Immunohistochemical Features of Prostatic Carcinoma in Southwest Nigeria: A Ten-Year Retrospective Study

Olabisi Ayo-Aderibigbe *

Department of Morbid Anatomy and Histopathology, Ladoke Akintola University of Technology, Ogbomoso, Oyo State, Nigeria.

Donatus Sabageh

Department of Morbid Anatomy and Histopathology, Ladoke Akintola University of Technology, Ogbomoso, Oyo State, Nigeria.

Oluwole Olaniyi Odujoko

Department of Morbid Anatomy and Histopathology, Ladoke Akintola University of Technology, Ogbomoso, Oyo State, Nigeria.

Adebayo Ayoade Adekunle

Department of Morbid Anatomy and Histopathology, Ladoke Akintola University of Technology, Ogbomoso, Oyo State, Nigeria.

*Author to whom correspondence should be addressed.


Background: The diagnosis of prostatic adenocarcinoma relies on a constellation of architectural and cytological features. However, some cases may pose some diagnostic challenges especially where there are only small foci of cancer where only a few atypical glands are present, especially in needle biopsies. Therefore, immunohistochemistry may be used to differentiate benign from malignant proliferations, primary prostatic lesions and secondary lesions from other sources.

Objectives: To determine the immunohistochemical profile of prostatic carcinoma seen at the Department of Morbid Anatomy and Histopathology, Ladoke Akintola University of Technology Teaching Hospital, Osogbo, using high molecular weight cytokeratin, alpha-methylacyl co-enzyme A racemase and Ki-67 markers.

Methods: This was a retrospective study involving all cases of diagnosed prostatic carcinoma in the Department of Morbid Anatomy and Histopathology of the Ladoke Akintola University of Technology Teaching Hospital, Osogbo, Osun State, Nigeria. The histologic slides were reviewed for the histological variant of prostatic carcinoma as well as the Gleason histologic grade of the tumour and the presence of high-grade prostatic intraepithelial neoplasia (HGPIN). Immunohistochemistry was done using high molecular weight Cytokeratin (HMWCK), a basal cell marker, and alpha-methyl acyl CoA racemase (AMACR), a marker of malignant prostatic cells. Ki-67 antibody was used to assess the proliferating index of the tumour.  

Results: The majority of cases (72.8%) were seen between the ages of 61 and 80 years while the peak age of frequency was the 71-80-year age group. Prostatic carcinoma constituted 4.4% of all tumours and 18.7 % of malignant tumours. A total of 204 (54.8%) cases were well-differentiated tumours, 104 (27.9%) moderately differentiated, and 64 (17.2%) were poorly differentiated. The most common histologic type (73.7%) was acinar adenocarcinoma, while colloid carcinoma was the least common variant (0.2%). HGPIN was seen in 111 cases (29.9%). Most of the cases of prostatic carcinoma (78.8%) were negative for Ki-67. All well-differentiated tumours were negative for the marker.

Conclusion: Prostatic carcinoma is the commonest malignant tumour in males in this environment with a frequency that increases with age. Poorly differentiated tumours are more like to be associated with a younger age at presentation. HGPIN appears to be a true precursor lesion. Immunohistochemistry with HMWCK and AMACR should be reserved for equivocal cases only. The Ki-67 marker may help segregate tumours with poorer prognosis.

Keywords: Immunohistochemistry, prostate carcinoma, adenocarcinoma

How to Cite

Ayo-Aderibigbe , O., Sabageh , D., Odujoko , O. O., & Adekunle , A. A. (2023). Immunohistochemical Features of Prostatic Carcinoma in Southwest Nigeria: A Ten-Year Retrospective Study. Asian Oncology Research Journal, 6(1), 85–93. Retrieved from


Download data is not yet available.


Epstein JI, Algaba F, Allsbrook Jr WC , Bastacky S, Boccon-Gibod AM, De Marzo AM et al. Tumours of the prostate: Pathology and genetics of tumours of the urinary system and male genital organs. WHO Tumours of the Urinary System and Male Genital Organs. IARC Lyon; 2004.

Meyer FJ, Gumerlock PH, Chi SG, Borchers H, Decters AD, Devere –White RW . Very frequent p53 mutations in metastatic prostate carcinoma and match primary tumors. The Am Cancer Society Cancer. 1998;83(12):25394-25399.

Roylance R, Spurr N, Sheer D. The genetic analysis of prostate carcinoma. Seminars in Cancer Biology. 1997;8:37–44.

Meid FH, Gygi CM, Leisinger HJ, Bosman FT, Benhattar J. The use of telomerase activity for the detection of prostatic cancer cells after prostatic massage. Journal of Urology. 2001;165:1802–1805.

Waghray A, Schober M, Feroze F, Yao F, Virgin J, Chen YQ. Identification of differentially expressed genes by serial analysis of gene expression in human prostate cancer. Cancer Research. 2001;61:4283–4286.

Ingles Ingles SA, Ross RK, Yu MC, Irvine RA, La Pera G, Haile RW et al. Association of prostate cancer risk with genetic polymorphisms in vitamin D receptor and androgen receptor. J Natl l Cancer Inst. 1997;89:166–170.

Pisters LL, Troncoso P, Zhau HE, Li W, von Eschenbach AC, Chung LW. c-met proto-oncogene expression in benign and malignant human prostate tissues. J Urology. 1995;l 154:293–298.

Herawi M, Parwin AV, Irie J, Epstein JL. Small glandular proliferation in needle biopsies; most benign mimickers of prostatic adenocarcinoma sent in for expert second opinion. Am J Surg Pathol. 2005;29(7):874-80.

Jorda M, Morales A, Ghorab Z, Fernandez G, Nadji M, Block N. Her2NEU expression in prostatic cancer: A comparison with mammary carcinoma. J Urol. 2002;168:1412–1414.

Leibovich Leibovich BC, Cheng L, Weaver AL, Myers RP, Bostwick DG. Outcome prediction with p53 immunostaining after radical prostatectomy in patients with locally advanced prostate cancer. J Urol. 2000;163:1756–1760.

Quinn DI, Henshall SM, Head DR, Golovsky D, Wilson JD, Brenner PC et al. Prognostic significance of p53 nuclear accumulation in localized prostate cancer treated with radical prostatectomy. Cancer Res. 2000;60:1585–1594.

Cher M, MacGrogan D, Bookstein R, Brown JA, Jenkins RB, Jensen RH. Comparative genomic hybridization, allelic imbalance, and fluorescence in situ hybridization on chromosome 8 in prostate cancer. Genes Chromosomes Cancer. 1994;11:153–162.

Henke RP, Kruger E, Ayhan N, Hubner D, Hammerer P, Huland H. Immunohistochemical detection of p53 protein in human prostatic canceC. J. Urol. 1994;152:1297–1301.

Cairns P, Okami K, Halachmni S, Halachmni N, Estellar M, HermanJG et al. Frequent inactivation of PTEN/MMAC1 in primary prostate cancer. The AmJ Cancer. 1997;57:4997-5000.

Menamin MC. Loss of PTEN expression in paraffin-embedded primary prostate cancer correlates with, high Gleason score and advanced stage. Cancer Res. 1998;59:4291–4296.

Zhou M, Jiang Z, EpsteinJL. Expression and diagnostic utility of alpha-methyl acylCoA racemase (P504S) in a foamy glands pseudohyperplastic prostatic cancer. Am J Surg Pathol. 2003;27:772-778.

Cairns -Cairns P, Okami K, Halachmi S, Halachmi N, Esteller M, Herman JG et al. Frequent inactivation of PTEN/MMAC1 in primary prostate cancer. Cancer Res.`1997:57:4997–5000.

Colombel M, Symmans F, Gil S, O'Toole KM, Chopin D, Benson M et al. Detection of the apoptosis-suppressing oncoprotein bc1-2 in hormone-refractory human prostate cancers. Am J Pathol. 1993;143:390-400.

Hockenbery DM, Zutter M, Hickey W, Nahm, Korsmeyer SJ. BCL2 protein is topographically restricted in tissues characterized by apoptotic cell death. Proc. Natl. Acad. Sci. 1991;88:6961– 6965.

Raffo AJ, Perlman H, Chen MW, Day ML, Streitman JS, Buttyan R. Expression of bcl-2 protects prostate cancer cells from apoptosis In vitro and confers resistance to androgen depletion in vivo. Cancer Res. 1995;55:4438–4445.

Bubendorf L, Kononen J, Koivisto P, Schraml P, Moch H, Gasser TC et al. Survey of gene amplifications during prostate cancer progression by high-throughput fluorescence in situ hybridization on tissue microarrays. Cancer Res 1999; 59:803–806.

Dorai T, Olsson CA, Katz AE, Buttyan R. Development of a hammerhead ribosome against bcl-2. I. Preliminary evaluation of a potential gene therapeutic agent for hormone-refractory human prostate cancer. Prostate. 1997;32:246–258.

Leav I, Plescia J, Goel HL, Li J, Jiang Z, Cohen RJ et al. Cytoprotective Mitochondrial Chaperone TRAP-1 As a Novel Molecular Target in Localized and Metastatic Prostate Cancer. Am J Pathol. 2010;176 (1):393–401.

Zha J, Huang YF. TGF-beta/Smad in prostate cancer: An update. Zhonghua Nan Ke Xue (in Chinese). 2009;15(9):840–843.

Senapati S, Rachagani S, Chaudhary K, Johansson SL, Singh RK, Batra SK. Overexpression of macrophage inhibitory cytokine-1 induces metastasis of human prostate cancer cells through FAK–RhoA signaling pathway. Oncogene. 2010;29 (9):1293–1302.

Watanabe SI, Miyata Y, Kanda S, Iwata T, Hayashi T, Kanetake H et al. Expression of X- linked inhibitor of apoptosis protein in human prostate cancer with or without neo-adjuvant therapy. J Cancer Res Clin Oncol. 2009;136;787-793.

Dimitropoulou P, Lophatananon A, Easton D, Pocock R., Dearnaley DP, Guy M et al. The UK genetic prostate cancer study collaborators. British Association of Urological Surgeons. Section of Oncology BJU International. 2009;103:178–185.

Michael F, Leitzmann MD, Elizabeth A, Platz SCD, Meior J, Stampfer MD et al. Ejaculation frequency and subsequent risk of prostatic cancer. JAMA. 2004;291:1578-1586.

Cheville JC, Reznicek MJ, Bostwick DG. The focus of “atypical glands, suspicious for malignancy” in prostate needle biopsy specimens: Incidence, histologic features, and clinical follow-up of cases diagnosed in a community practice. Am J Clin Pathol. 1997;108:633–640.

Oluwole OP. Taiwo JO, Awani KU, Adugba EO. Studies on prevalence of prostate cancer in Lokoja metropolis. Advance Tropical Medicine and Public Health International. 2011;2(1):15-20

Ekwere PD, Egbe SN. The changing pattern of prostatic cancer in Nigerians: Current status in southeastern states. J Natl Med Assoc. 2002;94:1340-1343

Eke N, Saspira MK. Prostate cancer in Port Harcourt, Nigeria: Features and outcome. Niger J Surg Res. 2002;4:34-44.

Osegbe DN. Prostatic cancer in Nigeria: Facts and non facts. J Urol. 1997;157:1340-1343.

Cowen D, Troncoso P, Vincent S, Khoo, Gunar K, Zager S et al. Ki-67 staining is an independent correlate of biochemical failure in prostate cancer treated with radiotherapy. Clinical Cancer Research. 2002;8(5):275-280.