Radiography/Radiology

Activity for 2016

Activity No: A5(16)

Topic

Radiology and prostate cancer

Articles

Prostate cancer – Double vision but solitary lesion Interventional uroradiology in the management of prostate cancer

Diffusion-weighted MRI for detecting prostate tumour in men at increased genetic risk

Approved for (2) Clinical Continuing Educational Unit’s (CEU’s)

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Prostate Cancer - Double Vision but Solitary LesionLim HY*1, Perchyonok Y2, Fitt G2, Lokan J3, Wada M4, Fabinyi G5, Azad A1, Cher L1 and Gan HK1

1Department of Medical Oncology, Austin Health, Heidelberg, Australia2Department of Radiology, Austin Health, Heidelberg, Australia3Department of Anatomical Pathology, Austin Health, Heidelberg, Australia4Radiation Oncology Centre, Austin Health, Heidelberg, Australia5Department of Neurosurgery, Austin Health, Heidelberg, Australia*Corresponding author: Lim HY, Department of Medical Oncology, Austin Health, PO Box 5555, Heidelberg, Victoria 3084, Australia, Tel: +61 431 175 522 / +61 3 9496 5763, Fax: +61 3 9457 6698, E-mail: HuiYin.Lim@austin.org.au

Case Report Open Access

Citation: Lim HY, Perchyonok Y, Fitt G, Lokan J, Wada M, et al. (2014) Prostate Cancer - Double Vision but Solitary Lesion. J Case Rep Stud 2(2): 201. doi: 10.15744/2348-9820.1.501

AbstractA 53 year old man with a background of castrate-sensitive prostate cancer on intermittent androgen deprivation therapy (ADT) presented with right sixth nerve palsy secondary to a solitary right petroclival lesion involving adjacent dura and bone. The clinical and imaging characteristics of the lesion were consistent with a number of differential diagnoses (including metastatic prostate cancer, meningioma and chondrosarcoma). The patient initially declined biopsy and ADT was recommenced but the lesion continued to enlarge despite an excellent biochemical response. A subsequent biopsy of the petroclival mass demonstrated a WHO grade I meningioma and the patient proceeded to have definitive stereotactic radiotherapy. This case illustrates an unusual solitary skull base lesion in a man with prostate cancer. Whilst bony metastases, usually multiple, in the skeleton are common, solitary skull or brain lesions should be investigated as alternate diagnoses are likely in such circumstance.

IntroductionProstate cancer is the most common cancer in Australian men and the third most common cause of cancer deaths, comprising 13% of all cancer deaths in Australian men [1]. One in five Australian men will develop prostate cancer by age 85 with 1 in 25 risk of dying from prostate cancer [1]. However, many cases are indolent and patients often die from competing risks. Whilst the risk of mortality is only 3% in low risk patients, it increases in intermediate risk (7%) and high risk disease (18%) [2].

Keywords: Petroclival lesion; Prostate cancer; Meningioma; MetastasisList of Abbreviations: ADT-Androgen deprivation therapy; CT-Computed tomography; FDG-avid PET-Fludeoxyglucose-avid positron emission tomography; PSA-Prostate specific antigen

Approximately 90% of patients with metastatic prostate cancer develop bony metastases, which are characteristically multiple osteoblastic lesions to the axial skeleton [3]. Bone metastases to the skull (8%) and skull base (1.7%) are much less frequent [3,4]. Similarly, patients with parenchymal central nervous system disease are also rare, being reported in less than 1% of patients [5], although the prognosis is usually very poor in such cases [5,6]. Where these cases are reported, most (79%) involve the brain parenchyma itself although some (21%) involve dura only [5]. Importantly, the finding of solitary metastasis to the central nervous system from prostate cancer is exceedingly rare [5].

Here, we report a patient with castrate-sensitive prostate cancer in biochemical remission who presented with progressive right sixth nerve palsy secondary to a solitary right petroclival lesion involving adjacent dura and bone.

Case ReportA 53-year-old man was referred by his primary physician for the management of an asymptomatic screen-detected prostate cancer, with a prostate specific antigen (PSA) level of 22.5 (institutional reference range 0.0 – 3.5 μg/L). He subsequently underwent a radical prostatectomy and lymph node dissection in March 2010 which revealed a T3bN1 carcinoma (Gleason 4+5) with lymphovascular and perineural invasion, positive margins and extra-capsular extension in one of two involved lymph nodes. Post-

Received Date: January 16, 2014 Accepted Date: April 28, 2014 Published Date: April 30, 2014

Volume 2 | Issue 2Journal of Case Reports and Studies

ISSN: 2348-9820

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Figure 1: (a) Axial post contrast T1 MR. (b) Bone window CT images demonstrate a durally-based, homogeneously enhancing petroclival mass (arrow) with associated bone lysis when compared to the bone density on the left. (c) Corresponding MRI 10 months and (d) 18 months later with increase in lesion size and progressive bone invasion. (e) High power images (400x) showing characteristic morphological features of meningioma with syncytia, nests and whorls of meningothelial cells. (f) A ki67 stain of the lesion showing moderately elevated ki67 proliferative index.

In July 2011, the patient began experiencing mild diplopia on right gaze which progressed over several months. Examination findings were consistent with mild right-sided sixth nerve palsy. Investigations showed a 10 mm x 3 mm extra-axial, durally-based, homogenously enhancing mass arising from the petroclival ligament. There was evidence of bony invasion with lysis but no sclerosis (Figure 1a & 1b). Concurrently, his PSA rose from 0.01 μg/L to 0.04 μg/L over 5 months but importantly, re-staging CT and bone scan showed no evidence of other visceral or bony disease. The lesion was only minimally FDG-avid on PET. The patient was offered a biopsy to differentiate between the differential diagnoses of a solitary prostate cancer metastasis or, more likely, an unrelated pathology such as meningioma or chondrosarcoma. The patient declined a biopsy and requested recommencement of ADT for presumed petroclival metastasis from prostate cancer.

With ADT, the patient’s PSA fell steadily over the next 6 months but unfortunately, his diplopia worsened and the lesion continued to enlarge (Figure 1c & 1d). He also developed subtle signs of right trigeminal nerve involvement, manifested by reduced corneal sensation. The patient agreed to a biopsy and limited decompression of the lesion. Histopathology demonstrated a grade 1 meningioma with an elevated ki67 index, without evidence of carcinoma (Figure 1e & 1f). The patient underwent definitive stereotactic radiotherapy 50 Gy in 20 fractions prescribed to 90% isodose (5 fractions per week over 4 weeks), with stabilisation of his neurological deficits

operatively, his PSA nadir level was 4 μg/L but without evidence of macroscopic metastases. He was commenced on ADT with goserelin acetate for 6 months and achieved biochemical complete remission (PSA<0.01) in March 2011. However, treatment was poorly tolerated and an intermittent schedule was adopted.

DiscussionThis case highlights the diagnostic challenge of a solitary base of skull lesion in a patient with prostate cancer presenting with a sixth nerve palsy. Although cases of diplopia from cranial nerve palsies [6,7] or ocular rectus muscle invasion [8] from metastatic prostate cancer have been reported, these are relatively rare. Whilst it would have been tempting to make a presumptive diagnosis

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This is a rare case of a concomitant atypical meningioma, possibly further stimulated by the use of ADT for prostate cancer treatment. Solitary lesions in the brain or skull of patients with a history of prostate cancer should be aggressively investigated given their rarity and the range of alternate diagnoses which can present similarly. The prognosis and management of many of these alternate diagnoses also differ substantially from those of metastatic prostate cancer and a high index of suspicion would aid an earlier diagnosis.

Conclusion

References

2) Daskivich TJ, Fan KH, Koyama T, Albertsen PC, Goodman M, et al. (2013) Effect of age, tumor risk, and comorbidity on competing risks for survival in a U.S. population-based cohort of men with prostate cancer. Ann Intern Med 158: 709-17.3) Bubendorf L, Schöpfer A, Wagner U, Sauter G, Moch H, et al. (2000) Metastatic patterns of prostate cancer: An autopsy study of 1589 patients. Hum Pathol 31: 578-83.4) Long MA, Husband JE (1999) Features of unusual metastases from prostate cancer. Br J Radiol 72: 933-41.

5) Tremont-Lukats IW, Bobustuc G, Lagos GK, Lolas K, Kyritsis AP, et al. (2003) Brain metastasis from prostate carcinoma: The M. D. Anderson Cancer Center experience. Cancer 98: 363-8.6) McAvoy CE, Kamalarajab S, Best R, Rankin S, Bryars J, et al. (2002) Bilateral third and unilateral sixth nerve palsies as early signs of metastatic prostatic carcinoma. Eye 16: 749-537) Riemenschneider MJ, Beseoglu K, Hanggi D, Reifenberger G (2009) Prostate adenocarcinoma metastasis in the pituitary gland. Arch Neurol 66: 1036-7.

8) Leonard GD, Battiwalla M, Stockle JB, Harris RA, Monahan BP, et al. (2003) Extraocular muscle palsy from metastatic prostate cancer. Lancet Oncol 4: 358.9) Fervenza FC, Wolanskyj AP, Eklund HE, Richardson RL (2000) Brain metastasis: an unusual complication from prostatic adenocarcinoma. Mayo Clin Proc 75: 79-82.10) Salvati M, Frati A, Russo N, Brogna C, Piccirilli M, et al. (2005) Brain metastasis from prostate cancer: Report of 13 cases and critical analysis of the literature. J Exp Clin Cancer Res 24: 203-7.11) Pallini R, Sabatino G, Doglietto F, Lauretti L, Fernandez E, et al. (2009) Clivus metastases: Report of seven patients and literature review. Acta Neurochir 151: 291-6.12) Sade B, Chahlavi A, Krishnaney A, Nagel S, Choi E, et al. (2007) World Health Organization Grades II and III meningiomas are rare in the cranial base and spine. Neurosurgery 61: 1194-813) Radhakrishnan K, Mokri B, Parisi JE, O’Fallon WM, Sunku J, et al. (1995) The trends in incidence of primary brain tumors in the population of Rochester, Minnesota. Ann Neurol 37: 67-73.14) Zeidman LA, Ankenbrandt WJ, Du H, Paleologos N, Vick NA (2008) Growth rate of non-operated meningiomas. J Neurol 255: 891-5.

15) Chen TY, Lee HJ, Wu TC, Tsui YK, Wu TC (2011) Intracranial dural metastatic prostate cancer can mimic meningioma: a report of two cases. Clin Imaging 35: 391-4.16) Lath CO, Khanna PC, Gadewar S, Patkar DP (2005) Intracranial metastasis from prostatic adenocarcinoma simulating a meningioma. Australas Radiol 49: 497-500.

17) Lyons MK, Drazkowski JF, Wong WW, Fitch TR, Nelson KD (2006) Metastatic prostate carcinoma mimicking meningioma: case report and review of the literature. Neurologist 12: 48-52.18) van Groeninghen JC, Kiesel L, Winkler D, Zwirner M (1998) Effects of luteinising-hormone-releasing hormone on nervous-system tumours. Lancet 352: 372-3.

19) Lee KL, Terris MK (2003) Luteinizing hormone-releasing hormone agonists and meningioma: a treatment dilemma. Urology 62:351

20) Hirota Y, Tachibana O, Uchiyama N, Hayashi Y, Nakada M, et al. (2009) Gonadotrophin-releasing hormone (GnRH) and its receptor in human meningiomas. Clin Neurol Neurosurg 111:127-33.

1) Australian Institute of Health and Welfare (2012) ACIM (Australian Cancer Incidence and Mortality), Canberra, Australia

Our patient was ultimately diagnosed and treated for a meningioma. The diagnosis of meningioma was considered in his initial differential diagnosis but the rarity of skull base meningiomas (2.8%) [12] and the rapid rate of change argued for a diagnosis of metastatic disease, given that most meningiomas tend to remain asymptomatic and are slow growing (one series showed 35 of 57 patients displayed no growth over a 29-month follow-up period) [13,14]. There is also sparse literature showing that metastatic prostate cancer can simulate meningiomas [15-17]. One intriguing possibility is the hypothesis that the unusual behaviour of the meningioma in this case may be the result of using luteinising hormone releasing hormone (LHRH) agonists as there is emerging data that some meningiomas may be regulated by the LHRH receptor expression [18-20].

of metastatic prostate cancer, a number of features in this case raised the possibility for an alternate diagnosis: the general rarity of solitary metastatic lesions in the brain or skull; the relatively low absolute levels of PSA; and the radiological appearance of the osteolytic focus in the petroclival region. It should be noted that a negative PSA does not exclude the presence of brain metastasis [9,10]. However, a diagnostic biopsy was initially declined by the patient on several occasions. The most common causes of clival lesions are primary tumours such as chordomas or chondrosarcomas (83%) with the rest being meningiomas and metastatic disease from sites such as the lung, prostate, liver or skin (melanoma) [11].

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40 n APPLIED RADIOLOGY©

www.appliedradiology.com September 2015

Jeffrey C. Hellinger, MD, MBA; Seth Blacksberg, MD, MBA; Jonathan Haas, MD; and John Melnick, MD

Interventional uroradiology in the management of prostate cancer

Prostate cancer is the most common cancer arising in men and the second most com-mon cause of death among men. In 2011,

nearly 210,000 new cases were diagnosed, with just over 27,000 deaths related to prostate can-cer.1 For 2015, it is estimated that the rate of new cases will be approximately 220,000. The major-ity of patients continue to be 65 or older and often have co-morbid disease in other body systems.2

As promoted throughout September—Prostate Cancer Awareness Month in the United States—routine screening through physical examinations and measurement of prostate-specific antibody are important for early detection. When detected early, most prostate cancers are confined to the gland without metastatic spread. Presentation as early, localized disease versus advanced and potentially metastatic disease will impact diag-nostic and therapeutic considerations.

Depending upon the stage of disease and extent of metastatic spread, management may include radiation therapy, minimally invasive ablations, chemotherapy and/or surgery. Interventional radiologists can play a significant role along with urologists, medical oncologists and radiation oncologists in the care of these patients. The role of the interventional radiologist is enhanced when disease is confined to the prostate gland.

Image-guided urologic interventions for pros-tate cancer include diagnostic biopsies, fiducial marker placements for external beam radiation, ultrasound-guided and primary ablative thera-pies, and fluid collection drainages. Each proce-dure is performed in close collaboration with the management team. With correct patient selection and procedural preparation and technique, mor-

bidity and mortality are minimized for optimum patient outcomes.

Direct prostate gland biopsies most commonly occur with transrectal ultrasound (TRUS) guid-ance. Alternatively, magnetic resonance imaging (MRI) may be utilized for transrectal guidance. With both modalities, patients are typically placed in a decubitus position. Self-limiting hematuria may frequently occur. TRUS guided biopsies are relatively easy to perform in an outpatient office setting. MRI guidance offers more precise tumor localization, but requires greater procedural inten-sity and time, leading to higher costs. In select cases when a transrectal approach is not feasible, a trans-gluteal approach with computed tomography guidance many be a consideration.3

Current state-of-the-art external beam therapy for prostate cancer utilizes hypofractionation, in which a reduced number of higher therapeutic radiation doses are delivered to the tumor. This therapy is termed stereotactic body radiotherapy (SBRT) when performed with five or fewer frac-tions. One of the challenges with hypofractionation is the unpredictable movement of the prostate gland during treatment. This motion occurs as x, y, and z orthogonal translation and rotation, in part second-ary to bladder and rectal filling in addition to pros-tate interfraction transient inflammation.4 As SBRT uses smaller margins to allow for high daily radia-tion deposition, uncorrected prostate motion can result in suboptimal dose to the target and an exces-sive dose to surrounding nontarget structures. It is important therefore to track and correct prostate motion during SBRT.5

Under image guidance, fiducial markers can be placed into the prostate gland to track the prostate

Dr. Hellinger is the Direc-tor of Interventional Radiol-ogy, Lenox Hill Radiology and Medical Imaging, New York, NY; Dr. Blacksberg is Associate Director for Radiation Oncology, Win-throp-University Hospi-tal, Long Island, NY; Dr. Haas is Director of Radia-tion Oncology, Winthrop-University Hospital, Long Island, NY; and Dr. Melnick is Medical Director, Lenox Hill Radiology and Medical Imaging, New York.

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n 41September 2015

during treatment and then to correct for motion. Fiducial markers are particularly needed with the use of robotic accelerator radiation delivery SBRT systems, such as the Cyberknife (Accuray Inc., Sunnyvale, CA). The Cyberknife delivers isodose profiles directly to the prostate tumor, utilizing 1) a rapid dose fall-off for adjacent non-target structures and 2) real-time image guidance during radiation delivery to correct for the trans-lational and rotational changes in the prostate gland position. Real-time correction of motion is accomplished with two orthogonal digital x-ray monitoring of fiducial marker positions.

For image-guided fiducial placement, prior to Cyberknife planning gold fiducial markers are placed within the prostate gland, via a transperi-neal or transrectal approach under TRUS guid-ance. To employ 6-dimensional correction, at least 3 fiducials are required. Markers should be depos-ited with at least 2 cm of separation and at least a 15° angle between any fiducial triplets. A common methodology in our practice involves transperineal placement of the markers at the left base, left apex, right base, and right apex using double-fiducial loaded needles with a spacer between each fidu-cial (Figure 1). With optimal techniques, fiducial markers can be placed with minimal (<1mm) posi-tional migration at 1 week, potentially affording planning on the same day of marker implantation.6

Alternative image-guided ablative uroradio-logic interventions for prostate cancer include high intensity focused ultrasound (HIFU) and cryother-apy. HIFU utilizes 0.8 to 3.5MHz sound waves via transrectal probe, to cause hyerthermic tumor cell necrosis and destruction. MRI can be used dur-ing HIFU for contiguous temperature monitoring,

thermal dose mapping, and intraprocedural adjust-ments. Cryotherapy results in tumor-cell destruc-tion by freezing and thawing. Typically argon gas or liquid nitrogen is delivered for tumor freezing under TRUS guidance. A transrectal approach is used for delivering liquid nitrogen, while a trans-rectal or transperineal approach may be used for argon. Helium is utilized for warming, typically via the transurethral approach.7

Following radiation therapy, ablative thera-pies, and surgical resections for prostate can-cer, simple fluid collections and abscesses can occur within the pelvis. Diagnosis is typically made with CT, which is then utilized for proce-dural planning. Depending upon the location of the collection and adjacent viscera and vascular structures, drainage may occur via a transgluteal, transabdominal/pelvic, or transrectal approach under CT (transgluteal, transabdominal/pelvic) or ultrasound guidance (transrectal).

RefeRences1. Centers for Disease Control and Prevention. http://www.cdc.gov/cancer/prostate/statistics/. Accessed Aug. 24, 2015.2. American Cancer Society. http://www.cancer.org/cancer/prostatecancer/detailedguide/prostate-cancer-key-statistics. Accessed Aug. 24, 2015. 3. Goenka AH, Remer EM, Veniero JC, et al. CT-guided trans-gluteal biopsy for systematic random sampling of the pros-tate in patients without rectal access. Am J Roentgenol. 2015; 205(3):578-583.4. Xie, et al. Int J Radiat Oncol Biol Phys. 2008;72(1):m236-246.5. Lovelock DM, et al. Int J Radiat Oncol Biol Phys. 2015;91(3): 588-594.6. Kumar KA, Wu T, Tonlaar N, et al. Image-guided radiation therapy for prostate cancer: A computed tomography-based assessment of fiducial marker migration between placement and 7 days. Pract Radiat Oncol. 2015;5(4):241-247. 7. Nomura T, Mimata H. Focal therapy in the management of prostate cancer: An emerging approach for localized prostate cancer. Adv Urol. 2012; 2012:1-8.

FIGURE 1. Cyberknife treatment-planning pelvis CT demonstrating successfully placed prostate gland fiducial markers.

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European Journal of Radiology Open 1 (2014) 22–27

Diffusion-weighted MRI for detecting prostate tumour in men at increasedgenetic risk

Nandita M. deSouza a,∗, Veronica A. Morgan a, Elizabeth Bancroft b, S. Aslam Sohaib c,Sharon L. Giles a, Zsofia Kote-Jarai b, Elena Castro b, Steven Hazell d, Maysam Jafar a,

Rosalind Eeles b

a CRUK and EPSRC Cancer Imaging Centre, Institute of Cancer Research and Royal Marsden NHS Foundation Trust, Downs Road, Surrey SM2 5PT, UKb Genetics and Epidemiology, Institute of Cancer Research and Royal Marsden NHS Foundation Trust, Downs Road, Surrey SM2 5PT, UK

c Department of Radiology, Royal Marsden NHS Foundation Trust, Downs Road, Surrey SM2 5PT, UKd Department of Histopathology, Royal Marsden NHS Foundation Trust, Downs Road, Surrey SM2 5PT, UK

Received 21 August 2014; accepted 24 August 2014Available online 7 September 2014

Abstract

Background: Diffusion-weighted (DW)-MRI is invaluable in detecting prostate cancer. We determined its sensitivity and specificity and establishedinterobserver agreement for detecting tumour in men with a family history of prostate cancer stratified by genetic risk.Methods: 51 men with a family history of prostate cancer underwent T2-W + DW-endorectal MRI at 3.0 T. Presence of tumour was noted at rightand left apex, mid and basal prostate sextants by 2 independent observers, 1 experienced and the other inexperienced in endorectal MRI. Sensitivityand specificity against a 10-core sampling technique (lateral and medial cores at each level considered together) in men with >2× population riskbased on 71 SNP analysis versus those with lower genetic risk scores was established. Interobserver agreement was determined at a subject level.Results: Biopsies indicated cancer in 28 sextants in 13/51 men; 32 of 51 men had twice the population risk (>0.25) based on 71 SNP profiling.Sensitivity/specificity per-subject for patients was 90.0%/86.4% (high-risk) vs. 66.7%/100% (low-risk, observer 1) and 60.0%/86.3% (high-risk) vs.33.3%/93.8% (low-risk, observer 2) with moderate overall inter-observer agreement (kappa = 0.42). Regional sensitivities/specificities for high-riskvs. low-risk for observer 1 apex 72.2%/100% [33.3%/100%], mid 100%/93.1% [100%/97.3%], base 16.7%/98.3% [0%/100%] and for observer2 apex 36.4%/98.1% [0%/100%], mid 28.6%/96.5% [100%/100%], base 20%/100% [0%/97.3%] were poorer as they failed to detect multiplelesions.Conclusion: Endorectal T2W + DW-MRI at 3.0 T yields high sensitivity and specificity for tumour detection by an experienced observer inscreening men with a family history of prostate cancer and increased genetic risk.© 2014 The Authors. Published by Elsevier Ltd. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/3.0/).

Keywords: Prostate cancer; MRI; Diffusion-weighted; Genetic risk; Screening; Detection

Abbreviations: ADC, apparent diffusion coefficient; DW, diffusion-weighted; FoV, field of view; HIPAA, Health Insurance Portability andAccountability Act; iCOGS, Illumina Collaborative Oncological Gene-Environment Study; MRI, magnetic resonance imaging; PSA, prostate specificantigen; SNP, single nucleotide polymorphism; STARD, Standards for theReporting of Diagnostic Accuracy Studies; TR, repetition time; TE, time toecho; TRUS, transrectal ultrasound.

∗ Corresponding author at: CRUK/EPSRC Imaging Centre, MRI Unit, Insti-tute of Cancer Research and Royal Marsden NHS Foundation Trust, DownsRoad, Surrey SM2 5PT, UK. Tel.: +44 20 8661 3119/3289;fax: +44 20 8661 0846.

E-mail address: nandita.deSouza@icr.ac.uk (N.M. deSouza).

1. Introduction

Men with a strong family history of prostate cancer (definedas a first degree relative with histologically or death certificateproven prostate cancer diagnosed at <70 years or 2 relatives onthe same side of the family where at least one is diagnosed at <70years or ≥3 relatives on the same side of the family diagnosedat any age) carry an increased risk of the disease compared tothe general population [1,2]. Seventy-six single nucleotide poly-morphisms have been shown to be significantly associated with

http://dx.doi.org/10.1016/j.ejro.2014.08.0022352-0477/© 2014 The Authors. Published by Elsevier Ltd. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/3.0/).

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prostate cancer in these men [3,4]. The detection of prostatecancer in this population however, remains reliant on random,non-targetted multiple biopsies of the gland, which are painfuland carry a significant morbidity whilst not necessarily samp-ling a relevant lesion. Diffusion-weighted MRI, when used inconjunction with T2-W MRI has been shown to be sensitive atdetecting clinically significant prostate cancers [5] especiallywhen random sampling in men with raised prostate specificantigen (PSA) is initially negative [6]. Moreover, the quantifiedapparent diffusion coefficient (ADC), which reflects the waterdiffusivity in the extracellular space, is increasingly restricted astumours increase in cellularity [7] so that ADC correlates withGleason grade [8,9] and is invaluable in detecting significantcancers. DW-MRI is easy to implement as a standard techniqueon current MRI platforms, and an ADC map derived using scan-ner software can be visually assessed for the presence of tumouras an area of restricted diffusion, as well as being quantifiable.The purpose of this study therefore was to determine the sen-sitivity and specificity of T2W + DW-MRI as a screening toolin men with a family history of prostate cancer stratified bygenetic risk and establish interobserver agreement for detectingtumour.

2. Methods

2.1. Subjects

This pilot diagnostic accuracy study had Institutional ReviewBoard approval and was performed as a single institutionstudy at a National Cancer Centre. Ethical standards com-plied with the Helsinki Declaration of 1975 as revised in2013. Between January 2010 and July 2012, men aged 41–68years (mean 53.4 ± 8.5 years) with a positive family historyof prostate cancer defined as (i) one first degree relative withhistology or death-certificate proven prostate cancer at <70years, (ii) 2 relatives on the same side of the family withprostate cancer where one is diagnosed at <70 years or (iii)≥3 relatives on the same side of the family of any age,were invited into the study. Those with a previous cancerand with a terminal prognosis of <5 years or with a previ-ous diagnosis of prostate cancer but with a current negativebiopsy were excluded. Fifty-four patients were approachedto undergo MRI within this study: 2 declined because ofclaustrophobia, the third had a high body mass index andhad previously experienced discomfort being positioned in anMRI scanner, so declined. Fifty-one consecutive men willingto undergo endorectal MRI followed by a 10-core transrec-tal ultrasound guided biopsy therefore were prospectivelyrecruited. All subjects were imaged following written informedconsent. PSA was 1.9 ± 1.7 ng/mL (mean ± standard devia-tion). The median interval between imaging and subsequentbiopsy was 15 days (lower quartile 6.5 days, upper quar-tile 29 days). Although limited by the non-targetted approachto biopsy, transrectal ultrasound guided random sampling ofthe prostate remains the gold-standard for prostate cancerdiagnosis.

2.2. SNP analysis and scores

The participant’s DNA was genotyped on the iCOGS (Illu-mina, Collaborative Oncological Gene-Environment Study)chip. iCOGS is a custom Illumina iSelect genotyping array,designed to test genetic variants related to three hormone relatedcancers of which prostate cancer is one [3]. Data was availablefor 71 of the 76 previously identified known prostate cancersusceptibility SNPs; 61 were directly genotyped and for 10loci we used data for a proxy SNP with a linkage disequili-brium >0.75 (3). The cumulative SNP risk score for each patientwas calculated by summing 71 risk alleles using the weightedeffect (log-additive model) as estimated in previous studies [10].Patients were divided into those having a low risk (score <0.25)or high risk (score ≥0.25), where 0.25 represented twice thelifetime risk of 1 in 8 (0.125) in a normal population [11].

2.3. Imaging methods

Images were acquired on a 3 T Philips Achieva (Best,Netherlands) using an endorectal coil (Medrad Inc., PA, USA) incombination with an external phased array coil. The endorectalballoon was inflated with 60 ml of perfluorocarbon. Hyoscinebutyl bromide was administered routinely as an antiperistalticagent. T2-W images were obtained in 3 planes orthogonal tothe prostate (FSE, TR 2500 ms, TE 110 ms, FoV 14 cm, slicethickness 2.2 mm, matrix 220 × 184 extrapolated to 256 × 256)and were complemented by diffusion weighted images in thetransverse plane (single shot EPI, TR 5243 ms, TE 72 ms, b = 0,100, 800 s/mm2, FOV 180 mm, slice thickness 2.2 mm, matrix80 m × 71 m, extrapolated to 128 × 128). Whole pelvis imagingwas not deemed to be a requirement in this cohort.

2.4. Biopsy procedure and histology analysis

Ten cores were obtained using a random sampling technique(lateral and medial gland base, lateral and medial mid glandand apex from right and left lobes) under transrectal ultrasound(TRUS) guidance. The systematic biopsies were not formallyregistered to the MR data, although the MR images and reportswere available to the operator performing the biopsies, so thatvisual account could be taken of the position of any identifiedlesions. Routine antibiotic prophylaxis was administered withCiprofloxacin 500 mg twice daily and intrarectal Metronidazole1 g capsule 1–2 h prior to the procedure.

Sections obtained using 18-G Tru-cut needles were stainedwith haematoxylin and eosin and the presence or absence ofcancer and its Gleason grading were noted by a specialisturopathologist. For the purposes of comparison with imaging thelateral and medial cores at the base and mid gland of each sidewere scored together as either positive or negative for tumour.

2.5. Data analysis

Apparent diffusion coefficient (ADC) maps were derived forevery voxel in the image using all b-values and a monoexpo-nential fit of the data. Images were assessed by 2 observers; the

24 N.M. deSouza et al. / European Journal of Radiology Open 1 (2014) 22–27

first had a considerable experience of endorectal imaging and ofreporting prostate imaging in a population managed by activesurveillance, the second was a dedicated uroradiologist with-out experience of endorectal MRI and did not have experienceof regular reporting a low-risk (Gleason 3 + 3) prostate can-cer population. The differences in observer performance weredeliberately addressed in order to understand how this techniquemight perform outside very specialist hands. The T2-W images,diffusion-weighted images and ADC maps were viewed togetherand each sextant (superior third = basal, middle third = mid andinferior third = apex for right and left sides) scored as positiveor negative for tumour by each observer independently. Tumourwas defined as a focal area of low signal-intensity within theperipheral zone of the prostate that corresponded to an areaof restricted diffusion on the ADC map; in the central glandof the prostate criteria included homogeneity of the focal lowsignal-intensity lesion with mass effect in order to exclude stro-mal nodules of benign prostatic hyperplasia. Sensitivity andspecificity for identifying tumour within the prostate on a per-subject as well as on a per-sextant basis was determined for eachobserver. A kappa statistic was used to determine interobserveragreement.

All statistical tests used a value of less than 5% to denotesignificance.

3. Results

No adverse events were experienced by any subject as a resultof endorectal MRI. Following biopsy, twenty eight sextants in13/51 men were positive for tumour (1 sextant in 5 men, 2 in 5men, 3 in 1 man, 4 in 1 man and 6 in 1 man). All lesions wereGleason 3 + 3; percentage of tumour length to total core lengthranged from 0.4% to 10% (median 1.6%). 32 of 51 patients hadcumulative risk scores of >0.25 based on 71 SNPs. As biopsywas performed after MRI in all cases, there was no artefact fromhaemorrhage on imaging.

3.1. Per-subject analysis

On MRI, lesions were sited in the peripheral zone in all but 1case where it was located across both peripheral zone and centralgland. In the high-risk group, the incidence of positive biopsywas 31.3% (10 of 32 cases), of which MRI detected 9 cases byobserver 1 and 6 cases by observer 2. In the low-risk group, theincidence of positive biopsy was 15.8% (3 of 19 cases), of whichMRI detected 2 cases by observer 1 and 1 case by observer 2.Sensitivity and specificity for each observer by group are givenin Table 1, and the Standards for the Reporting of DiagnosticAccuracy Studies (STARD) flow chart is given in Fig. 1. For thewhole cohort at a per-subject level, agreement between observerswas moderate (kappa = 0.42).

3.2. Per-sextant analysis

In the high-risk group 23 of 192 sextants were positive on his-tology (12%) of which 15 were detected by observer 1 and 7 byobserver 2. In the low-risk group 5 sextants of 114 (4.4%) were

Table 1Sensitivity, specificity, by 2 independent observers for identifying tumour withinthe prostate in a screening population at high risk.

Observer 1 risk score Observer 2 risk score

>0.25 <0.25 >0.25 <0.25

Whole prostate Sens% 90.0 66.7 60 33.3Spec% 86.4 100 86.3 93.8PPV% 75.0 100 66.7 50.0NPV% 95.0 94.1 82.6 88.2

Apex Sens % 72.7 33.3 36.4 0Sens% 100 100 98.1 100Spec% 100 100 80.0 0PPV% 94.6 94.6 88.1 92.1

Mid Sens% 100 100 28.6 100Spec% 93.1 100 96.5 100PPV% 60.0 100 50.0 100NPV% 100 100 91.7 100

Base Sens% 16.7 0 16.7 0Spec% 98.3 100 100 97.3PPV% 50.0 0 100 0NPV% 91.9 97.4 92.1 97.3

positive on histology of which 2 were detected by observer 1 and1 by observer 2. Sensitivity and specificity for each observer ona regional (apex, mid, base) basis is given in Table 1. For the 8men with 2 or more sextants positive, observer 1 identified mul-tiple abnormal sextants in 5 cases, while observer 2 identifiedmultiple abnormal sextants in 1 case only. A true positive caseis illustrated in Fig. 2 and a false positive case in Fig. 3.

4. Discussion

This study has indicated that TRUS random sampling biopsypicked up prostate cancer in 31% of men with a family his-tory of the disease stratified as high-risk (risk twice that ofnormal population) based on 71 SNP analysis and that DW-MRI by an experienced observer identified 90% of these with a86% specificity. This is in keeping with previous data from anactive surveillance population where similar levels of sensitivityand specificity were recorded in a population all of whom hadprevious positive biopsies [12]. As with the active surveillancepopulation, the sensitivity achieved is likely related to lesion sizeand Gleason grade as many of these cancers are of small size andlow Gleason grade. The sensitivity of ADC as a biomarker hasbeen linked to Gleason grade [9] and ADC has been shown to besignificantly lower in aggressive disease [13]. Also the spatialresolution of the technique used in this study, with a pixel sizeof ∼6 mm2 meant that lesions of <3 contiguous pixels of lowADC (18 mm2) were unlikely to be recognised as tumour.

The difference in sensitivity and specificity betweenobservers is also in line with previous data where lower sensitiv-ity and specificity was observed with observers inexperiencedin low risk disease such as in an active surveillance population[12]. These data are in keeping with that from other studies,where sensitivities and specificities improved from 54% to 81%with minimal loss of specificity (91–84% respectively) for Glea-son 3 + 3 lesions of ∼4 mm by an experienced observer when

N.M. deSouza et al. / European Journal of Radiology Open 1 (2014) 22–27 25

Eligible pa�ents n=54

MRI perf ormed n=51

Abn ormal result on MRIn=12 [9]

Normal result on MRIn=20 [23]

Abnormal result on MRIn=2 [2]

Normal result on MRI n=17 [17 ]

Gene�c risk >0.25 based on 71 SNP profiling

Gene�c risk >0.25 based on 71 SNP profiling

Histo Tumour present n=9 [6]

Histo Tumour absent n=3 [3]

Histo Tumour present n=1 [4]

Histo Tumour present n=2 [1]

Histo Tumour present n=1 [2]

Histo Tumour absent n=19 [19 ]

Histo Tumour absent n=0 [1]

Histo Tumour absent n=16 [15 ]

Reference standar d tra nsr ectal ultrasoun d 10-core biopsy Reference standar d tra nsr ectal ultrasoun d 10-core biopsy

Fig. 1. STARD flow chart for index test (endorectal diffusion-weighted MRI at 3.0 T) for detecting tumour by observer 1 and observer 2 against a standard 10-corerandom sampling transrectal ultrasound biopsy technique in men with a family history of prostate cancer stratified by genetic risk.

Fig. 2. True positive for prostate cancer in a 58 year old man: transverse T2-W images (FSE 2500/80 ms [TR/TE]) images (A) through the mid prostate obtainedwith an endorectal coil at 3.0 T and corresponding ADC maps (B) generated from a monoexponential fit of diffusion-weighted data (EPI 8000/69 ms [TR/TE], b = 0,100, 800 mm2/s). Outlines for whole prostate and central gland are given on the ADC maps. A lesion is not visible on the T2-W images, but a focally restricted areaon the ADC maps (arrow) corresponded to a positive biopsy from that sextant.

Fig. 3. False positive for prostate cancer in a 46 year old man: transverse T2-W images (FSE 2500/80 ms [TR/TE]) images (A) through the mid prostate obtainedwith an endorectal coil at 3.0 T and corresponding ADC maps (B) generated from a monoexponential fit of diffusion-weighted data (EPI 8000/69 ms [TR/TE], b = 0,100, 800 mm2/s). Outlines for whole prostate and central gland are given on the ADC maps. Although a lesion is not visible on the T2-W image, a small focallyrestricted area on the ADC maps (arrow) was seen medially. However, all 12 biopsies from this subject were negative for tumour.

26 N.M. deSouza et al. / European Journal of Radiology Open 1 (2014) 22–27

DWI was added to the T2W imaging [14]. Other multiobserverstudies have similarly recorded a wide range in sensitivity andspecificity: in a multireader (n = 6) study, variation in theseparameters ranged from 26 to 51% and 47 to 72% respectively[15]. Although the reason for these variations has not been inter-rogated, it is likely to relate to lesion size and the fact that subtlevariations in ADC with lower Gleason grade tumours adverselyinfluence interpretation.

The sensitivity and specificity for detecting tumour at a sex-tant level were poorer. Two factors are likely to have contributedto this: firstly in patients with multiple tumours, MRI only iden-tified one or some of the lesions. In 6 patients with multiplelesions, not all the lesions were identified on imaging. It is alsopossible that these were part of the same tumour, and so con-tiguous on MRI, whereas histology identified them on 2 separatecores. It is possible that a multiparametric approach, for exam-ple the inclusion of DCE MRI may have improved this [16], butthe increased complexity in scan time, analysis time and costis not warranted in a screening setting. Secondly, definitions ofapex, mid and base are arbitrary and while we divided the glandvisually into “thirds” on MRI, this level of discrimination wouldnot have been possible during transrectal biopsy sampling mak-ing registration between adjacent sextants on MRI and histologyimperfect. Finally, the contrast between tumour and normal tis-sue at the base of the prostate is reduced by the MR appearancesof the normal central zone, which classically has a much shorterT2 relaxation than the normal peripheral zone. This is due to itsunique histology comprising crowded tall columnar cells asso-ciated with thick muscle bundles at the bladder neck [17]. Thismay explain the lower sensitivity for recognizing tumour at thegland base.

This pilot study has some limitations. Most importantly, thepresence of cancer was based on 10 core TRUS biopsy whichuses a random sampling technique. Our negative cases maytherefore not have been truly negative had a more aggressivesampling scheme such as template biopsy been considered. Tem-plate biopsies in healthy men in a screening context are poorlyacceptable to patients. They often necessitate a general anaes-thetic and carry a significant morbidity, which is difficult tojustify in a screening population. In the first instance, there-fore we undertook a pilot study with TRUS biopsy to determinewhether we were able to pick up anything before a formalstudy that incorporated template biopsy. Secondly, the diffusion-weighted techniques employed although they used an endorectaltechnique at 3 T, could be improved by newer reduced field ofview techniques such as zonal oblique multislice imaging [18]which allow much greater spatial resolution without significantreduction in signal to noise ratio or increased acquisition time.In a screening population where safety of the diagnostic inter-vention is paramount, use of a technique that does not involveionizing radiation or administration of a contrast agent is ideal.At a very minimum 4 sequences would be required, bringingscan time down to 20 min; it is likely that future improvementsin scanner hardware and software reduce this further. However,cost–benefit is also an issue and MRI although now widely avail-able incurs a significant financial burden. The restriction of itsuse to those genetically stratified as being at high-risk or by a

combination of PSA and genetic risk will be of major impor-tance in implementing this technique in a screening population.In the first instance, establishing the robustness and accuracy ina larger multicentre trial is warranted.

In summary, we have shown in a pilot study that T2W + DW-MRI is able to detect 90% of men with prostate cancer in ascreening population with a family history of the disease and a>2× population risk based on genetic profiling, but that experi-enced observer interpretation is required. Improvements in theprocess of automated analysis would advance this technique ina larger population study, which are currently in the process ofsetting up.

Funding

The Imaging Centre is supported by CRUK and EPSRCin association with MRC and Department of HealthC1060/A10334. We gratefully acknowledge NIHR support tothe Clinical Research Facility in Imaging and funding to theNIHR Biomedical Research Centre at The Institute of CancerResearch and The Royal Marsden NHS Foundation Trust. REis supported by CRUK 5047/A15007.

Conflicts of interest

The authors have no conflicts of interest to declare with regardto the subject matter of this research.

Acknowledgements

We thank Natalie Taylor and Lucia D’Mello, research nursesfor their assistance with the studies.

References

[1] Kote-Jarai Z, Leongamornlert D, Saunders E, Tymrakiewicz M, Castro E,Mahmud N, et al. BRCA2 is a moderate penetrance gene contributing toyoung-onset prostate cancer: implications for genetic testing in prostatecancer patients. Br J Cancer 2011;105:1230–4.

[2] Madersbacher S, Alcaraz A, Emberton M, Hammerer P, Ponholzer A,Schröder FH, et al. The influence of family history on prostate cancerrisk: implications for clinical management. BJU Int 2011;107:716–21.

[3] Eeles RA, Olama AA, Benlloch S, Saunders EJ, Leongamornlert DA, Tym-rakiewicz M, et al. Identification of 23 new prostate cancer susceptibilityloci using the iCOGS custom genotyping array. Nat Genet 2013;45:385–91.

[4] Goh CL, Saunders EJ, Leongamornlert DA, Tymrakiewicz M, Thomas K,Selvadurai ED, et al. Clinical implications of family history of prostatecancer and genetic risk single nucleotide polymorphism (SNP) profiles inan active surveillance cohort. BJU Int 2013;112:666–73.

[5] Thoeny HC, Forstner R, De Keyzer F. Genitourinary applica-tions of diffusion-weighted MR imaging in the pelvis. Radiology2012;263:326–42.

[6] Park BK, Lee HM, Kim CK, Choi HY, Park JW. Lesion localization inpatients with a previous negative transrectal ultrasound biopsy and per-sistently elevated prostate specific antigen level using diffusion-weightedimaging at three Tesla before rebiopsy. Investig Radiol 2008;43:789–93.

[7] Gibbs P, Liney GP, Pickles MD, Zelhof B, Rodrigues G, Turnbull LW.Correlation of ADC and T2 measurements with cell density in prostatecancer at 3.0 Tesla. Investig Radiol 2009;44:572–6.

[8] Kitajima K, Takahashi S, Ueno Y, Miyake H, Fujisawa M, Kawakami F,et al. Do apparent diffusion coefficient (ADC) values obtained using high

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b-values with a 3-T MRI correlate better than a transrectal ultrasound(TRUS)-guided biopsy with true Gleason scores obtained from radicalprostatectomy specimens for patients with prostate cancer. Eur J Radiol2013;82:1219–26.

[9] Nagarajan R, Margolis D, Raman S, Sarma MK, Sheng K, King CR, et al.MR spectroscopic imaging and diffusion-weighted imaging of prostatecancer with Gleason scores. J Magn Resonan Imaging 2012;36:697–703.

[10] Macinnis RJ, Antoniou AC, Eeles RA, Severi G, Al Olama AA, McGuffogL, et al. A risk prediction algorithm based on family history and com-mon genetic variants: application to prostate cancer with potential clinicalimpact. Genet Epidemiol 2011;35:549–56.

[11] http://www.cancerresearchuk.org/cancer-info/cancerstats/incidence/risk/statistics-on-the-risk-of-developing-cancer#Lifetime5.

[12] Morgan VA, Kyriazi S, Ashley SE, deSouza NM. Evaluation of the potentialof diffusion-weighted imaging in prostate cancer detection. Acta Radiol2007;48:695–703.

[13] deSouza NM, Reinsberg SA, Scurr ED, Brewster JM, Payne GS. Mag-netic resonance imaging in prostate cancer: the value of apparent diffusion

coefficients for identifying malignant nodules. Br J Radiol 2007;80:90–5.

[14] Haider MA, van der Kwast TH, Tanguay J, Evans AJ, Hashmi AT, Lock-wood G, et al. T2-weighted and diffusion-weighted MRI for localizationof prostate cancer. Am J Roentgenol 2007;189:323–8.

[15] Kajihara H, Hayashida Y, Murakami R, Katahira K, Nishimura R, HamadaY, et al. Usefulness of diffusion-weighted imaging in the localization ofprostate cancer. Int J Radiat Oncol Biol Phys 2009;74:399–403.

[16] Riches SF, Payne GS, Morgan VA, Sandhu S, Fisher C, Germuska M,et al. MRI in the detection of prostate cancer: combined apparent diffusioncoefficient, metabolite ratio, and vascular parameters. Am J Roentgenol2009;193:1583–91.

[17] Srodon M, Epstein JI. Central zone histology of the prostate: a mim-icker of high-grade prostatic intraepithelial neoplasia. Hum Pathol2002;33:518–23.

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QUESTIONNAIRE A5(16)

Radiography and prostate cancer

INSTRUCTIONS Read through the article and answer the multiple choice questions provided below

Some questions may have more than one answer; in which case you must please mark all the correct answers

Prostate cancer – Double vision but solitary lesion

Question 1: Approximately what percentage of patients with metastatic prostate cancer develop bone metastases?

A: 60% B: 70% C: 80% D: 90%

Question 2: With regard to the case report, which one of the following imaging modalities was initially used that demonstrated a durally-based, homogenously enhancing mass arising from the petroclival ligament?

A: CT scan B: Doppler studies C: MRI D: Ultrasound

Question 3: Is it TRUE or FALSE that cases of diplopia from cranial nerve palsies or ocular rectus muscle invasion from metastatic prostate cancer are commonly reported?

A: TRUE B: FALSE

Question 4: Which of the following features in this case raised the possibility for an alternate diagnosis other than metastatic prostate cancer?

A: The relatively low absolute levels of PSA B: The general rarity of solitary metastatic lesions in the

brain or skull C: The radiological appearance of the osteolytic focus in

the petroclival region D: All of the above

Question 5: Is it TRUE that most meningiomas tend to remain asymptomatic and are slow growing?

A: YES B: NO

Interventional uroradiology in the management of

prostate cancer Question 6: Which of the following statements are TRUE with regard to prostate cancer?

A: Prostate cancer is the least common cancer in men B: Prostate cancer is the second most common cause

of death among men C: The majority of patients are between 45 and 56 D: The majority of prostate cancer patients often have

co-morbid disease in other body systems

Question 7: Is it TRUE that when detected early, most prostate cancers are confined to the gland without metastatic spread?

A: YES B: NO

Question 8: Image-guided urologic interventions for prostate cancer include which of the following?

A: Fluid collection drainages B: Fiducial marker placements for external beam

radiation C: Ultrasound-guided and primary ablative therapies D: Diagnostic biopsies E: All of the above

Question 9: Direct prostate gland biopsies most commonly occur with which of the following guidance?

A: MRI B: CT C: TRUS D: SBRT

Question 10: Is it TRUE or FALSE that even though SBRT uses smaller margins to allow for high daily radiation deposition, uncorrected prostate motion cannot result in suboptimal dose to target?

A: TRUE B: FALSE

Question 11: For image-guided fiducial placement, to employ 6-dimensional correction, how many fiducials are required?

A: 1 B: Less than 3 C: 1 or 2 D: At least 3

Question 12: Alternative image-guided ablative uroradiologic interventions for prostate cancer include which of the following?

A: Only high intensity focused ultrasound B: Cryotherapy but not HIFU C: Cryotherapy and HIFU D: Low intensity focused ultrasound and cryotherapy

Question 13: MRI can be used during HIFU for which of the following?

A: Contiguous temperature monitoring B: Intraprocedural adjustments C: Thermal dose mapping D: All of the above

Question 14: Is it TRUE or FALSE that CT is used to diagnose simple fluid collections and abscesses occurring within the pelvis following radiation therapy, ablative therapies and surgical resections for prostate cancer?

A: TRUE B: FALSE

Diffusion-weighted MRI for detecting prostate tumour in

men at increased genetic risk Question 15: How many single nucleotide polymorphisms have been shown to be significantly associated with prostate cancer in men with a strong family history of prostate cancer?

A: 85 B: 76 C: 61 D: 56 E: 45

Question 16: Is diffusion-weighted MRI, when used in conjunction with T2-W MRI, sensitive at detecting clinically significant prostate cancers?

A: YES B: NO

Question 17: Of the 31% of men with a family history of prostate cancer that was picked up with TRUS random biopsy sampling as having prostate cancer, what percentage of these men were identified through DW-MRI by an experienced observer?

A: 30% B: 50% C: 70% D: 80% E: 90%

Question 18: Is It TRUE or FALSE that in patients with multiple tumours, MRI identified all the lesions?

A: TRUE B: FALSE

Question 19: It it TRUE that the contrast between tumour and normal tissue at the base of the prostate is reduced by the MR appearances of the normal central zone which may explain the lower sensitivity for recognizing tumour at the gland base?

A: YES B: NO

Question 20: Is it TRUE or FALSE that in a screening population where safety of the diagnostic intervention is paramount, use of a technique that does not involve ionizing radiation or administration of a contrast agent is ideal?

A: TRUE B: FALSE

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