Clonal abnormalities in a recurrent laryngeal papilloma
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Cancer Genetics and Cytogenetics 159 (2005) 190–191 Letter to the editor Clonal abnormalities in a recurrent laryngeal papilloma Although clonal chromosomal aberrations are usually considered hallmarks of neoplasm, the occurrence of nonran- dom changes has been documented in several benign condi- tions, namely, Dupuytren contracture [1–4], carpal tunnel syndrome [5], and Peyronie disease of the penis [6,7]. We have recently found trisomy 8 and loss of the Y in a recurrent laryngeal papilloma, and therefore would add that lesion to the list of hyperproliferations with clonal changes. Our patient, a 77-year-old man, recalls multiple surgical procedures in early childhood for laryngeal papillomas. He is not sure of the number or of his age at the times of surgery. There is no information available regarding possible maternal condyloma. He was followed with periodic exami- nations but with no recurrence in adolescence. At age 20 years, however, upon discharge from the U.S. Army, he again had surgery for removal of a lesion. An examination at age 50 years was normal. Increasing hoarseness led to a self-referral at age 77 years. The patient has never smoked, nor been exposed to significant workplace air pollution. At this recent referral, a single lesion was seen and subse- quently removed. Pathologic examination showed papillary squamous proliferation made up of fibrovascular cores lined with benign squamous epithelium. There were a few mitotic figures within the basal cells, but there was no dysplasia (Fig. 1). Papilloma tissue was cultured and karyotyped using standard methods. Four cell lines were found: 47,XY,8[4]/ 45,X,Y[2]/46,Y,8[2]/46,XY[11]. The patient’s past medical history is significant, in that he was diagnosed with cutaneous T-cell lymphoma (CTCL) at age 67 years; a single lesion, biopsied at age 34 years and deemed to be “parapsori- asis” was probably a first manifestation, although no further CTCL lesions occurred for 33 years. Laryngeal papillomas are benign lesions usually caused by papillomaviruses. Juvenile onset is associated with mater- nal genital condylomata, the incidence of affected offspring being 7 of every 1,000 children born to affected mothers [8]. Most cases of juvenile laryngeal papillomas regress with puberty. It is not known under what circumstances the papil- loma virus may be reactivated. Smoking and alcohol have been suggested as possible risk factors. A recent case of recurrence was reported in a 44-year-old woman who, in addition to being a heavy smoker, had a concomitant candida infection of the glottis [9]. Our patient has never smoked, nor ever been a heavy drinker. The viral reactivation may be a reflection of his CTCL rendering him immunologically 0165-4608/05/$ – see front matter 2005 Elsevier Inc. All rights reserved. doi:10.1016/j.cancergencyto.2004.11.001 compromised. Alternatively, it may be associated with the radiologic or chemotherapeutic interventions for CTCL. No karyotypic changes were found in the only previous report of recurrent laryngeal papillomas, seen in two children and five adults [10]. In out patient, several aberrant clones were found: trisomy 8 with or without loss of Y, as well as a cell line with loss of Y. Although the latter may be a function of the patient’s age, both loss of Y and trisomy 8 have been described separately and together in other benign proliferations. In three series of patients [2,3,5] with Dupuy- tren contracture, carpal tunnel syndrome, or both and with karyotypic changes, trisomy 8 was the predominant finding. Although clonal changes were present in patients in two other clinically similar series [1,4], trisomy 8 was not found. Fig. 1. A papillary squamous proliferation made up of fibrovascular cores lined with benign squamous epithelium (200×). The inset shows a core at higher magnification (400×). There are a few mitotic figures within the basal cells, but there is no dysplasia.
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Transcript of Clonal abnormalities in a recurrent laryngeal papilloma
Cancer Genetics and Cytogenetics 159 (2005) 190–191
Letter to the editor
Clonal abnormalities in a recurrent laryngeal papilloma
Although clonal chromosomal aberrations are usuallyconsidered hallmarks of neoplasm, the occurrence of nonran-dom changes has been documented in several benign condi-tions, namely, Dupuytren contracture [1–4], carpal tunnelsyndrome [5], and Peyronie disease of the penis [6,7]. Wehave recently found trisomy 8 and loss of the Y in a recurrentlaryngeal papilloma, and therefore would add that lesion tothe list of hyperproliferations with clonal changes.
Our patient, a 77-year-old man, recalls multiple surgicalprocedures in early childhood for laryngeal papillomas. Heis not sure of the number or of his age at the times ofsurgery. There is no information available regarding possiblematernal condyloma. He was followed with periodic exami-nations but with no recurrence in adolescence. At age 20years, however, upon discharge from the U.S. Army, heagain had surgery for removal of a lesion. An examination atage 50 years was normal. Increasing hoarseness led to aself-referral at age 77 years. The patient has never smoked,nor been exposed to significant workplace air pollution.
At this recent referral, a single lesion was seen and subse-quently removed. Pathologic examination showed papillarysquamous proliferation made up of fibrovascular cores linedwith benign squamous epithelium. There were a few mitoticfigures within the basal cells, but there was no dysplasia(Fig. 1). Papilloma tissue was cultured and karyotyped usingstandard methods. Four cell lines were found: 47,XY,�8[4]/45,X,�Y[2]/46,�Y,�8[2]/46,XY[11]. The patient’s pastmedical history is significant, in that he was diagnosed withcutaneous T-cell lymphoma (CTCL) at age 67 years; a singlelesion, biopsied at age 34 years and deemed to be “parapsori-asis” was probably a first manifestation, although no furtherCTCL lesions occurred for 33 years.
Laryngeal papillomas are benign lesions usually causedby papillomaviruses. Juvenile onset is associated with mater-nal genital condylomata, the incidence of affected offspringbeing 7 of every 1,000 children born to affected mothers[8]. Most cases of juvenile laryngeal papillomas regress withpuberty. It is not known under what circumstances the papil-loma virus may be reactivated. Smoking and alcohol havebeen suggested as possible risk factors. A recent case ofrecurrence was reported in a 44-year-old woman who, inaddition to being a heavy smoker, had a concomitant candidainfection of the glottis [9]. Our patient has never smoked,nor ever been a heavy drinker. The viral reactivation may bea reflection of his CTCL rendering him immunologically
0165-4608/05/$ – see front matter � 2005 Elsevier Inc. All rights reserved.doi:10.1016/j.cancergencyto.2004.11.001
compromised. Alternatively, it may be associated with theradiologic or chemotherapeutic interventions for CTCL.
No karyotypic changes were found in the only previousreport of recurrent laryngeal papillomas, seen in two childrenand five adults [10]. In out patient, several aberrant cloneswere found: trisomy 8 with or without loss of Y, as wellas a cell line with loss of Y. Although the latter may be afunction of the patient’s age, both loss of Y and trisomy 8have been described separately and together in other benignproliferations. In three series of patients [2,3,5] with Dupuy-tren contracture, carpal tunnel syndrome, or both and withkaryotypic changes, trisomy 8 was the predominant finding.Although clonal changes were present in patients in twoother clinically similar series [1,4], trisomy 8 was not found.
Fig. 1. A papillary squamous proliferation made up of fibrovascular coreslined with benign squamous epithelium (200×). The inset shows a core athigher magnification (400×). There are a few mitotic figures within thebasal cells, but there is no dysplasia.
Letter to the editor / Cancer Genetics and Cytogenetics 159 (2005) 190–191 191
In several studies [1,3,5], normal skin cells, grown as con-trols, showed no clonal changes, confirming the relationshipof the changes to the hyperplasia. Clonal changes includingtrisomy 8 and loss of Y also predominated in plaque-derivedabnormal cultures from patients with Peyronie disease [6,7].It is curious that trisomy 8, one of the most ubiquitous find-ings in a wide variety of malignancies, is also the mostfrequently occurring autosomal clonal numerical abnormal-ity in benign hyperplastic conditions.
Ahmed SolimanDepartment of Otolaryngology/Head and Neck Surgery
Temple University School of MedicinePhiladelphia, PA
Jasvir S. KhuranaDepartment of Pathology and Laboratory Medicine
Temple University School of MedicinePhiladelphia PA
Hope H. PunnettDepartment of Pathology and Laboratory Medicine
St. Christopher’s Hospital for ChildrenErie Avenue at Front Street, Philadelphia, PA 19134
andDrexel University College of Medicine
Philadelphia, PA
References
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[2] Sergovich FR, Botz JS, McFarlane RM. Nonrandom cytogenetic ab-normalities in Dupuytren’s disease. N Engl J Med 1983;308:162–3.
[3] Wurster-Hill DH, Brown F, Park JP, Gibson SH. Cytogenetic studiesin Dupuytren contracture. Am J Hum Genet 1988;43:285–92.
[4] Casalone R, Mazzola D, Meroni E, Righi R, Minelli E, Granata P,Panattoni A, Viotto AM, Modesti M, Pilato G. Cytogenetic andinterphase cytogenetic analyses reveal chromosome instability but noclonal trisomy 8 in Dupuytren contracture. Cancer Genet Cytogenet1997;99:73–6.
[5] Bonnici AV, Birjandi F, Spencer JD, Fox SP, Berry AC. Chromosomalabnormalities in Dupuytren’s contracture and carpal tunnel syndrome.J Hand Surg 1992;17:349–55.
[6] Somers KD, Winters BA, Dawson DM, Leffell MS, Wright GLJr, Devine CJ Jr, Gilbert DA, Horton CE. Chromosome abnormalitiesin Peyronie’s disease. J Urol 1987;137:672–5.
[7] Guerneri S, Stioui S, Mantovani F, Austoni E, Simoni G. Multipleclonal chromosome abnormalities in Peyronie’s disease. Cancer GenetCytogenet 1991;52:181–5.
[8] Silverberg MJ, Thorsen P, Lindeberg H, Grant LA, Shah KV. Condy-loma in pregnancy is strongly predictive of juvenile-onset recurrentrespiratory papillomatosis. Obstet Gynecol 2003;101:645–52.
[9] Daya H, Gallimore A. Recurrent laryngeal papillomatosis: a case offlorid papillomatosis following a remission of 30 years. J LaryngolOtol 1993;107:636–8.
[10] Zaslav A-L, Steinberg BM, Stamberg J, Lin YJ, Abramson AL. Chro-mosomal analysis of recurrent laryngeal papillomas. Arch OtolaryngolHead Neck Surgery 1988;114:1170–4.
