Penile Neoplasias, Cytological Findings · P Penile Neoplasias, Cytological Findings Ika Kardum-Skelin1,3,4, Ankica Vasilj2, Sandra Kojic-Katovic2 and Marina Pazur1 1Department of

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Penile Neoplasias, CytologicalFindings

Ika Kardum-Skelin1,3,4, Ankica Vasilj2, SandraKojic-Katovic2 and Marina Pazur11Department of Clinical Cytology andCytogenetics, Merkur University Hospital,Zagreb, Croatia2Department of Clinical Cytology, SestreMilosrdnice University Hospital Centre, Zagreb,Croatia3School of Medicine, University of Zagreb,Zagreb, Croatia4Croatian Academy of Medical Sciences, Zagreb,Croatia

Definition

Penile neoplasias include Penile intraepithelial neo-plasia (PeIN) as premalignant lesions andmalignantneoplasms (squamous cell carcinoma, melanoma,basal cell carcinoma, adenocarcinoma – Paget dis-ease of the penis, sarcoma. . ..).

Epidemiology

The incidence of penile neoplasias is related to theprevalence of HPV in the population. Penile can-cer is rare in Europe, present in less than one manin 100,000, and accounts for less than 1% ofcancers in men in the USA. Penile cancer is,

however, much more common in some parts ofAsia, Africa, and South America (AmericanCancer Society 2016).

Penile Intraepithelial Neoplasia (PeIN)Definition and introduction: Penileintraepithelial neoplasia (PeIN) is a premalignantlesion that can affect any part of the penile surface.PeIN shows different degrees of dysplasia and istherefore classified into PeIN 1, 2, and 3. Allgrades of epithelial dysplasia or PeIN are histo-logical prestages of carcinoma in situ that maygradually lead to penile squamous cell carcinoma(SCS). PeIN 3 is also known as carcinoma in situ.PeIN is believed to have a close association withhuman papilloma virus infection. Treatment ofPeIN can potentially prevent progression to penilecancer (Zreik et al. 2013).

Premalignant penile lesions can be broadlydivided into those related to HPV infection andthose that are not HPV related but caused bychronic inflammation. HPV-related lesionsinclude Bowen’s disease (BD), erythroplasia ofQueyrat (EQ), and Bowenoid papulosis (BP),which are associated with “high-risk” HPV types16 and 18. Low-risk HPV types 6 and 11 areassociated with other premalignant lesions, suchas giant condylomata acuminate (GCA) orBuschke-Lowenstein tumours. Non-HPV-relatedlesions are primarily linked to genital lichensclerosus et atrophicus (LS). However, they arealso associated with rarer chronic inflammatoryconditions such as penile cutaneous horn,

# Springer International Publishing AG 2016H.V. Krieken (ed.), Encyclopedia of Pathology,DOI 10.1007/978-3-319-28845-1_4673-1

leukoplakia, and pseudoepitheliomatous, kera-totic micaceous balanitis (PKMB) (Algabaet al. 2002; Backes et al. 2009; Barbagliet al. 2006).

A recent reclassification system based on cellmorphology, squamous differentiation, and path-ogenesis has been suggested. In the new proposedclassification system the term penileintraepithelial neoplasia (PeIN) is used to describeall premalignant lesions. It is further subclassifiedinto differentiated PeIN, the subtype most fre-quently associated with chronic inflammationand not HPV, and three other subtypes (warty,basaloid, and mixed warty-basaloid), which arelinked to HPV infection (Chaux et al. 2010;Wikström et al. 2012; Cubilla et al. 2000).

Pathology: Morphological criteria for differ-entiated PeIN included the presence of acanthosis,abnormal epithelial maturation with cellularatypia at the basal/parabasal regions or above inthe epithelium, enlarged keratinocytes with abun-dant eosinophilic cytoplasm, prominentintercellular bridges, vesicular nuclei, and occa-sional prominent nucleoli, hyperkeratosis/hyper-granulosis, elongation of rete ridges, andintraepithelial keratin pearl formation. Amongthe undifferentiated variants, in basaloid PeIN,the epithelium was replaced by a monotonouspopulation of small- to intermediate-sized, roundto ovoid, rarely spindle, immature cells with highnuclear/cytoplasmic ratio, abundant mitosis andapoptotic bodies, flat or slightly irregular epithe-lial surface, and abrupt parakeratosis; focalkoilocytosis was acceptable.

Warty PeIN was characterized by a thickenedepithelium with undulating/spiking papillary sur-face, parakeratosis, cellular pleomorphism andanaplasia, conspicuous, often pleomorphic,koilocytosis, and dyskeratosis. Warty-basaloidPeIN showed overlapping features of both wartyand basaloid types, with basaloid-type cells in thebottom half and warty features at the surface(Cubilla et al. 2000).

Cytologyfindings:Mild dysplasia (PeIN grade I).Cytological atypia is generally slight with only mildpleomorphismof cells or nuclei. Cytological samples

are brush and scarf. Corresponding cytologic sam-ples show abnormal cells with mature or superficial-type cytoplasm. Low-grade lesion typically involvessquamous cells with mature, intermediate, orsuperficial-type cytoplasm with well-defined polyg-onal cell borders. Nuclear enlargement is at leastthree times the size of a normal intermediate cellnucleus (Wikström et al. 2012). Although thenucleus is hyperchromatic, the chromatin is distrib-uted uniformly or it may appear degenerated andsmudged if associated with cytopathic changesinduced by HPV. Cells with HPV cytopathic effect(koilocytes) are also interpreted as low-grade dyspla-sia or PeIN I on cytologic smears. In these cases, thenucleus may not be enlarged, but is usually hyper-chromatic and “wrinkled” (Wikström et al. 2012).

Moderate dysplasia (PeIN grade II) demon-strates a proliferation of atypical cells extendinginto the middle third of the epithelium. The cyto-logical changes are more severe than in mild dys-plasia and changes such as hyperchromatism andprominent cell and nuclear pleomorphism may beseen. Increased and abnormal mitoses may bepresent, but these are usually located in the basallayers. Cytologically moderate dysplasia showscells with less cytoplasm, larger nuclei, and occa-sionally with asymmetrical nuclear outlines. Thechromatin is increased and granular (Wikströmet al. 2012) (Fig. 1).

In severe dysplasia (PeIN grade III) there isabnormal proliferation from the basal layer intothe upper third of the epithelium. These changesare seen in cytologic smears as immature cells,with scant cytoplasm and a high nuclear-cytoplasmic ratio. The abnormal cells can beseen singly or in crowded, dark sheets/groups(Wikström et al. 2012) (Fig. 2).

Differential diagnosis: Balanitis, psoriasis,contact dermatitis, and eczem are chronical skinconditions characterized by skin inflammationand irritation without cellular atypia, lichenplanus, lichen sclerosus and Erythroplasia ofQueyrat show hyperkeratosis, chronic inflamma-tions (infiltrate lymphocytes, plasma cells), andmild to moderate dysplasia with or without cyto-pathic changes induced by HPV, and Zoon’s

2 Penile Neoplasias, Cytological Findings

Penile Neoplasias, Cytological Findings,Fig. 1 Penile intraepithelial neoplasia (PeIN grade II).Cytological atypia is generally slight with only mild

pleomorphism of cells or nuclei (Dermal swab of leuko-plakia on the penis, May-Grünwald Giemsa, (a, b) �400and (c, d) �1000)

Penile Neoplasias, Cytological Findings,Fig. 2 Penile intraepithelial neoplasia (PeIN grade III).In severe dysplasia with changes are seen in cytologic

smears as immature cells, with scant cytoplasm and ahigh nuclear-cytoplasmic ratio (Dermal swab of thepenis, May-Grünwald Giemsa �1000)

Penile Neoplasias, Cytological Findings 3

balanitis looks similar to PeIN grade III but havedense plasma cell infiltrate.

The differential diagnosis between penileintraepithelial lesions can be difficult. At lowpower view, warty lesions are papillary andbasaloid lesions are flat. Cytologically, the formeris more keratinized and pleomorphic, with con-spicuous koilocytosis, whereas in basaloid PeIN,there is a uniform small, nonkeratinizing cell pat-tern. Basaloid PeIN should also be distinguishedfrom flat urothelial carcinoma in situ of distalurethra, which may secondarily involve the penilemeatal region. Squamous cell carcinoma is themost severe form of epithelial dysplasia.

Squamous Cell Carcinoma (SCC)Definition: SCC is the most frequent penile can-cer, usually originates from the epithelium of theglans or the foreskin (Hakenberg et al. 2014), andcan develop anywhere on the penis. Around 95%of penile cancers are SCCs. Early stage of SCC iscarcinoma in situ (CIS), without invasion by neo-plastic squamous cells into the deeper tissues(stroma) of the penis.

Pathology: Squamous cell carcinoma origi-nates in epidermis, squamous mucosa, or areasof squamous metaplasia. In skin, it arises fromthe epithelial cells of the epidermis as a smallgrey or brownish lesion with irregular margins toexophytic tumour or ulcer. The diagnosis of cSCCis primarily based on clinical features. A biopsy orexcision and histologic confirmation should beperformed in all clinically suspicious lesions inorder to facilitate the prognostic classification andcorrect management (Stratigos et al. 2015). Thehistologic subtype has also been considered as afactor in determining the prognosis. Several his-tologic subtypes of SCC are described, includingkeratoacanthoma, acantholytic, spindle cell,verrucous, clear cell, papillary, signet ring,pigmented, and desmoplastic SCC. These variantsof SCC are reviewed for their clinical and histo-logic features and the risk of recurrence andmetastasis (Rinker et al. 2001).

Cytology findings: Bowen disease (BD), squa-mous cell carcinoma in situ (SCCIS), is the mostsevere form of epithelial dysplasia. When thecytological changes are very marked this may

indicate that a lesion should be upgraded. Featuresthat favor a high-grade lesion include increasednumbers of abnormal cells, higher nuclear/cyto-plasmic ratios, greater irregularities in the outlineof the nuclear envelope, coarsening of nuclearchromatin, and chromatin clumping. Cell size,overall, is smaller in carcinoma in situ. Theyhave a more immature type of cytoplasm thatcan be lacy and delicate or dense/metaplasticwith rounded cell borders. At times it may not bepossible to exclude the possibility of invasivecarcinoma in such cases (Wikström et al. 2012).SCC of the penis, similarly to the cervix, vagina,vulva, or oropharynx, varies from well-differentiated keratinizing tumors to anaplasticcarcinomas with scant keratinization. Mosttumors are highly keratinized and moderately dif-ferentiated with bizarre enlarged cells includingtadpole and fiber cell forms with hyperchromaticand irregular nuclei in a hemorrhagic and necroticbackground (Figs. 3, 4, 5, and 6). Poorly differen-tiated carcinomas have variable amounts of spin-dle or giant cell with nonkeratinized cytoplasmand prominent nucleoli (American Cancer Society2016; Kocjan et al. 2013) (Fig. 7).

Differential diagnosis: Squamous cell carci-noma is an invasive malignant neoplasm.Depending on the degree of cell differentiaton,cells are bizarre large, elongated, and hyper-chromatic or multinucleated admixed in hemor-rhagic, necrotic background (Gray and Kocjan2010). Bowen disease is a squamous cell carci-noma in situ (SSCIS) showing epidermal dyspla-sia with an intact basement membrane (Baradet al. 2014). Atypical keratinocytes have less cyto-plasmic and/or nuclear pleomorhism withouthemorrhagic and necrotic background.

Basal Cell Carcinoma (BCC)Definition: BCC is the cancer that develops frombasal cells in the deepest layer of the skin. It is avery slow growing cancer and very rarely spreadsto distant parts of the body. Basal cell carcinomaof the penis is an extremely rare entity, accounts0.03% of all BCCs in men, with very good prog-nosis (Roewe et al. 2014).

Pathology: Basal cell carcinoma (BCC) is thetumor that affects mainly photoexposed areas,


most often in the head, and seldom appears ongenitalia and perigenital region (Dourmishevet al. 2013). The tumour infiltrates tissues in athree-dimensional fashion through the irregulargrowth of subclinical finger-like outgrowthswhich remain contiguous with the main tumourmass. Clinical appearances and morphology arediverse and include nodular, cystic, superficial,morphoeic (sclerosing), keratotic, and pigmentedvariants. Common histological subtypes includenodular (nBCC), superficial (sBCC), andpigmented forms in addition to morphoeic, micro-nodular, infiltrative, and basosquamous variantsthat are particularly associated with aggressivetissue invasion and destruction. Perivascular orperineural invasion are features associated withthe most aggressive tumours (Telfer et al. 2008).The currently most favoured classification is onebased predominantly on histological growth

pattern. This classification contributes to the use-ful concept of low- and high-risk histological sub-types of BCC (Saldanha et al. 2003).

Cytology findings: Smears of BCC are verycellular with cohesive sheets of small uniformcells without variation in nuclear size and shape(Fig. 8). Nuclei are hyperchromatic round or ovaland have granular chromatin. Cytoplasm is scantywith indistinct cell borders (Kocjan et al. 2013)(Figs. 9 and 10).

Differential diagnosis: Tumors with basaloidcells may be mistaken for the basal cell carcinomaas a pilomatrixoma or sebaceous gland tumors. Incase of pilomatrixoma, it helps clinical presenta-tion, “ghost” cells, and multinucleate giant cells.Merkel cell carcinoma has greater cellular disso-ciation. Metastatic small cell carcinoma hasshown moulding efect and sometimes necroticbackground (Gray and Kocjan 2010).

Penile Neoplasias, Cytological Findings, Fig. 3 Well-differentiated squamous cell carcinoma. (a–c) Elongatedcells including tadpole and fiber cell forms in a

hemorrhagic background (Swab of the shaft penis,May-Grünwald Giemsa �400)


Adenocarcinoma: Paget DiseaseDefinition: Adenocarcinoma – Paget disease isthe cancer of the glandular cells that producesweat in the skin of the penis, similarly to theperineum, vulva, axilla, and scrotum. It is a rarecutaneous, intraepithelial adenocarcinoma of theepidermis, which sometimes infiltrate into theunderlying dermis. Isolated Paget’s disease ofthe penis is extremely rare.

Pathology: Paget’s disease was described byPaget in 1874 as mammary and extramammary.Extramammary Paget’s disease is considered anadenocarcinoma originating from the skin or skinappendages in areas with apocrine glands. Theprimary location is the vulvar area, perianalregion, scrotum, penis, and axillae as an erythem-atous plaque of indolent growth, with well-defined edges, fine scaling, excoriations,

exulcerations, and lichenification (Lopes Filhoet al. 2015).

Cytology findings: With the imprint smears,various sizes of Paget’s cells were evident on amonolayer sheet but there was no overlapping.Their cell borders were defined, and theircytoplasma were abundant. The shape of thenuclei was mostly round or oval, and the nuclearrims were thin and irregular.

The chromatin patterns were finely granular orreticular (Sheue-mei et al. 1986) (Fig. 11).

Differential diagnosis: Paget’s disease is a raredisease which can mimic various types of derma-tosis. Differential diagnosis includes the follow-ing dermatoses: Bowen’s disease, tinea cruris,contact dermatitis, lichen simplex, lichen planus,psoriasis, and seborrheic dermatitis. The Paget’scells are larger than keratinocytes, have clear

Penile Neoplasias, Cytological Findings, Fig. 4 Well-differentiated squamous cell carcinoma. Large hyper-cromatic elongated or poligonal atypical cells with

hyperchromatic irregular nuclei and abundant cytoplasm(Swab of the shaft penis, May-Grünwald Giemsa �1000)


chromatin, a prominent nucleolus, and gray–bluecytoplasm, and they may appear vacuolated. Allthese characteristics of the Paget’s disease unlikevarious dermatoses are consistent with their glan-dular nature. A high index of suspicion isrequired, combined with biopsy and immunohis-tochemical staining in order to make the correctdiagnosis.

MelanomaDefinition:Malignant melanoma is a malignancyof melanocytes. Penile melanoma is a rare cancerwith a poorer prognosis than that of cutaneousmelanoma as there is usually a delay in the pre-sentation and diagnosis (Van Geel et al. 2007).The incidence of primary penile melanoma isthought to be between 0.1% and 0.2% of all mel-anomas, and the disease constitutes less than 2%

of all malignancies at this site. Melanoma of theglans penis may be epidermal or mucosal in ori-gin. Mucosal melanoma arises from the distalurethra while epidermal melanomas arise fromthe glans (Sanchez-Ortiz et al. 2005; Trittonet al. 2008).

Pathology: Penile melanomas usually presentsas a pigmented macule, papule, or ulceration withan irregular border; however, it can also beunpigmented. It is typically found on the glanspenis and less often on the prepuce. The AmericanJoint Committee on Cancer system for classifyingcutaneous melanomas includes the depth of inva-sion (Clark staging) and tumor thickness (Breslowlevel, direct measurement). Hematogenous metas-tases occur through the vascular structures of thecorporal bodies; lymphatic spread to the regionallymphatic ilioinguinal nodes occurs by lymphatic

Penile Neoplasias, Cytological Findings,Fig. 5 Squamous cell carcinoma. (a, b) Metastatic squa-mous cell carcinoma of the penis to iliac crest (Bone

marrow aspirate of iliac crest, May-Grünwald Giemsa�1000); (c) Immunocytochemistry. Pan-cytokeratin posi-tive cells (LSAB �100)


Penile Neoplasias, Cytological Findings,Fig. 6 Squamous cell carcinoma. (a–c) Bizarre enlargedcells including tadpole and fiber cell forms with

hyperchromatic and irregular nuclei in a hemorrhagic andnecrotic background (Swab of the glans penis,May-Grünwald Giemsa �400)

Penile Neoplasias, Cytological Findings,Fig. 7 Poorly diferentiated squamous cell carcinoma.Large poorly diferentiated atypical cells with irregular

nuclei (Swab of the glans penis, May-Grünwald Giemsa�1000)


permeation (Pettaway et al. 2007). Histopatholog-ical examination of specimens is performed basedon the cellular differentiation, pleomorphism,solidity, and grade of tumor according to WHO’sschema.

Cytology findings: Malignant cells from mel-anoma (epitheliod and pleomorphic subtype) usu-ally contain moderate amounts of cytoplasm, andcytoplasmic melanin pigment is identified intumor cells. Melanin pigment may also be seenin macrophages. The cells exhibit moderate tomarked nuclear pleomorphism and, in some

cases, contain binucleate and multinucleate cells.Nuclear chromatin is finely or coarsely granular,and nuclear membrane irregularities may be seen.Nucleoli are often prominent, and some cells maycontain large eosinophilic macronucleoli.Intranuclear cytoplasmic invaginations(pseudoinclusions) may be seen (Fig. 12). Some-times the background contains necrotic debris(Murali et al. 2008). Additionally, diagnosis issupported by immunostainings with a specificmarker for melanoma (Protein S-100 +,HMB – 45 +, Melan A) (Fig. 13).

Penile Neoplasias, Cytological Findings, Fig. 8 Basalcell carcinoma. (a, b) Clusters of small uniform cells and

many background stripped nuclei (Dermal swab of thepenis, May-Grünwald Giemsa �400)

Penile Neoplasias, Cytological Findings, Fig. 9 Basalcell carcinoma. (a, b) Small uniform cells with scantycytoplasm, hyperchromatic round or oval nuclei and

granular chromatin (Dermal swab of the penis,May-Grünwald Giemsa �1000)


Differential diagnosis: Differential diagnosisincludes: dysplastic nevi, pigmented basalioma,pigmented Bowens disease, and seborrheic kera-toses. Malignant cells from melanoma (epitheliod

and pleomorphic subtype) usually contain moder-ate amounts of cytoplasm, and cytoplasmic mela-nin pigment is identified in tumor cells.

Penile Neoplasias, Cytological Findings,Fig. 10 Basal cell carcinoma. Immunocytochemistry. (a,

b) Pancytokeratin positive cells, (c) cells negative forvimentin, (d) weak positivity to CK5/6 (LSAB �1000)


Penile Neoplasias, Cytological Findings,Fig. 11 Adenocarcinoma – Paget disease. Large Paget’scells with defined borders, abundant cytoplasm, round or

oval nuclei, and irregular nuclear rims (Dermal swab ofeczematosed lesion of the penis, May-Grünwald Giemsa�1000)


Penile Neoplasias, Cytological Findings,Fig. 12 Melanoma. (a–f) Various size of atypicalmono- andmultinucleated cells with large lobulated nuclei,prominent nucleoli, moderate amounts of cytoplasm with

melanin pigment in tumor cells, macrophages, and extra-cellular. (g, h) Amelanotic pleomorphic cells (Fine-needleaspirate of inguinal lymph node, metastatic melanoma ofthe penis, May-Grünwald Giemsa �1000)


References and Further Reading

Algaba, F., Horenblas, S., Pizzocaro, G., Solsona, E., &Windahl, T. (2002). European Association of Urology.EAU guidelines on penile cancer. European Urology,42, 199–203.

American Cancer Society. (2016). Cancer facts & figures.Penile cancer. Atlanta: American Cancer Society.

Backes, D. M., Kurman, R. J., Pimenta, J. M., & Smith,J. S. (2009). Systematic review of human papillomavi-rus prevalence in invasive penile cancer. CancerCauses and Control, 20, 449–457.

Barad, P., Fernandes, J., & Shukla, P. (2014). Bowen’sdisease: A favorable response to imiquimod. IndianDermatology Online Journal, 5(4), 546–547.doi:10.4103/2229-5178.142570.

Barbagli, G., Palminteri, E., Mirri, F., Guazzoni, G., Turini,D., & Lazzeri, M. (2006). Penile carcinoma in patientswith genital lichen sclerosus: A multicenter survey. TheJournal of Urology, 175, 1359–1363.

Chaux, A., Pfannl, R., Lloveras, B., Alejo, M., Clavero, O.,Lezcano, C., Muñoz, N., de Sanjosé, S., Bosch, X.,Hernández-Pérez, M., Velazquez, E. F., & Cubilla,A. L. (2010). Distinctive association of p16INK4aover-expression with penile intraepithelial neoplasia(PeIN) depicting warty and/or basaloid features:A study of 141 cases evaluating a new nomenclature.The American Journal of Surgical Pathology, 34,385–392.

Cubilla, A. L., Meijer, C. J., & Young, R. H. (2000).Morphological features of epithelial abnormalities andprecancerous lesions of the penis. Scandinavian Jour-nal of Urology and Nephrology, 205, 215–219.

Cubilla, A. L., Dillner, J., Schellhammer, P. F., &Horenblas, S. (2004). Tumours of the penis: Malignantepithelial tumours. In J. N. Eble, G. Sauter, J. I. Epstein,& I. A. Sesterhenn (Eds.), World Health Organizationclassification of tumours pathology & genetics oftumours of the urinary system and male genital organs(pp. 279–290). Lyon: IARC Press.

Penile Neoplasias, Cytological Findings,Fig. 13 Melanoma. Immunocytochemistry. (a, b) Malig-nant cells immunostained for HMB45, (c, d) cells positive

for Melan A (Fine-needle aspirate of inguinal lymph node,metastatic melanoma of the penis, LSAB �1000)


Dourmishev, L. A., Rusinova, D., & Botev, I. (2013).Clinical variants, stages, and management of basalcell carcinoma. Indian Dermatology Online Journal,4(1), 12–17. doi:10.4103/2229-5178.105456.

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Kocjan, G., Gray, W., Levine, T., Kardum-Skelin, I., &Vielh, P. (2013). Diagnostic cytopathology essentials.London: Churchill Livingstone.

Lopes Filho, L. L., Lopes, I. M., Lopes, L. R., Enokihara,M. M., Michalany, A. O., & Matsunaga, N. (2015).Mammary and extramammary Paget’s disease. AnaisBrasileiros de Dermatologia, 90(2), 225–231.doi:10.1590/abd1806-4841.20153189.

Murali, R., Loughman, N. T.,McKenzie, P. R.,Watson, G. F.,Thompson, J. F., & Scolyer, R. A. (2008). Cytologicfeatures of metastatic and recurrent melanoma in patientswith primary cutaneous desmoplastic melanoma.American Journal of Clinical Pathology, 130, 715–723.

Pettaway, C., Lynch, D., & Davis, J. (2007). Tumors of thePenis. In A.Wein, L. Kavoussi, A. Novick, A. Partin, &C. Peters (Eds.), Campbell-Walsh urology (9th ed.,p. 967). New York: Elsevier.

Rinker, M. H., Fenske, N. A., Scalf, L. A., & Glass, L. F.(2001). Histologic variants of squamous cell carcinomaof the skin. Cancer Control, 8(4), 354–363.

Roewe, R.J., Uhlman, M.A., Bockholt, N.A., & Gupta, A.(2014). Basal cell carcinoma of the penis: A case reportand review of the literature. Case Reports in Urology,Article ID 173076, 3 pages. doi:10.1155/2014/173076.

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Sanchez-Ortiz, R., Huang, S. F., Tamboli, P., Prieto, V. G.,Hester, G., & Pettaway, C. A. (2005). Melanoma of thepenis, scrotum and male urethra: A 40-year singleinstitution experience. The Journal of Urology, 173,1958–1965.

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Penile Neoplasias, Cytological Findings · P Penile Neoplasias, Cytological Findings Ika Kardum-Skelin1,3,4, Ankica Vasilj2, Sandra Kojic-Katovic2 and Marina Pazur1 1Department of