

Taiki Magome ◽

...

Keyword(s):

Prostate Cancer ◽

Cancer Radiotherapy ◽

Setup Errors ◽

Patient Setup ◽

Portal Images ◽

Prostate Cancer Radiotherapy

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Dual PI3 K/mTOR inhibition reduces prostate cancer bone engraftment altering tumor-induced bone remodeling

Tumor Biology ◽

10.1177/1010428318771773 ◽

2018 ◽

Vol 40 (4) ◽

pp. 101042831877177 ◽

Cited By ~ 2

Author(s):

Andrea Mancini ◽

Alessandro Colapietro ◽

Simona Pompili ◽

Andrea Del Fattore ◽

Simona Delle Monache ◽

...

Keyword(s):

Prostate Cancer ◽

Cancer Patients ◽

Therapeutic Potential ◽

Disease Free Survival ◽

Bone Lesions ◽

Metastatic Progression ◽

Mtor Inhibition ◽

Osteoblast Activity

Morbidity in advanced prostate cancer patients is largely associated with bone metastatic events. The development of novel therapeutic strategies is imperative in order to effectively treat this incurable stage of the malignancy. In this context, Akt signaling pathway represents a promising therapeutic target able to counteract biochemical recurrence and metastatic progression in prostate cancer. We explored the therapeutic potential of a novel dual PI3 K/mTOR inhibitor, X480, to inhibit tumor growth and bone colonization using different in vivo prostate cancer models including the subcutaneous injection of aggressive and bone metastatic (PC3) and non-bone metastatic (22rv1) cell lines and preclinical models known to generate bone lesions. We observed that X480 both inhibited the primary growth of subcutaneous tumors generated by PC3 and 22rv1 cells and reduced bone spreading of PCb2, a high osteotropic PC3 cell derivative. In metastatic bone, X480 inhibited significantly the growth and osteolytic activity of PC3 cells as observed by intratibial injection model. X480 also increased the bone disease-free survival compared to untreated animals. In vitro experiments demonstrated that X480 was effective in counteracting osteoclastogenesis whereas it stimulated osteoblast activity. Our report provides novel information on the potential activity of PI3 K/Akt inhibitors on the formation and progression of prostate cancer bone metastases and supports a biological rationale for the use of these inhibitors in castrate-resistant prostate cancer patients at high risk of developing clinically evident bone lesions.

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Embigin Promotes Prostate Cancer Progression by S100A4-Dependent and-Independent Mechanisms

Cancers ◽

10.3390/cancers10070239 ◽

2018 ◽

Vol 10 (7) ◽

pp. 239 ◽

Cited By ~ 3

Author(s):

I Ruma ◽

Rie Kinoshita ◽

Nahoko Tomonobu ◽

Yusuke Inoue ◽

Eisaku Kondo ◽

...

Keyword(s):

Prostate Cancer ◽

Cancer Patients ◽

Cancer Progression ◽

Immunoglobulin Superfamily ◽

Prostate Cancer Progression ◽

Transmembrane Glycoprotein ◽

Mtorc1 Signaling ◽

Ampk Activity ◽

In Vivo Growth

Embigin, a transmembrane glycoprotein belonging to the immunoglobulin superfamily, is involved in prostate and mammary gland development. As embigin’s roles in cancer remain elusive, we studied its biological functions and interaction with extracellular S100A4 in prostate cancer progression. We found by a pull-down assay that embigin is a novel receptor for S100A4, which is one of the vital cancer microenvironment milleu. Binding of extracellular S100A4 to embigin mediates prostate cancer progression by inhibition of AMPK activity, activation of NF-κB, MMP9 and mTORC1 signaling, and inhibition of autophagy, which increase prostate cancer cell motility. We also found that embigin promotes prostate cancer growth, spheroid- and colony-forming ability, and survival upon chemotherapy independently of S100A4. An in vivo growth mouse model confirmed the importance of embigin and its cytoplasmic tail in mediating prostate tumor growth. Moreover, embigin and p21WAF1 can be used to predict survival of prostate cancer patients. Our results demonstrated for the first time that the S100A4-embigin/AMPK/mTORC1/p21WAF1 and NF-κB/MMP9 axis is a vital oncogenic molecular cascade for prostate cancer progression. We proposed that embigin and p21WAF1 could be used as prognostic biomarkers and a strategy to inhibit S100A4-embigin binding could be a therapeutic approach for prostate cancer patients.

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Is it essential to use fiducial markers during cone-beam CT-based radiotherapy for prostate cancer patients?

Japanese Journal of Radiology ◽

10.1007/s11604-016-0590-y ◽

2016 ◽

Vol 35 (1) ◽

pp. 3-9 ◽

Cited By ~ 4

Author(s):

Berna A. Yildirim ◽

Cem Onal ◽

Yemliha Dolek

Keyword(s):

Prostate Cancer ◽

Cancer Patients ◽

Cone Beam Ct ◽

Cone Beam ◽

Fiducial Markers

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LINC01006 facilitates cell proliferation, migration and invasion in prostate cancer through targeting miR-34a-5p to up-regulate DAAM1

Cancer Cell International ◽

10.1186/s12935-020-01577-1 ◽

2020 ◽

Vol 20 (1) ◽

Author(s):

Enhui Ma ◽

Qianqian Wang ◽

Jinhua Li ◽

Xinqi Zhang ◽

Zhenjia Guo ◽

...

Keyword(s):

Prostate Cancer ◽

Prostate Gland ◽

Inhibitory Effect ◽

Luciferase Reporter ◽

Migration And Invasion ◽

Protein Coding ◽

Novel Target

Abstract Background Prostate cancer (PCa) is a kind of malignancy occurring in the prostate gland. Substantial researches have proved the major role of long noncoding RNAs (lncRNAs) in PCa. However, the role of long intergenic non-protein coding RNA 1006 (LINC01006) in PCa has not been investigated yet. Methods RT-qPCR was used to examine the expression levels of LINC01006 and its downstream targets. The function of LINC01006 in PCa was tested by in vitro and in vivo assays. With application of RNA pull down, RNA immunoprecipitation (RIP) and luciferase reporter assays, the interaction among LINC01006, miR-34a-5p and disheveled associated activator of morphogenesis 1 (DAAM1) were verified. Results LINC01006 expression presented high in PCa cell lines. LINC01006 silencing suppressed cell proliferative, migratory, invasive capacities while accelerated apoptotic rate. Besides, LINC01006 knockdown also suppressed tumor growth and metastasis in vivo. Furthermore, miR-34a-5p, a tumor suppressor in PCa, was sponged by LINC01006. Moreover, DAAM1 was targeted by miR-34a-5p and promoted PCa progression. More intriguingly, rescue assays suggested that the inhibitory effect of LINC01006 knockdown on PCa development was offset by DAAM1 overexpression. Conclusions LINC01006 promoted PCa progression by sponging miR-34a-5p to up-regulate DAAM1, providing a novel target for PCa therapy.

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