Skip to main content
NCBI home page
Journal of the West African College of Surgeons logoLink to Journal of the West African College of Surgeons
. 2016 Oct-Dec;6(4):31–65.

MANAGEMENT OF PROSTATE CANCER IN ACCRA, GHANA

ED, Yeboah 1,✉, AW Hsing 4,2, S Mante 3, JE Mensah 1, MY Kyei 1, J Yarney 1, V Vanderpuye 1, K Beecham 1, Y Tettey 1, RB Biritwum 1, AA Adjei 1, R Gyasi 1, K, Asante 1, KN Ampadu 1, GO Klufio 1, S Gepi-Attee 1, C, Owoo 1, D Kwami 1, Ahiaku 5, R Pandra 6, MB Cook 2
PMCID: PMC5667721  PMID: 29181364

Abstract

Introduction

Africans living with prostate cancer in Africa face problems of early diagnosis and appropriate treatment.

Aim

To study the clinical incidence of prostate cancer, risk factors, TNM stage, their management and outcomes.

Methods

A prospective study of Prostate Cancer cases managed at Korle Bu Teaching Hospital and hospitals in Accra, diagnosed by history, abnormal PSA/DRE, physical examination and histologically confirmed by biopsy from 2004 to 2013 was carried out. The cases were TNM staged and managed by approved protocol.

Results

There were 669 cases with a mean age 70±0.045SE years, median Gleason Score of 7, organ confined Prostate Cancer(PC) in 415(62%), locally advanced in 167(25%) and metastatic Prostate Cancer in 87(13%) cases. The cases were followed for median of 10 months to ≥ 84 months. Organ confined cases were managed by: Radical Prostatectomy (RP) 92 (13.8%) with a mortality of 0.3%; brachytherapy 70 (10.5%) with a mortality of 0.1% and External Beam Radiotherapy (EBRT) 155 (23%) with a mortality 0.7%. In all, 98 men constituting (14.1%) cases with a mean age of 75+0.25SE years, life expectancy <10 years were treated by hormonal therapy with a mortality of 1.7%. Twenty cases who were for active surveillance (GS6), PSA <10ng/ml, life expectancy <10 years later all opted for EBRT. Locally advanced cases 25% all had neoadjuvant hormonal therapy then Brachytherapy in 3 (0.4%) mortality 0.15% and EBRT in 64 (9.5%), mortality 0.59%. Hormonal therapy was given in 100 (15%) locally advanced cases, mortality 5%. Metastatic prostate cancer cases (13%) were managed by hormonal therapy, mortality 6%.

Conclusion

Improved facilities and dedicated skilled teams led to a significant rise in proportion of organ confined Prostate Cancer from 15.3% to 62% curable by Radical Prostatectomy, brachytherapy or EBRT with longer disease free survival.

Keywords: Prostate cancer, Gleason score, Stage, Management, Radical prostatectomy, Radiation therapy, Hormonal therapy

Introduction

Prostate Cancer (PC) is the commonest Cancer in living men and has high incidence in the African Caribbean’s, African Americans, Caucasians but low in Asiatics and Chinese. PC prevalence in Africans and Ghanaians has been under reported. The worldwide incidence of PC is variable. It is the 15th commonest cancer constituting 11.7% and of new cases, 19% in developed countries and 5% in developing countries. It is next to Liver cancer in Western men1,2, 3,4,5,6,7,8,9. In Africa, epidemiology studies have found low PSA testing, late presentation and low percentage of organ confined disease (T1 – T2) but high percentage of locally advanced 30% and metastatic PC in 55% of cases1,10,11making disease control difficult. Recent reports indicate high prevalence in Caribbean’s and Ghanaians12,13.

The risk factors reported for PC include familial, sporadic, presence of testis, ageing, ethnicity, race (highest African American > Caucasian American > Asian Americans), high activity of oncogenes, 5-DHT, 5 alpha reductase but decreased activity of anti-oncogenes. Others are hormonal imbalance, decreased cell death and genetics/GWAS have incriminated HPC1, HPC2, p53, 17q21, 8q24, BRAC1, BRAC2. Other risk factors are red meat and fatty diet, early sex activity, Viruses – HPV, HSV, chronic inflammation, prostatitis and high Basal Metabolic Index (BMI) 10,11,12,14,15,16,17,18,19.

OBJECTIVES

The study was to identify and establish the clinical incidence of prostate cancer, risk factors, TNM stage, their management and outcomes.

ETHICAL APPROVAL: The project was approved by the IRBs, College of Health Sciences/NCI/Ministry of Health Ghana.

SPONSORSHIP: The study was sponsored by NCI/NIH, University of Ghana Medical School and Korle Bu Teaching Hospital.

PATIENTS & METHODS

A prospective study of cases of prostate cancer(PC) suspected by abnormal PSA (TPSA >4ng/ml, abnormal PSA velocity >0.75ng/ml year, PSAD >0.15ng/ml, short PSA doubling time) or abnormal DRE was carried out. Prostate Cancer was histologically confirmed by TRUS guided/trucut biopsy, digitally guided biopsy or with TURP/open simple prostatectomy specimens. Histological diagnosis was by pathologists at Korle Bu Teaching Hospital(KBTH), Accra, Ghana and some validated by John Hopkins pathologists in Baltimore, USA. The centers involved in this study were Korle Bu Teaching Hospital, 37 Military Hospital, Nyaho Medical Centre, SSNIT Hospital and Ridge Hospital, all in Accra.

The subjects underwent detailed history, physical examination including DRE, anthropometric measurements and PSA determination. Other investigations included IPSS, EFI, prostatitis index, screening for STD’s and genetic/genome wide studies. Informed consent was obtained from all the subjects.

The staging procedures included X-ray’s (Chest, KUB, Skeletal Survey), abdomino-pelvic ultra sonographic scan(USG), CT Scan/MRI and radioactive bone scan and staged by TNM staging.Fig. 1

Fig. 1: T stages of Prostate Cancer.

Fig. 1:

Open in a new tab

Only cases with histologically proven prostate cancer (PC) were included in the study and patients with inadequate data were excluded from the study.

MANAGEMENT PROTOCOLS (as in Table 1)

Table 1. Table 1.

Stage (TNM) Grade(Gleason score) Treatment Protocols offered for Prostate Cancer in Ghana
Early (T1 and T2 N0 M0) GS ≤7 External beam radiotherapy EBRT 2D/3D 70 – 74GYBrachytherapy 160 GY – I seedsRadical Prostatectomy (RP) (Open retropubic or perineal/ Laparoscopic)
Active SurveillanceT1 – T2 N0M0 Low Risk GS ≤6 (No GS 4 no GS 5) Life expectancy <10 yrs. PSA <10ng/ml Follow up every 3 months for 1st year and every 6 months subsequently. Check TPSA, PSA velocity, DRE at each visit. If progression by TPSA, ↑PSA velocity >0.75ng/ml/yr., repeat biopsy and appropriate Rx by radiation or hormonal therapy
Early (T1 and T2a N0 M0) GS 7- 10 Neoadjuvant ADT/Radical Prostatectomy /Brachytherapy External beam radiotherapy 2D or 3D conformal + neoadjuvant or adjuvant hormonal therapy with antiandrogens or Luteinizing Hormone Releasing Hormone(LHRH) analogues ± Total Androgen Blockade(TAB)
Late LOCALLY ADVANCED(any T3 and T4) N0 M0 GS ≤7 Neoadjuvant hormonal therapy with antiandrogens ± TAB orBilateral orchidectomy/Hormonal therapy TAB and EBRT/ Brachytherapy
Late(any T3 and T4) M1 High Risk GS 7 – 10 Bilateral orchidectomy Hormone therapy LHRH analogues ± TAB ADT ↑supportive therapy
Hormone Refractory Stilboestrol, Cyclophosphamide, antiandrogen withdrawal, docetacel, prednisolone
Open in a new tab

(A)ORGANNCONFINED 1. EARLY PC Life expectancy >15 years, 1. T1-T2 N0M0 GS≤7. - These were managed by (a) Radical Prostatectomy (RP) (b) Brachytherapy or (c) External Beam Radiotherapy (EBRT)

2. EARLY T1 – T2 G>7 was managed by neoadjuvant Androgen Deprivation Therapy(ADT) then RP, Brachytherapy or EBRT

(B)LOCALLY ADVANCED T3 T4 N0M0 GS ≤7 – Neoadjuvant hormonal therapy, brachytherapy, EBRT or hormonal therapy.

(C)METASTATIC disease treated by hormonal therapy.

(D)HORMONE REFRACTORY Cases managed by Stilboestrol, chemotherapy e.g. Ketoconazole.

(E)ACTIVE SURVEILLANCE for organ confined PSA < 10ng/ml T1-T2 N0M0 GS6 (no G4 or 5) Life expectancy <10 years.

Post Treatment Follow up

Post RP or radiation therapy we follow patients every 3 months for 1 year, then every 12 months. DRE, TPSA PSDT, PSA Velocity and PSA doubling time are estimated at the follow-up visits. If changes suggest biochemical failure, then salvage post-surgery radiotherapy is given or hormonal treatment if post RP radiotherapy rejected or contraindicated.

For patients on active surveillance, the follow up protocol was every 3 months for 1 year then every 6 months. At each visit, DRE, TPSA, PSA Velocity, PSA doubling time are performed and if any indicate progression then we treat by RP or radiotherapy with or without hormonal therapy

PATIENTS WITH BONY METASTASES – Symptomatic patients were given bisphosphonates orally or infusions for 1 year. Hormone therapy was given to metastatic cases who were not castrated (confirmed by serum testosterone levels) but EBRT 8GY – 30GY was given to relieve spinal cord compression, relief of pain and obstructive symptoms. Bone metastases with hypocalcemia was managed by infusions of Zolendronic acid.

PATIENTS WITH IMMINENT CORD COMPRESSION – these were treated by a course of dexamethasone + Bilateral Total Orchiectomy (BTO) or hormonal therapy (Stilbestrol, ADT Ketoconazole).

HORMONE REFRACTORY CASES(HRPC)/CASTRATE RESISTANT (CRPC)

These cases were given palliative hormonal chemotherapy: - Stilbestrol or ketoconazole or docetaxel 75mg/m2 given 3 weekly with prednisolone or abiraterone. A few cases were given oral cyclophosphamide plus prednisone. These were guided by affordability issues.

PATIENTS WITH COMORBIDITIES such as obesity, diabetes mellitus (DM), congestive cardiac failure (CCF), severe hypertension (HPTN), Ischaemic heart disease (IHD), chronic kidney disease (CKD), chronic liver failure (CLF), chronic anemia and elderly had their conditions managed by conventional methods to prevent untoward morbidity or mortality influenced by affordability issues.

PATIENTS WITH URINARY OBSTRUCTIVE SYMPTOMS– Those with moderate to severe symptoms (cases with IPSS ≥ 8, QOL ≥ 3) high Post Void Residua(PVR)l urine and decreased Peak Flow Rate(PFR) were given alpha adrenergic blockers ± finasteride. Cases with severe bleeding, severe symptoms, refractory recurrent retention, calculi, diverticuli are treated by TUIP/ TURP, bladder neck resection or radical prostatectomy if localized T1– T2 N0M0 disease

The data obtained including demographic, clinical features, relevant investigations, management offered and outcome were analyzed using Statistical Package for Social Science (SPSS) version 20.

Data results were expressed as percentages and means ± standard deviations. A p-value of less than 0.05 was considered significant.

Results

A total of 697 cases were recruited out of which 669(96%) had completed medical records abstractions with adequate data. The remaining 22 without adequate data were excluded from the study. The median age was 70±0.48SE years with a range of 41 – 94 years (Fig. 2a) while the median PSA was 52.5ng/ml with a range of 2.5 – 9,900ng/ml (Fig. 2b).

Fig 2a: Age Ranges of the patients.

Fig 2a:

Open in a new tab

Fig 2b: Initial PSA levels of the patient.

Fig 2b:

Open in a new tab

Hospital logbooks cases were obtained from Korle Bu Teaching Hospital (KBTH) in 401 (60%) cases, 37 Military in 54 (8%) cases, Nyaho Medical Center in 210 (31%), 4 (0.6%) from SSNIT and Ridge hospitals in Accra, Ghana. Their ethnicity are as follows: Akan 320 (48%), Ga- Adangbe 160 (24%), Ewes 80 (12%), Northern 34 (5%), non-Ghanaian 4, not stated 71 (10.6%); their social status include: retired 46.1%, middle income 20.5%, high income 11.4%, low income 9%, while Christians made up 54%, moslem 7%, other 39%. Biopsy types included TRUS-guided biopsies in 63.5%, digitally guided biopsies in 21.7% (Fig. 2c)

Fig 2c: Biopsy methods used.

Fig 2c:

Open in a new tab

Stages and Gleason scores(GS) (Fig. 2d)

Fig. 2d: TNM Stage.

Fig. 2d:

Open in a new tab

The 669 cases were staged thus: localized disease T1 – T2 N0 M0 in 415 (62%) cases, locally advanced disease T3-T4 N0M0 in 167(25%), metastatic disease in 87 (13%) cases while the Gleason Scores(GS)-High risk GS ≥7 was 67.7% whereas low and intermediate risk GS ≤ 6 was 32.3% (Table 3)

Table 3. Gleason Scores of the patients.

Gleason Score N %
G≤ 4 29 4.4 Low Risk
G5 40 6 Moderate
G6 147 21.9 Risk
G7 225 33.7 High Risk67.7%
G8 110 16.4
G9 96 14.3
G10 22 3.3
Open in a new tab

1. ORGAN CONFINED (LOCALISED)

T1-2 N0M0 415 (62%), Median GS <7, presentation PSA ≥ 4ng/ml 95.6%, PSA ≤ 4, 4.4%, LUTS (LUTO/IRRITATIVE) 25%, retention of urine (ROU) 10%, medical management of obstructive symptoms with alpha blocker ± finasteride in 23%. The co-morbidities were hypertension (HPTN) 21%, diabetes mellitus (DM) 4%, HPTN & DM 3.3%, anemia with Hb <12gm/dl in 3.3% and renal impairment with creatinine >120umol/L in 10% cases.

Management PC n = 415 (62%) (a)Radical Prostatectomy (RP) - localized disease T1 – T2 M0 number was 92/669 (13.8%) Fig. 3mean age 61.8 years ± 0.88SE with a range of 51 – 72 years. Radical (Open) Prostatectomy cases 85 (12.7%), radical retropubic open prostatectomy 81 (12%), perineal radical prostatectomy 4 (0.6%), laparoscopic RP 7 (1%). Mean pre-operative PSA 17.9 ng/ml ± 2.58SE (range 4 – 100ng/ml) versus mean post-operative PSA 0.43 ± 0.26SE (range 0.01 – 12ng/ml) p< 0.0001 in 12.8%, median GS ≤ 7, median follow up 10 months (range 10 months – 84 months+), lost to follow up 6 (0.9%).

Fig 3: RADICAL PROSTATECTOMY n = 86 T1T2 N0M0 PC PRE VS POST TREATMENT PSA.

Fig 3:

Open in a new tab

RP specimen organ confined disease was 76 (11.4%), BPH 3 (0.4%) and positive margins 13 (2%). Cases with positive margins were treated by hormones/EBRT. Biochemical failure(BF) were 18(2.7%) and were treated by EBRT + Androgen Deprivation Therapy (ADT)

Post-operative complications were erectile dysfunction (EDYS) 10 (1.5%), bladder neck stenosis 10 (1.5%), overactive bladder (OAB) 6 (0.9%), UTI 12 (1.8%), and deaths 2 (0.3%) from pulmonary embolism/myocardial infarction (PE/MI). Deep vein thrombosis (DVT) 5 (0.7%) treated by anticoagulants, urinary Incontinence temporary 6 (0.7%) treated by oxybutynin, detrusitol and pelvic exercises.

(b) Brachytherapy for n = 70 (10.5%). I125 seeds deliver dose 160GY. Mean age 60.8 ± 0.587SE (Range 51 – 76 years) Table 4, Fig. 4.Lost to follow up 9 (1.3%), and one death 1/669 (0.1%). Pre-treatment versus post-treatment PSA n = 61 (9.1%) PSA 13.34ng/ml ± 0.08SE versus mean post PSA 0.166ng/ml ± 0.03SE p<0.0001 . Mean pre-treatment PSA Stage T1 (n = 20) 13.32ng/ml ± 0.24SE versus post mean PSA 0.134ng/ml ±0.06 SE p<0.0001. Mean pre-treatment PSA T2 (n41) 13.38ng/ml ± 0.34SE versus post 0.234ng/ml ± SE 0.05 p<0.0001 in 9.1%. Fig. 4

Table 4. Brachytherapy for 70 cases with T1 T2 No Mo.

T Stage T1 T2
PRE-Rx n 23 47
G2 – 6 10 15
7 1 9
8 – 10 1 3
Mean Pre-Rx PSA ng/ml 13.32 ± 0.24SE(6.1 – 38.07) 13.38 ± 0.34SE (2.5 – 69)
Post Follow up(10 – 72 mths)Mean 12 mths 20 41
POST Rx PSAng/ml meanrange 0.134 ± 0.06SE(0.01 – 7.9) 0.234 ± 0.056SE(0.01 – 57.3)
pre vs post PSA P< 0.0001 P< 0.0001
Biochemical Failure (BF) 1 2 Rx EBRT/ Hormone therapy
Open in a new tab

Fig 4: BRACHYTHERAPY 61 cases T1 T2 N0M0 of PC.

Fig 4:

Open in a new tab

Follow up median 12 months (10 – 72 months), 9 (1.3%) defaulted, complications were, BF 3 (0.4%) with PSA 6.41, 20 and 40ng/ml, median time to failure 23 months. Treatment of BF was by hormone therapy Zoladex/BTO + EBRT 40 – 50GY. Radiation cystitis 6 (0.9%) treated by tranexamic acid, tamsulosin oxybutynin/ detrusitol, prednisolone Ciprofloxacin, EDYS 6 (0.9%), treated with Tardanafil/sildenifil citrate, DVT 1 (0.1%) treated by anticoagulants, death 1 (0.1%) from PE.

(c)EBRT for n= 155(23%). Table 5,Table 6, Fig. 5Cobalt 60, 70 – 74GY 2D/3D, 20 of 155 were on surveillance and recruited later, mean age 61.75 ± 0.2462SE. Outcomes mean pre-treatment PSA (n = 137) PSA 16.513 ±0.80SE versus post treatment PSA 0.33 ± 0.11 p<0.0001. T1 cases mean pre-treatment versus post-treatment PSA 13.35ng/ml ± 0.86SE versus 0.232ng/ml ± 0.011SE p< 0.0001 and for T2 pre-treatment 17.2ng/ml ± 0.95SE versus post 0.35ng/ml ± 0.013SE and p<0.0001 in 52/669 (7.7%)

Table 5. External Beam Radiotherapy (EBRT) in 155 cases (T1T2 N0M0).

T Stage T1 T2
N 24 131
Pre-treatment PSA Mean ng/ml 13.35 ± 0.8SE 17.2 ± 0.925SE
Range 3.8 – 22.5 2.7 – 93.8
No follow up Median 10 months range7 months – 8 years 21 116
Mean post treatment PSA ng/ml 0.23 ± 0.11SE 0.35 ± 0.13SE
Range 0.01 – 3.56 0.01 – 14.54
Pre vs post PSA P< 0.0001 P< 0.0001
Biochemical Failure (BF) 3 15
Open in a new tab

Table 6. MANAGEMENT offered for various stages of prostate cancer.

STAGE Modality Treatment TNM Stage Lost to follow up
N T1 T2 T3 T4 T 1-4 N 1-3 M1
Organ confined T1-T2 N0M0 n=415 Radical Prostatectomy RRP 81 PRP 4Laparoscopic 7 92 17 75 6
Brachytherapy 70 23 47 9
EBRT 155 24 131 18
Hormonal/ Chemotherapy 98 24 74 14
Locally advanced T3-T4 M0 n=167 Androgen Deprivation Neoadjuvant 167 16
Brachytherapy 3 - - 3 -
EBRT 64 57 7 (7)
Hormonal therapy 100 40 60 (9)
Advanced metastatic T1-4 N1-3 M1 n=87 Hormonal androgen deprivation therapy 87 87 8
Total 669 88 327 100 67 87 71
RRP (Radical Retropubic Prostatectomy), PRP (Perineal Radical Prostatectomy)Lost to follow up (71/669) 10.6%, Mortality in 8 years in advanced and metastatic cases were 91/669 (13.6%) due to bleeding 2(0.3%), obstructive uropathy 20(3%), urosepsis 20 (3%), paraplegia 31(4.6%) and sepsis 18 (2.7%).
Open in a new tab

Fig 5: EBRT for 137 cases T1 T2 N0M0 of PC PRE VS POST Treatment PSA.

Fig 5:

Open in a new tab

Median follow up 10 months (7 months – 8+ years), lost to follow up 18 (2.7%), BF 18 (2.7%), 3% treated by hormone/chemotherapy, mortality 5 (0.7%) (3 from massive haematuria, radiation cystitis, 2 – DVT and PE)

(d)LOCALISED DISEASE WITH PROGRESSION AND HAD HORMONAL THERAPY n=98 (14.6%) (T1-T2 N0M0)

High risk G ≥7, mean age 75 ± 0.25SE (Range 68 – 94yrs) of these 6 (0.1%) have had simple prostatectomy for BPH. Comobidities included HPTN 4.2%, Ischaemic heart disease (IHD)1.6%, DM 3.7%, Obesity 2.2%, CCF 1.5%. Methods LHRH analogue/ chemotherapy 30 + 18*(4.5% + 2.7%), Stilboestrol 2.5mg + aspirin 30 (4.5%), BTO 20 (3%) ± bicalutamide/ flutamide. BF noncompliant with LHRH agonists 18* were treated by BTO 18 (2.7%) (Total BTO 38 5.7%), T1 24 (3.6%), T2 74 (11%). Mean pretreatment PSA 24ng/ml ±0.84SE (range 3.8 – 90.8ng/ml) versus post mean treatment nadir PSA 0.34ng/ml ± 0.01SE (range 0.2ng/ml – 50ng/ml) p< 0.002. in 66/669(9.8%). Median follow up 10 months (range 12 months – 7 years), mortality 9 (1.3%), CVA 2 (0.3%), DVT and PE 1 (0.5%), castrate resistance PC (CRPC) 6 (0.9%), Lost to follow up T1 18 (2.7%), T2 14 (2.1%).

2.LOCALLY ADVANCED

T3-4 M0 N0 DISEASE n=167(25%) (T3 100, T4 67)

Mean age 70± 0.535SE, Median GS > 7, mean pre-treatment PSA 48.5ng/ml ± 0.96SE (range 7.1 – 2793ng/ml) versus post-treatment mean PSA 0.6ng/ml ± 0.34SE (range 0.2 – 50ng/ml). Of these 4 (0.6%) had had previous simple prostatectomy for BPH.

Presentation – LUTS/LUTO 40 (6%), acute retention of urine (AROU) 7 (9%), chronic retention of urine (CROU) 3 (0.4%), obstructive uraemia 4 (0.6%), hematuria 10 (1.5%), EDYS 5 (7.5%), Pain back/perineal/supra- pubic 17 (2.5%).

Management – Neoadjuvant hormonal ± TAB LHRH analogue 87 (13%) ± TAB /Stilboestrol 20 (3%) ± TAB BTO 60 (9%) followed by (a)brachytherapy 3 (0.4%), (b) EBRT 64 (9.6%)

a) Locally Advanced Management treated by Brachytherapy

T3 3 (0.4%), pre-treatment median PSA was 14.3ng/ml (range 9.4 – 17.3ng/ml) and post treatment median PSA was 0.11ng/ml (range 0.11 – 0.12ng/ml). Complications were 1 death 0.15% from progression of disease (Fig. 6a).

Fig. 6a: LOCALLY ADVANCED PC Rx BRACHYTHERAPY PRE & POST Rx.

Fig. 6a:

Open in a new tab

b) Locally Advanced treated by EBRT (Fig. 6b).

Fig. 6b: PRE VS POST TREATMENT PSA LOCALLY ADVANCE PC T3 T4 N0M0D TREATED BY EBRT.

Fig. 6b:

Open in a new tab

n = 64 (9.5%), Lost to follow up 7 (1%), pre-treatment mean PSA T3 57 (8.5%) 32.4ng/ml ± 0.85SE, T4 7 median PSA 64.6ng/ml versus post-treatment mean PSA T3 0.4ng/ml ± 0.12SE p< 0.0001, post T4 median PSA 0.45ng/ml Fig. 6b. Lost to follow up 7. Complications were 21 (3%): - BF 5 (0.7%) (T3 1 T4 4), radiation cystitis 7 (1%), proctocolitis 4 (0.6%), rectal bleeding 5 (0.7%), Deaths 4 hematuria- 1 (0.15%), disease progression 3 0.4%.

(c)Locally Advanced PC managed by hormonal therapy

Number of cases were 100 (15%), of these 4 (0.6%) had had previous simple prostatectomy for BPH, T3 40 (5.9%), T4 60 (9%). Mean pre-treatment PSA was T3 (40) 34.1ng/ml ± 0.78 and T4 60 pre-treatment mean PSA 41.05 ng/ml ± 0.81SE versus mean post treatment PSA T3 was 0.4ng/ml ± 0.11SE p< 0.002 and T4 0.48ng/ml ± 0.11SE p< 0.002 in 13%

Management Methods were LHRH ± TAB (ADT bicalutamide /flutamide) 47 – 7%, Stilboestrol ± aspirin 6 – 0.8% and BTO 47 – 7%. 50 (7.5%) of cases with LUTO/LUTS AROU/CROU were treated by alpha blockers ± finasteride 43 – 5%, TUIP/TURP Bladder neck resection 17 – 2.5%. Complications were HRPC/CRPC 31 – 4.6%, hot flashes 36 – 5%, EDYS 98 – 15%. The median follow up was 12 months (rang 1 year – 7 years), lost to follow up 9 – 1.34% (T3 3 and T4 6), hospital mortality 34 – 5% due to urosepsis 16 – 2.4%, bedsores and sepsis 5 – 0.7%, PE 3 – 0.4%, obstructive uraemia 6 – 0.9%, and anemia from hematuria 4 – 0.6%.

(3) Metastatic Disease

T1-4 N1-3 M1 n 87 13%, mean age 70 ± 0.587SE, median GS ≤7 (r4 – 10), mean pre-treatment PSA 98ng/ml ± 1.344 (r7 – 9,900ng/ml), mean post-treatment PSA 0.46ng/ml ± 0.138 (r0.04 – 86ng/ml). Presentation: LUTS/LUTO 31 – 4.6%, AROU 8 – 1%, uremia CROU 5 – 0.7%, metastatic – skeletal: pelvis 40 – 6%, spine 8 – 1%, pelvis/spine 15 – 2.2%, pelvic/groin lymph nodes (PLN) positive 15 – 2.2%, hematuria 9 – 1.3%, paraplegia 9 –1.3%, pulmonary secondary’s 4 – 0.6%, cerebral secondary’s 3 – 0.4%, lymphedema penis & scrotum 3 – 0.4%, lymphedema legs 4 – 0.6%, pain skeletal /waist 58 – 8.6%, anemia 18 – 2.7%, headaches 3 – 0.4%. Treatment was by hormonal/ chemotherapy and conventional methods for complications.

Management AROU/CROU – Catherization, α-blockers ± finasteride 13 (1.9%), TURP 8 (1.2%), LHRH analogue ± TAB 20 (3%), Stilboestrol TAB 15 (2.2%), BTO 52 (7.8%).

Complications Hot flashes 26 (3.9%), EBRT used for localized vertebra bone secondaries to relieve compression in 6 cases 0.9%, BF 30 – 4.4% managed as HRPC/CRPC - 4.5% by stilboestrol, ketoconazole/prednisolone, docetaxel, cyclophosphamide and prednisolone. Hospital mortality 40 – 6%, urosepsis 14 – 2%, obstructive uropathy/uremia 10 – 1.5%, anemia hematuria 6 – 0.9%, bedsores sepsis 5 – 0.7%, DVT PE 5 – 0.7%, Lost to follow up 8 – 1.2%.

SUMMARY OF FINDINGS Table 6

Summary of Management of 669 cases

  • •

    Stages at Presentation. Stages found were T1 T2 M0 -62%, T3T4 M0 -25%, metastatic PC-13%.

  • •

    Risk Factors established in our Study are males with testes, advanced age and high BMI. Genome wide studies have shown chromosome 10p14 associated with PC in Ghana, aggressive PC GS ≥7 (67.7%) high PSA >52ng/ml associated with SNPS 5q31.3 and low grade GS ≤6 (32.3%) PSA <52ng/ml associated with SNPs Xq28 & 6q21. These findings have been published elsewhere and will be discussed.

  • •

    The comorbidities were hypertension (HPTN) 25%, DM 5.4%, HPTN/DM 5.1%, anemia 3.3%, CKD 11.1%. Lost to follow up 71 (10.6%) Table 6.

  • •

    Initially, there were significant falls in PSA in most groups in the immediate post treatment period.

  • •

    Management of PC in Ghana has improved since 2004 from study of 669 cases with long disease free survival with improved urological practices with 62% presenting as organ confined allowing curative treatment such as: radical prostatectomy 92 (14%), mortality 2 (0.3%), brachytherapy 73 (11%), mortality 2 (0.3%), EBRT 155 T1-T2, (23%), mortality 5 (0.7%), Active surveillance (3%) 20 cases (T1 8 & T2 12), later opted for EBRT, so analyzed with EBRT.

The locally advanced 167, (25%) cases were managed by neoadjuvant hormonal/chemotherapy followed by EBRT and brachytherapy 67 (10%), hormonal chemotherapy 100 (15%). The metastatic cases 13% were managed by hormonal ± chemotherapy. Hormonal therapy long/short term for localized disease (98) and locally advanced (167) and metastatic disease (87) that is in 52.6% cases using LHRH analogues BTO, stilboestrol + aspirin ± TAB.

Discussion

More and more of prostate cancers (PC) in the Western hemisphere are diagnosed at an earlier stage because of rising numbers of PSA testing. Cooperberg14 showed proportion of low risk tumor rose from 29.8% in 1989 to 45.3% in 2001 and the proportion of locally advanced disease fell from 19.2% to 4.4% and the metastatic cases declined from 14.1% to 3.3% in USA. Reports from USA and Jamaica indicate that late stage of presentation is associated with low income Whites, African Americans and Jamaicans3.

This trend has also been observed in communities with PSA screening which caused stage down migration of radical prostatectomy specimens.14,15 Our study has shown stage down migration T1 – T2 62%, locally advanced 25%, metastatic 13% versus T1 – T2 15.35%, locally advanced 32.3%, metastatic 52.5% in our retrospective study13 statistically significant p<0.0001. In our population study T1-T2 82%, locally advanced 12% and metastatic 6%. This is in line with Western trends.

T1 – 2 N0M0 ORGAN CONFINED 415 (62%)

Our survival of 98% for RP is comparable to results from other centers 20,21,22,23,24,25,26. There were initial significant falls in pre-versus post-operative PSA p<000.1 in 86/92(93.4%). We have had limited experience with laparoscopic RP 7 (1%) cases which is purported to have low incidence of mortality, erectile dysfunction or complications27,28 but no experience with robotic RP which is reported to give better results with morbidity and mortality than open and laparoscopic RP27,28. Unlike Weldon, Isenlin, Ruenes and Gueye who have done several cases of radical perineal prostatectomy23,29,30, we have had only 4 (0.6%) cases of perineal RP which did well. Kyei has reported his experiences with RP at KBTH in Accra which did well22. The biochemical failure of 13 (2%) in 92 cases were due to positive margins and were managed successfully by EBRT /hormonal therapy 31,32.

The therapeutic value of brachytherapy is generally comparable to RP 33,34,35. Brachytherapy has good outcomes with 8year PSA relapse free survival of low risk PC 88%, intermediate risk PC 81% and the initial high risk PC 65%. Randomized control study has established that RP and brachytherapy have comparable 5-year biochemical recurrence rates but brachytherapy has favorable side effect profile of potency than radical prostatectomy33,34,36. Our study has confirmed these observations as 70 (10.5%) of our patients who had brachytherapy with a median follow up of 12 months (range 10 – 84 months) had significantly low PSA nadir values recorded in post treatment PSA with only 0.4% BF which responded to hormonal therapy and one (0.1%) death from PE as a result of DVT.

Current literature supports the role of EBRT in management of localized PC as comparable to RP even though it has been claimed that surgery offered better results than EBRT21,22,33,37,38,39. Our results have been encouraging since large numbers of cases 155 (23.1%) were treated in one center; the national radiotherapy center (NRC) KBTH compared to 92 (13.8%) RP at KBTH and 37 Military Hospital. There were significant falls in post treatment PSA. The national radiotherapy center (NRC) at KBTH is capable of offering services to patients from all parts of Ghana. There is another radiotherapy center at Komfo Anokye Teaching Hospital but they have not published their experiences with PC. The 3 (0.4%) deaths from bleeding due to radiation cystitis have not occurred since the introduction of conformal techniques. The efficacy of radiation therapy has been reported by ASTRO (American Society of Radiation Oncology) and AUA (American Urological Association) Joint guidelines on PC therapy31,32,35,36,37,38,40.

LOCALISED DISEASE PC WITH PROGRESSION n 98 (14.4%) – MANAGED BY HORMONAL THERAPY

The efficacy of hormonal/chemotherapy for advanced PC has been established41,42,43. Biochemical failure, castrate resistant PC occurred in 6 (0.9%) who also had CVA 2%, DVT/pulmonary embolism 2% and CCF 2%. Even though hormonal therapy is not recommended as therapy for early PC and those with life expectancy more than 10 years, these cases survived longer in the face of comorbidities. Our cases of >72 years and short life expectancy were 98 (14.4%), some elderly frail and others with serious comorbidities such as DM 3.7%, obesity 2.2% were managed by hormonal therapy when they progressed. There was significant fall in pre-treatment nadir values in PSA p< 0.002. The survival was from 36 months to 7 years which shows this is good option for these groups of patients41,42,44,45,46,47. The complications of DVT 2%, CRPC 0.9% could be expected from this form of therapy, even though soluble aspirin seems to reduce incidence of DVT.

LOCALLY ADVANCED PC T3 T4 NxM0 n = 167 (25%)

  • a

    Sixty-seven (10%) locally advanced cases were managed by neoadjuvant hormonal and radiation therapy. Figs. 6abc

Neoadjuvant hormonal therapy in 67 followed by radiation EBRT 9.6% and brachytherapy 0.4%. There were significant falls in post radiation nadir PSA in the EBRT group p< 0.0001. The survival rate in this group of cases was impressive. Promising results from several phase III trials for combining radiotherapy (brachytherapy or EBRT) with total androgen blockage (TAB) lie in the synergistic effects of both treatments32,44,48. Reports from radiation therapy oncology group(RTOG) suggest that patients with GS 7 or higher also have improved survival rate when treated by TAB and radiotherapy31,44,48,49. This holds promise for our patients with locally advanced PC who can benefit from TAB plus radiotherapy37,38,44,47,48,49,50.

  • a

    LOCALLY ADVANCED PC – managed by hormonal therapy only n 100 (15%)

One hundred cases (15%) were managed by hormonal therapy alone. The initial fall in pre-treatment PSA was significant p<0.002. The complications encountered were erectile dysfunction >12%, gynaecomastia 3%, hot flashes/flushes 9%, HRPC/CRPC 4.5%. Five percent (5%) died in hospital from progression of disease by PE, obstructive uropathy, urosepsis, bed sores and sepsis and anemia as have been previously reported41,42,43,47.

METASTATIC DISEASE

n = 87 (13%) median GS7, median prior PSA 98ng/ml. The median post treatment falls in PSA are impressive but were not subjected to statistical analysis because of non-comparable variables. These were managed by hormonal therapy and comorbidities managed by conventional methods. As expected, hospital mortality was high in these from urosepsis, obstructive uraemia and progression to hormone refractory PC or castrate resistance PC (HRPC/CRPC). Unfortunately, most of our cases could not afford docetacel, abiraterone and other efficacious therapies for CRPC.

Androgen deprivation is established as effective against advanced and metastatic PC but unfortunately with time almost all PC will become androgen refractory (HRPC/CRPC)41,42,43,45,46,47,50. The current forms of androgen deprivation function by either lowering the circulating androgens or blocking the binding of androgen to the androgen receptors39,40,41,42. But almost all androgen refractory PC remain sensitive to androgen and therefore ADT should be continued in CRPC disease, unfortunately the alternate drugs such as docetacel, carbazitazel, denossumab, bevacizumb, abiraterone and ipilimumab are very expensive and are not affordable by most of our cases or not available in Ghana. However, with limited experience stilboestrol and prednisolone have been effective in some of our cases with CRPC/HRPC cases50. The side effects of hormonal therapy include erectile dysfunction, hot flashes, sweating, gynecomastia and breast tenderness, pains from tumour flare, weight gain, memory problems, mood swings, depression, osteoporosis and risk of early heart attack. Intermittent androgen deprivation may slow down progression to CRPC with fewer side effects and is being used in some of our patients 42,45.

Cytotoxic drugs used for our CRPC were docetaxel and carbazitaxel which have been shown to be effective and improve overall survival for limited period in CRPC but are expensive and not affordable by most of our patients.

Bone pain in metastatic cases can be ameliorated by zolendonic acid and denosumad.

Novel approaches for HRPC/CRPC include immunotherapy by use of sipuleucel-T in men with asymptomatic CRPC. Abiraterone is effective with patients progressing after docetaxel but these are very expensive for our patients and effective for limited periods45.

RISK FACTORS IN PC

The risk factors reported in PC include familial 10%, sporadic 80 – 90%, presence of testes, ageing hormones, genetic factors and race. PC prevalence is highest in Caribbean Africans, African Americans, Caucasian American and least in Asians2,10,11,16,17,25,52,53. Others are increased activity of oncogenes, decreased activity of antioncogenes, increased dihydrotestosterone levels and increased activity of 5 alpha reductase, hormonal imbalance, and decreased cell death, raised BMI, early sex and Genetic /GWAS studies have incriminated HPC1, HPC2, p53, 17q21, 8q24, BRAC1 & BRAC2. Vaguely incriminated are HPV, HSV, chronic inflammation, high red meat and fatty diet.

Our genome wide studies are continuing, to date we found the following risk factors from the Ghana study. African race PC has high prevalence of 6.3 – 7% in Ghana. Our GWAS have also incriminated chromosome 10p14 with PC, aggressiveness and high PSA >52.5ng/ml GS>7 with 5q31.3. Low grade PSA <52.5ng/ml GS<7 with chromosomes Xq28 and 6q2153,54,55.

The weakness of this study included lack of follow up in some patients, high cost of treatment and the lack of insurance cover for treatment of prostate cancer. Also, complications of the curative methods RP, brachytherapy and EBRT which should be avoided.

Conclusions

Improved facilities and dedicated skilled teams led to a significant rise in proportion of organ confined Prostate Cancer from 15.3% to 62% curable by Radical Prostatectomy, brachytherapy or EBRT with longer disease free survival. Since it has been established that both the quality of life and cancer free survival for organ confined PC disease can be achieved by the above treatment modalities, physicians and urologists should be able to pick organ confined cancer by PSA testing and DRE so that patients can be diagnosed at an early stage and receive curative treatments to achieve long cancer free survival and better quality of life.

Table 2. Prostate cancer incidence vs PSA level.

PSA (ng/ml) Number Percentage%
0 – 4 9 1.5
4.1 - 10 56 8
10.1 – 20 125 18.6
> 20 460 68.7
Initial PSA not stated 19 2.8
Open in a new tab

Acknowledgment

We acknowledge the help of Medical doctors, residents, nurses, health professionals and paramedical staff, staff of pathology and medical illustration and abstractors. We also acknowledge Mrs. Evelyn Tay for coordination of the project and Ms. Victoria Okyne for coordination and secretarial services. We are also grateful to the CEO’S of Korle Bu, 37 Military Hospital, Nyaho Medical Center, SSNIT Hospital, Ministry of Health, Ghana health Service and IRB’s of NCI/NIH, CHS University of Ghana, Noguchi Memorial Institute of Medical Research and MOH for giving permission for the study which has achieved most of the objectives we set ourselves.

References

  • 1.Crawford ED. Epidemiology of prostate cancer. Urology. 2003;62:3–12. doi: 10.1016/j.urology.2003.10.013. [DOI] [PubMed] [Google Scholar]
  • 2.Hsing AW. International Trends and Patterns of cancer incidence and mortality. Int J Cancer. 2000;95:60–67. doi: 10.1002/(sici)1097-0215(20000101)85:1<60::aid-ijc11>3.0.co;2-b. [DOI] [PubMed] [Google Scholar]
  • 3.Glover Jr FE, Coffey DS, Douglas LL, Cadogan M, Russell H, Tulloch T, Baker TD, Wan RS, Walsh P. The Epidemiology of prostate cancer in Jamaica. J Urol. 1998;159(6):1984–1987. doi: 10.1016/S0022-5347(01)63220-8. [DOI] [PubMed] [Google Scholar]
  • 4.Center MM, Jeme A, Lorte-Tievlent J, Ward E, Ferlay J, Brawley O, Bray F. International variables in PC incidence and mortality rates. Eur Urol. 2012;61:1079–1092. doi: 10.1016/j.eururo.2012.02.054. [DOI] [PubMed] [Google Scholar]
  • 5.Haas GP, Delongchamps N, Brawley OW, Wang CY, de la Roza G. The worldwide epidemiology of Prostate Cancer: perspectives from autopsy studies. Can J Urol. 2008;15:3866–3871. [PMC free article] [PubMed] [Google Scholar]
  • 6.Parkin DM, Ferlay J, Curado MP, Bray F, Edwards B, Shin HR, Forman D. Fifty years of cancer incidences. International Journal of Cancer. 127(12):2918–2927. doi: 10.1002/ijc.25517. [DOI] [PubMed] [Google Scholar]
  • 7.Parkin D, Whelan SL, Ferlay J, Hambi-Cherif M, Silas F, Thomas JO, Wablington H. IARC. France: Press Lyon; 2002. Prostate Cancer in Africa Epidemiology and Prevention. [Google Scholar]
  • 8.Chu LW, Richey J, Devesa SS, Quraishi SM, Zhang H, Hsing AW. Prostate cancer incidence rates in Africa. Prostate cancer. 2011 doi: 10.1155/2011/947870. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 9.Gronberg H. PC Epidemiology. The Lancet. 361(9360):859–864. doi: 10.1016/S0140-6736(03)12713-4. [DOI] [PubMed] [Google Scholar]
  • 10.Hsing AW. Hormones and prostate cancer, what’s next? Epidemiol/Rev. 2000;23:42–58. doi: 10.1093/oxfordjournals.epirev.a000795. [DOI] [PubMed] [Google Scholar]
  • 11.Rebbeck TR, Devesa SS, Chang BL, Cheng I, Bunker CH, Cooney K, Gueyes SM, Yeboah ED, Hsing AW, Zeigler-Johnson CM. Global patterns of PC incidence, aggressiveness and mortality in men of African Descent. Prostate Cancer. 2013:1–12. doi: 10.1155/2013/560857. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 12.Bunker CH, Patrick AL, Konety BR, Onir R, Brufsky AM, Vivas CA, Beach MJ. High prevalence of screening-detected prostate cancer among Afro-Caribbeans: The Tobago prostate cancer survey . Cancer Epidemiology Biomarkers and prevention. 2002;8:726–729. [PubMed] [Google Scholar]
  • 13.Hsing AW, Yeboah ED, Biritwum R, Tettey Y, DeMarzo AM, Adjei AA, Netto G, Yu K. “High prevalence of screen detected PC in West African Men Implications for Racial Disparity in Prostate Cancer”. J Urology. 2014;192(3):730–735. doi: 10.1016/j.juro.2014.04.017. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 14.Cooperberg MR, Dubeck DP, Meng MY, Mehtan SS, Farall P. The changing face of Prostate Cancer: Trends in clinical presentation and primary management. J Clinic Onco . 2004;22(11):2141–2149. doi: 10.1200/JCO.2004.10.062. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 15.Cooperberg MR, Mevi JW, Carrol P. The changing face of low risk PC. Trends in clinical presentation and primary management. J Clinic Onco. 2005;23(11):8146–8151. doi: 10.1200/JCO.2004.10.062. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 16.Ritchey J, Biritwum RB, Yeboah ED, Tettey Y, Adjei A, Chokkallinghan A, Quaraishi S, Hsing AW. Body size and other epidemiologic characteristics in West African men implications for Racial Disparity in Prostate Cancer. American Journal of Epidemiology (AJE) 2008:01354p. [Google Scholar]
  • 17.Mutetwa B, Taioli E, Ahong-Rogers Prostate cancer characteristics and survival in males of African Ancestry according to place of birth. Data from Brooklyn – New York, Guyana, Tobago and Trinidad. Prostate. 2010;70(10):1102–1109. doi: 10.1002/pros.21144. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 18.Gann PH. Risk factors in PC. Rev Urol. 2002;4(5):3–10. [PMC free article] [PubMed] [Google Scholar]
  • 19.Laponite J, Chinde LI, Higgins JP, de Rijin MJ, Bair E, Montgomery K, Ferrari M, Egevad L. Gene expression profiling identifies clinically relevant subtypes of Prostate Cancer.; Proceedings National Academy of Sciences USA.; 2008. pp. 811–816. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 20.Walsh PC. Radical prostatectomy for localised prostate cancer provides durable cancer control with excellent quality of life. A structured debate. J of Urol. 2000;163(6):1802–1807. [PubMed] [Google Scholar]
  • 21.Walsh PC, De Weere TL, Eisenberger MA. Clinical practice localised prostate cancer. N Eng J Med. 2007;357(2):696–705. doi: 10.1056/NEJMcp0706784. [DOI] [PubMed] [Google Scholar]
  • 22.Kyei MY, Mensah JE, Gepi-Atee S, Kwami D, Ampadu K, Asante K, Klufio GO, Yeboah ED. Outcomes after Radical Prostatectomy in Ghanaians; a surgeons early experience. ISRN Urol. 2013:1–15. doi: 10.1155/2013/832496. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 23.Weldon VE, Tavel FR, Neuwitt H. Continence, potency and morbidity after radical perineal prostatectomy. J Urol. 1997;158:1470–1475. [PubMed] [Google Scholar]
  • 24.Link RE, Su LM, Sullivan W. Health related quality of life before and after laparoscopy. J Urol. 2005;173:175–179. doi: 10.1097/01.ju.0000147190.67218.1b. [DOI] [PubMed] [Google Scholar]
  • 25.Morrison BF, Conrad K, Strachan G, Miller R, W Aiken, Mayhew Radical Prostatectomy outcomes at University hospital of West Indies 2000 – 2007. West Indian Medical Journal. 60(1):68–72. [PubMed] [Google Scholar]
  • 26.Catalona WJ, Carvalhal GF, Mager DE, Smith DM. Potency continence and complication rates in 1,870 consecutive radical retropubic prostatectomies”. Journal of Urol. 1999;162(2):433–438. [PubMed] [Google Scholar]
  • 27.Patel VE, Palmer KI. Robotic Assisted laparoscopic RP perioperative outcomes of 1500 cases. J Endo Urol. 2008;22:2209–2305. doi: 10.1089/end.2008.9711. [DOI] [PubMed] [Google Scholar]
  • 28.Stolzenberg JU, Rabenat R, Do M, Kallidonis P, Liatsikos EN. Endoscopic extraperitoneal RP University of Leipsig experience of 2000 cases. J Endourol. . 2008;22(10):2319–2325. doi: 10.1089/end.2008.9714. [DOI] [PubMed] [Google Scholar]
  • 29.Isenlin CE, Robertson JE, Paulson DF. Radical perineal prostatectomy oncological outcome during a 20 year period. J Urology. 1999;161:163–168. doi: 10.1016/s0022-5347(01)62088-3. [DOI] [PubMed] [Google Scholar]
  • 30.Fiecarra VI, Nonara G, Artibani W, Cestari A, Galfano A, Graefen M, Guazzoni G. Retropubic laparocopic and robot assisted Radical Prostatectomy. A systemic review and cumulative analysis of comparative studies. Eur Urol. 2009;55:1037–1063. doi: 10.1016/j.eururo.2009.01.036. [DOI] [PubMed] [Google Scholar]
  • 31.MulCathy N. AUA and ASTRO issue Joint Guidelines for post-surgery Radiotherapy. Medscape Medical news. 2013.
  • 32.Aral IA. External Beam radiotherapy in Prostate Cancer. MEDSCAPE Medical News. 2014. pp. 1–13.
  • 33.Dong SP. Current Status of brachytherapy for prostate cancer. Korean J Urology. 2012;53(II):743–749. doi: 10.4111/kju.2012.53.11.743. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 34.Mensah JE, Yarney J, Vanderpuiye V, Akpakli E, Tagoe S, Sasu E. Prostate Brachytherapy in Ghana. Our initial experience. Journal of Contemporary Brachytherapy. 2016;8(5):289–285. doi: 10.5114/jcb.2016.62972. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 35.Keyes M, Norris J. Results of men treated in provisional brachytherapy program are among the best in the world. BC MJ. 2010;52(2):76–83. [Google Scholar]
  • 36.D’Amico AVI, Moul JW, Carrol PR, Sun L, Chen L. Surrogate endpoint for prostate cancer specific mortality after radical prostatectomy or radiation therapy. J Natl Cancer Institute. 2003;85:136–138. doi: 10.1093/jnci/djg043. [DOI] [PubMed] [Google Scholar]
  • 37.Paulson DF. Ramdomised series of treatment with surgery vs radiation for prostate adenocarcinoma. NCI Monogr. 1988:137–13. [PubMed] [Google Scholar]
  • 38.Zeleftsky MI, Fuks Z, Hunt M, Manon YY, Ling CC. High dose intensity modulated radiation therapy for PC early toxicity, and biochemical outcome in 772 patients. 2002;53(5):1111–1116. doi: 10.1016/s0360-3016(02)02857-2. [DOI] [PubMed] [Google Scholar]
  • 39.Bagshaw MA, Cox RS, Ramback JE. Radiation therapy for localized Prostate Cancer justification by long term follow up. UROL Clinics North Am. 1990;17(4):787–802. [PubMed] [Google Scholar]
  • 40.Schroder FH, Roacha M, Scandino P. Clinical decision making management of Prostate cancer. New Eng J Med. 2008;3592:2602–2609. [Google Scholar]
  • 41.Huggins C, Stevens RE, Hodges V. Studies on PC II The effects of castration on advanced PC. Archives of Surgery. . 1941;43:209–223. [Google Scholar]
  • 42.Nanniki M, Ueno S, Kitagawa Y, Fukagai T, Akaza H. Effectiveness and adverse effects of hormonal therapy for prostate cancer. Japanese experience perspective. Asian Journal of Androl. . 2012;14(3):451–457. doi: 10.1038/aja.2011.121. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 43.Prostate Cancer Trialists’ Maximum androgen blockade in advanced prostate cancer an overview of randomized trials. Lancet. 2000;255:1491–1498. [PubMed] [Google Scholar]
  • 44.Bolla M, Warde P, Collete L, Blank L, Dubois JB, Mirimane H, Storme G. Long term results with immediate androgen suppression and EBRT in patients with locally advanced PC (an EORTIC Study) a phase III randomized trial. Lancet. 2002;306:103–108. doi: 10.1016/s0140-6736(02)09408-4. [DOI] [PubMed] [Google Scholar]
  • 45.D’Lorenzo G, Buosherba C, Autorino R, Placido SD, and Scenberg CN. Castration resistant prostate cancer current and emerging treatment strategies, Drugs. 2010;70(6):963–1000. doi: 10.2165/10898600-000000000-00000. [DOI] [PubMed] [Google Scholar]
  • 46.Andriole GL, Levin DL, Crawford ED, Gelmann EP, Pinsky PF, Chia D, Kramer BS. Prostate cancer screening in prostate, lungs, colorectal and ovarian (PLCO) cancer screening Trial: Findings from initial screening round of randomized Trial. . Journal National Cancer Institute. 2005;97(6):433–438. doi: 10.1093/jnci/dji065. [DOI] [PubMed] [Google Scholar]
  • 47.Shroder FH, Huggosson J, Rovbal MJ, Teuvo LJ, Tammela TLJ, Gatto S. Screening and prostate cancer mortality in randomized European Study. N Eng J Med. 2009;360(13):1320–1328. doi: 10.1056/NEJMoa0810084. [DOI] [PubMed] [Google Scholar]
  • 48.Grimm P, Billet I, Botswick D, Dicker AP, Frank S, Immerzeel J, Kupelian P. Comparative analysis of PSA free survival outcomes of patients with low, intermediate and high risk Prostate Cancer treated by radical therapy. Results from PC results Study Gp. BJU. 2012;109(22):22–29. doi: 10.1111/j.1464-410X.2011.10827.x. [DOI] [PubMed] [Google Scholar]
  • 49.D’Amico AV, Chen MH, Renshaw AA, Loffredo RN, Kantoff PW. Androgen suppression and radiation vs radiation alone for locally advanced PC. JAMA. 2012;299(3):289–295. doi: 10.1001/jama.299.3.289. [DOI] [PubMed] [Google Scholar]
  • 50.Pollack A, Zagare FK, Starkswell PC response to radiation dose response. Results of MD Anderson phase III randomized trial. Int J Radiology Oncology. 2002; 53:1097–1103. doi: 10.1016/s0360-3016(02)02829-8. [DOI] [PubMed] [Google Scholar]
  • 51.Philips AA, Jacobson JS, Magai C, Consedius N, Horowicz-Mhler NC, Negut I. Cancer incidence and mortality in the Caribbean. Cancer Investigation. 2007;5(6):476–483. doi: 10.1080/07357900701359841. [DOI] [PubMed] [Google Scholar]
  • 52.Yeboah ED, Mensah JE, Klufio GO, Mante SD. Ketoconazole and bisphosphats in advanced hormone refractory prostate cancer in Ghanaians. BJU Int. 2002;90(2):304. [Google Scholar]
  • 53.Powell IJ, Heilbrun L, Littrup PL, Franklin A, Parzuchowski J, Gelfend D, Sakr W. Outcome of African American men screened for prostate cancer: the Detroit Education and Early Detection (DEED) study. J Urol. 1997;159(1):146–149. doi: 10.1097/00005392-199707000-00045. [DOI] [PubMed] [Google Scholar]
  • 54.Haiman CA, Chen GK, Blot WJ, Strom SS, Berndt SK, Inzes RA, Yeboah ED, Tettey Y, Adjei AA, Biritwum R. Genome wide Association study of PC in Men of African Ancestry identifies, a susceptibility locus at 17q21”. Nature Genet. 2011;43(6):570–573. doi: 10.1038/ng.839. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 55.Cook MB, Wang Z, Yeboah ED, Tettey Y, Biritwum RB, Adjei AA, Tay E, Truelove Genome wide association study of Prostate Cancer in West African Men. Human Genetics. 2014;133(5):509–521. doi: 10.1007/s00439-013-1387-z. [DOI] [PMC free article] [PubMed] [Google Scholar]

Articles from Journal of the West African College of Surgeons are provided here courtesy of Wolters Kluwer -- Medknow Publications

RESOURCES