PubMed Health⌕ Search

Biomedical subjects

C P Crum

Publications and source records attributed to C P Crum.

At least 55 records · Page 3Linked to original sources

In vivo cyclin E expression as a marker for early cervical neoplasia.

Identification of human papillomavirus (HPV)-related early cervical neoplasia and its distinction from benign epithelial alterations is based on either subjectively applied morphologic criteria or on identification of associated papillomaviruses. The direct and indirect consequences of HPV infection, however, potentially include upregulation of some host genes. We investigated one candidate, cyclin E, as a possible marker for HPV-related early squamous lesions. Serial paraffin sections from 92 archival cervical biopsy specimens were analyzed, including 19 non-neoplastic biopsy specimens, 30 low-grade and 31 high-grade squamous intraepithelial lesions (SILs), and 12 invasive carcinomas. Four parameters (histologic diagnosis, cyclin E staining, HPV status and, in selected cases, Ki-67 staining) were scored, and their relationship(s) were evaluated by the chi2 independence test. Twenty-one, 73, 79, and 75% of nonlesional epithelia, low-grade SILs, high-grade SILs, and invasive squamous cell carcinomas, respectively, were HPV positive (P < .001 for HPV status vs. diagnosis). Cyclin E staining was nuclear in distribution, and the frequency of positive staining, ie., moderate or strong intensity, was significantly higher (P < .001 for cyclin E staining vs. diagnosis) in all of the lesional epithelia (92.3, 51.6, and 50% of low-grade and high-grade SILs and carcinomas, respectively) compared with nonlesional epithelium (5.9%). Cyclin E positivity and/or HPV positivity was seen in 100% of the low-grade SILs. Epithelial Ki-67 and cyclin E staining were strikingly different in frequency and distribution. Cyclin E was undetectable in basal cells of normal mucosa (which were positive for Ki-67) and limited to suprabasal epithelium in noninvasive lesions. Cyclin E expression correlates strongly with morphologic features of HPV-related preinvasive and invasive cervical disease. This correlation is most pronounced in low-grade SILs. The possibility that in vivo cyclin E staining is a generic marker for HPV infection in low-grade SILs merits additional study.

Biomarkers, Tumor↗

Koilocytotic atypia in Papanicolaou smears. Reproducibility and biopsy correlations.

BACKGROUND: It would be useful if cervical smears containing koilocytes alone could be reliably separated from those containing other forms of nuclear atypia within the spectrum of low grade squamous intraepithelial lesions (LSIL) and that this separation was predictive of differences in biopsy follow-up. In this article, the authors sought to test this possibility. METHODS: Consecutive smears diagnosed as LSIL from 140 patients who had follow-up colposcopic biopsies were reviewed independently by three observers. The inter- and intraobserver reproducibility in diagnosing smears with koilocytes alone was assessed by the kappa statistic. Comparison of each reviewer's cytologic diagnosis with a reviewed biopsy diagnosis was assessed using chi-square analysis. The quantity of abnormal cells was compared with the presence or absence of a lesion on biopsy. RESULTS: Kappa values for any 2 observers agreeing on koilocytosis as a separate category ranged from 0.22-0.47 (poor to good). Intraobserver reproducibility across all cytologic categories ranged from 0.35-0.62 (poor to good). A cytologic diagnosis of koilocytosis predicted a lower rate of high grade SIL (HSIL) on initial biopsy for one of the observers, but not for the other two. Koilocytosis did not predict a lower rate of LSIL on initial biopsy or HSIL in follow-up biopsies for any observer. The quantity of cells on the initial smear did not correlate with a lesion on biopsy. CONCLUSIONS: Separation of LSIL into two diagnostic categories is not feasible because of its poor cytologic reproducibility and inability to predict differences in biopsy diagnosis. The quantity of abnormal cells in LSIL is not predictive of the detection of a lesion on biopsy.

Biopsy↗

Cervical cancer in young women in Taiwan: prognosis is independent of papillomavirus or tumor cell type.

The objective of this study was to address the hypotheses that younger patients with cervical cancer have a uniquely worse clinical outcome and/or are more likely to have adverse tumor cell types or specific human papillomaviruses (HPV). Cases of stage Ib-IIa cervical cancer among women 35 years of age or younger (82) and over 35 (54) were analyzed and compared with respect to the following: (1) histologic type (squamous vs nonsquamous), (2) human papillomavirus (HPV) type via polymerase chain reaction, and (3) clinical parameters, including tumor size, nodal metastases, and recurrence/persistence. Patients 35 years of age or younger had a survival similar (71.2% vs 72.4%) to that of older women from the same institution. In the younger group, outcome was not correlated with the presence or absence of HPV or HPV type. Nonsquamous carcinomas, including adenocarcinoma and small cell carcinoma, were strongly associated with HPV18, were more prevalent in the younger group, and had a slightly higher risk of recurrence/persistence; however, these differences were not significant and 71% of the recurrences were squamous cell carcinomas. Thus, in young Taiwanese women with stage Ib-IIa cervical cancer, the majority of deaths cannot be attributed to a specific HPV type or unique tumor morphology.

Adult↗

Low prevalence of human papillomavirus infection in esophageal squamous cell carcinomas from North America: analysis by a highly sensitive and specific polymerase chain reaction-based approach.

Several studies have documented the frequent occurrence of human papillomavirus (HPV) DNA in esophageal squamous cell carcinomas (ESCC) in patients from geographic regions where the incidence of this type of cancer is high, such as parts of China. However, the prevalence of HPV infection in ESCC in patients from low incidence geographic regions, such as North America, remains controversial. Therefore, this study evaluates the prevalence of HPV in ESCC in patients from North America, a region where the population is considered at low risk for the development of this neoplasm. ESCCs in 51 patients from three North American cities were analyzed for the presence of HPV DNA by a highly sensitive and specific polymerase chain reaction (PCR) method. Tumor DNA was extracted from formalin-fixed, paraffin-embedded tissue specimens and assayed by PCR using an L1 HPV consensus sequence primer, as well as HPV 16 and HPV 18 E7 region primers. The use of consensus primers to the L1 region allows for detection of most known HPV types and many novel HPV types. Appropriately sized reaction products were analyzed by restriction fragment length polymorphism (RFLP) to confirm the presence and type of HPV, and to exclude products produced by amplification of human DNA sequences. After complete analysis, only one case (2%) of ESCC was HPV DNA positive. This case was independently confirmed using L1 and E7 consensus primers as HPV type 16 and was the only case that tested positive with either assay. These results show that, in contrast to geographic regions where ESCC is prevalent, HPV infection occurs infrequently in association with ESCC in patients from North America.

Adult↗

MN antigen expression in normal, preneoplastic, and neoplastic esophagus: a clinicopathological study of a new cancer-associated biomarker.

Recently, a novel tumor-associated protein, termed MN, has been described in carcinomas of the uterine cervix, where its expression has been shown to be associated with malignant transformation. Because malignant transformation in the esophagus develops through a dysplasia-carcinoma sequence similar to that which occurs in the cervix, this study was performed to evaluate MN expression in normal, preneoplastic, and neoplastic tissues of the esophagus. Esophageal tumor resection specimens from 27 patients (12 squamous cell carcinomas, one multifocal squamous dysplasia, 10 Barrett's-associated adenocarcinomas, two Barrett's esophagus with dysplasia, two adenosquamous carcinomas) were immunohistochemically stained with a monoclonal antibody (clone M75) directed against the MN antigen. The localization of MN antigen, as well as the proportion of positively stained cells, were determined in sections of normal, dysplastic, and carcinomatous tissues. The staining characteristics were correlated with the pathological features of the tumors. Weak intracellular MN expression was detected only in the basal cells of normal squamous epithelium. However, inflamed and reactive squamous epithelium showed increased staining in the basal layer and in the overlying mature squamous cells. MN expression was significantly increased in dysplastic squamous epithelium (P < .001). All esophageal squamous cell carcinomas (100%) stained positively for MN antigen, where the pattern of staining was predominantly membranous. However, the degree of MN staining did not correlate with any of the pathological features of the tumors. In Barrett's epithelium, MN stained positively in all types of metaplastic cells and showed no difference in dysplastic epithelium. In contrast to squamous cell carcinomas, only 80% of esophageal adenocarcinomas were positive for MN, but the degree of MN expression was inversely correlated with histological tumor differentiation (P < .015). The results of this study suggest that (1) the tumor-associated MN antigen may play a role in proliferation and regeneration in esophageal squamous epithelium, and (2) loss of MN expression may be related to cancer progression in Barrett's-associated adenocarcinomas.

Adult↗

Disparities in mean age and histopathologic grade between human papillomavirus type-specific early cervical neoplasms.

Noninvasive squamous and glandular precursor lesions associated with human papillomavirus (HPV) types 16 and 18 have been reported to vary in morphology. HPV 16 is associated predominantly with high-grade squamous intraepithelial lesions (HSIL; cervical intraepithelial neoplasia (CIN 2 and 3), and HPV 18 is associated with low-grade squamous intraepithelial lesions (condyloma/CIN 1) and CIN 3/adenocarcinoma in situ (ACIS). This study explored the relationship of morphologic growth pattern in these precursor groups with age of presentation. One hundred fourteen CIN lesions (including those with ACIS), associated with HPV 16 or 18, were subdivided into well-differentiated low- and high-grade SIL (CIN 1 and 2, respectively), poorly differentiated HSIL (CIN 3) with or without ACIS. HPV was detected by polymerase chain reaction (PCR) amplification with L1 consensus or type-specific E7 primers and typed by restriction fragment length polymorphism (RFLP) analysis. Age of the patient was obtained from the pathology report. Mean age for each group was as follows: Low-risk HPVs, 25 years; HPV 18 CIN 1-2, 21.6 yrs; HPV 18 CIN 3/ACIS, 35.2 yrs; HPV 16 CIN 1,2, 25.9 yrs; and HPV 16 CIN 3, 29.8 yrs. There were significant differences in mean ages between HPV 18 CIN 1 and 2 and HPV 16 CIN 1 to 2 (P = .04), HPV 16 CIN 1-2 and CIN 3 (P = .01) and HPV 18 CIN 1 to 2 and HPV 18 CIN 3/ACIS (P = .00001). None of the cases of HPV 18-associated CIN3/ACIS was associated with a CINI lesion. The disparity in mean ages between well and poorly differentiated HPV 16/18 related that precursor lesions could reflect factors such as morphologic progression with increasing age, different rates of lesion persistence, depending on grade, or efficiency of detection between the two groups. The marked difference in mean age between HPV 18-associated CIN 1-2 and CIN 3/ACIS, combined with their lack of coexistence in the same cervix, raises alternate possibilities that specific viral or host factors may determine the morphological phenotype associated with some HPV 18 infections. In the latter, the possibility that age independently confers an increased risk for higher-grade lesions should be considered.

Adenocarcinoma↗

Cervical squamous cell carcinoma in situ with intraepithelial extension to the upper genital tract and invasion of tubes and ovaries: report of a case with human papilloma virus analysis.

A 55-year-old woman, who was found to have malignant squamous cells on a routine cervical smear, underwent a conization biopsy, followed by hysterectomy with bilateral salpingo-oophorectomy. No gross tumor was present in the uterus, but both ovaries, which were of normal size, contained multiple cysts filled with light brown, soft material. Microscopic examination showed squamous cell carcinoma in situ of the cervix with contiguous spread to the endometrium, fallopian tubes, and ovaries; squamous cell carcinoma extensively replaced the endometrial and tubal epithelium, focally invaded the wall of the fallopian tubes, and involved the parenchyma of both ovaries. Although an invasive cervical carcinoma occasionally spreads to the ovary, this case illustrates that exceptionally an in situ tumor spreads along the epithelium of the upper genital tract and the ovarian surface and invades the ovary and tubes. The detection of human papillomavirus DNA in the cervical, endometrial, tubal, and ovarian tumors by the polymerase chain reaction suggests a role for human papilloma virus infection in this case.

Carcinoma in Situ↗

Monoclonal origin of vulvar intraepithelial neoplasia and some vulvar hyperplasias.

Squamous neoplasms of the female genital tract, including vulvar intraepithelial neoplasia, presumably are derived from a single cell. This study addressed this hypothesis and determined the clonal status of other squamous epithelial alterations associated with vulvar carcinoma, including hyperplasia and lichen sclerosis. X chromosome inactivation patterns of 22 epithelial lesions and matched normal epithelium were determined using a polymerase chain reaction (PCR)-based assay targeting the X-linked human androgen receptor gene (HUMARA). Clonality was inferred by comparing matched lesional and control tissues as follows: 1) monoclonal, if intensity of either PCR product was skewed relative to normal reference epithelium (control), 2) polyclonal, if both lesional and control were unskewed, and 3) unknown, if both lesion and control tissues were skewed toward the same allele. Two cases were excluded because of noninformative homozygous HUMARA alleles. Of 8 vulvar intraepithelial neoplasias analyzed, 7 were scored monoclonal and 1 polyclonal. Of 12 hyperplasias, 6 were monoclonal, including one with lichen sclerosis, 2 were polyclonal, and in 4, the clonal status could not be determined. The PCR-based clonal assay supports a monoclonal derivation for vulvar intraepithelial neoplasia and, in some cases, vulvar hyperplasia, and lichen sclerosis. The finding of monoclonal hyperplasia and lichen sclerosis suggests that clonal expansion may evolve before the development of morphological atypia in these epithelia.

Carcinoma in Situ↗

Pathobiology of vulvar squamous neoplasia.

Vulvar squamous carcinoma is an uncommon neoplasm that afflicts a spectrum of women and has been associated with granulomatous vulvar diseases, papillomaviruses, and chronic inflammatory disorders of the vulva. Histopathological, molecular, and epidemiological studies have revealed two subsets of vulvar squamous neoplasia, which are distinguished by their association with human papillomaviruses and patient demographics. This review summarizes the evidence both supporting the diverse pathogenesis of these tumors and the existence of factors that may be common to both groups. Ultimately, the pathway to both human papillomavirus positive and negative vulvar cancers may involve not only obvious precancerous changes but also biological events in the vulvar mucosa that precede the onset of morphological atypia.

Carcinoma, Squamous Cell↗

Association between cervical neoplasia and apoptosis as detected by in situ nuclear labeling.

Invasive cervical cancer is thought to arise from the progression of precancerous lesions. How these lesions proceed from precancers to cancer remains unknown. Data regarding other tissues indicate that altered programmed cell death (apoptosis), in addition to cellular proliferation, is associated with the development of neoplasia. Therefore, in order to better understand the development of cervical neoplasia, we investigated the rate of apoptosis in cervical precancer and cancer. Archival cervical samples from normal epithelium (n = 11), low-grade squamous intraepithelial lesions (LSIL, n = 11), high-grade squamous intraepithelial lesions (HSIL, n = 10), and squamous cancers (n = 10) were evaluated for chromatin cleavage, a hallmark of programmed cell death. We used in situ end-labeling of DNA strand breaks by terminal deoxynucleotidyltransferase incorporation of biotinylated deoxyuridine to 3'-OH ends of DNA, identified by a nickel-avidin-peroxidase. The apoptotic index (sum of apoptotic bodies divided by the total nuclei times 100) significantly decreased (P < 0.001) as the degree of neoplasia increased: 3.5% (+/-0.4) in normal cervical epithelium (4.8 +/- 0.4) in LSIL, 1.4% (+/-0.4) in HSIL, and 0.4% (+/-0.1) in squamous cancers. Compared to normal epithelium, the total cell number per 10 mm2 increased significantly (P < 0.001): 124 (+/-12) in normal epithelium, 162 (+/-9.7) in LSIL, 315 (+/-31) in HSIL, and 413 (+/-32) in squamous cancers. We conclude that increasing cervical atypicality is associated with a decrease in apoptosis. We hypothesize from our data that one factor involved in the progression of neoplasia in the uterine cervix is a decrease in the rate of normal cellular deletion.

Apoptosis↗

A comparison of early (E7) and late (L1) primer-mediated amplification of papillomaviral DNA in cervical neoplasia.

Studies have demonstrated that in 50-90% of cervical carcinomas, human papillomavirus (HPV) DNA sequences are covalently bound (integrated) to the chromosomal DNA. All evidence shows that when integration takes place disruption of the viral genome occurs downstream to the E7 open reading frame, which is invariably retained in functional form. Theoretically, this phenomenon could result in loss of HPV sequences (L1) not critical to the presumed tumourigenic functions and if so, could influence primer selection for HPV DNA detection in these tumours. A series of cervical carcinomas (CA, n = 133), adenocarcinomas in situ (ACIS, n = 28) and high grade squamous intraepithelial lesions (HSIL, n = 30) were analysed for HPV nucleic acids using primers designed to amplify the E7 and L1 regions. Primer sizes and sensitivities were adjusted to produce equivalent amplification efficiency. Of 191 cases studied, 134 (70%) scored positive for HPV16 or 18 with either the E7 or L1 primer set. Of these, 116 (87%) were positive with both primer pairs. There were no significant differences in proportions of HPV 16/18 positives or lesion types scoring positive exclusively with the E7 vs the L1 primer sets. However, HPV18 associated, E7 positive carcinomas were slightly less likely than HPV16 associated carcinomas to be L1 positive (P = 0.07). Although a high proportion of HPV16 and particularly HPV18 positive carcinomas have been associated with exclusively integrated HPV DNA, there is little evidence that this influences detection sensitivity with E7 vs L1 primers. The combination of E7 and L1 primers provided the maximum sensitivity in this study, with 18 of 134 cases scoring positive with only one primer set.

Carcinoma↗

Absence of papillomavirus DNA in normal tissue adjacent to most cervical intraepithelial neoplasms.

OBJECTIVE: To determine if human papillomavirus (HPV) DNA is present in the normal mucosa adjacent to cervical intraepithelial neoplasia (CIN). METHODS: Serial sections of 28 CIN lesions were studied. Lesional and normal epithelia and stroma were microdissected; the DNA was extracted and amplified by polymerase chain reaction (PCR) using primers designed to amplify both HPV late (L1) and human beta-globin sequences. Human papillomavirus was typed by restriction fragment length polymorphism analysis following digestion of PCR products. RESULTS: Twenty-five of 28 (89%) lesional epithelia scored positive for HPV nucleic acids. In' four of 25 (16%) HPV-positives, the normal squamous epithelium scored positive for HPV nucleic acids, two of which (8%) also scored positive in the stroma. Repeat microdissection and PCR analysis of three of these cases was performed and all were negative in both normal epithelium and stroma, suggesting laboratory contamination. CONCLUSION: Human papillomavirus nucleic acids are present uncommonly in normal-appearing squamous epithelium adjacent to CIN. This does not exclude occult infection in the natural history of CIN but indicates that when lesions develop, occult infection is not normally maintained in the normal mucosa. This is consistent with the low recurrence rates following ablation as well as low indices of HPV positivity in normal cervices during follow-up. This finding should be taken into consideration when counseling patients and is relevant to the concept of HPV testing during follow-up after cone biopsy.

DNA Probes, HPV↗

Human papillomavirus-associated cervical intraepithelial neoplasia following lesbian sex.

BACKGROUND: Less than 3% of lesbians develop cervical dysplasia, with increasing risk correlating with previous heterosexual activity. Because they are not currently sexually active with men, many lesbians do not perceive themselves to be at risk for developing dysplasia and do not obtain regular Papanicolaou smears. There are no standard recommendations for Papanicolaou smear intervals for lesbians. CASE: A 36-year-old, nonsmoking woman had a Papanicolaou smear history of a high-grade squamous intraepithelial lesion of the cervix, which was confirmed by biopsy and successfully treated by laser ablation. Human papillomavirus type 16 was identified in the cervical biopsy by polymerase chain reaction amplification and restriction fragment polymorphism analysis. The patient gave a clear history of having had sexual activity only with women. CONCLUSION: Regular Papanicolaou testing should be recommended to all lesbians, regardless of type of sexual activity. Papanicolaou testing intervals should be determined using standards similar to those used for heterosexual women: annually after onset of sexual activity or after age 18, and possibly less often after three normal smears at her physician's discretion. An extensive number of sexual partners, current smoking, and prior dysplasia may influence the physician to advise continued yearly Papanicolaou testing for lesbians, similar to advice given to heterosexual patients.

Adult↗

Viral and histopathologic correlates of MN and MIB-1 expression in cervical intraepithelial neoplasia.

A recently studied tumor antigen, MN, has been associated with cervical carcinomas and cervical intraepithelial neoplasms (CIN), suggesting that it may serve as a marker for cervical cancer or cancer risk. To determine if expression of the MN antigen paralleled parameters reflecting viral or biological events in precursor epithelium, MN expression was correlated with MIB-1 expression, morphological phenotype, and human papillomavirus (HPV) distribution and type in a series of CINs. Seventy-three percent, 62% and 83% of CIN I, II, and III, respectively, were MN antigen positive. The proportion of neoplastic cells immunoreactive for MN did not correlate with the CIN grade or with HPV types stratified by their association with cancer. Evaluation of serial sections showed no correlation between the frequency of MN antigen staining, the proportion of MIB-1 immunoreactive cells, or the proportion of HPV positive cells detected by in situ hybridization (ISH). CINs associated with prototypical high risk (HPV 16) types exhibited increased immunostaining for the MIB-1 antigen and were more often classified as HSIL in contrast to the other types. Thus, although MN expression previously has been associated strongly with squamous carcinoma, it did not emerge as a specific marker for either cancer-associated HPV types or high grade CIN. CIN I lesions associated with low and high risk HPV types were not distinguished by MIB-1 expression and viral replication. This emphasizes the interrelationship between vegetative viral functions (including viral replication) and morphological phenotype, irrespective of HPV type.

Antigens, Neoplasm↗

Bethesda classification of cervicovaginal smears: reproducibility and viral correlates.

Fifty-five cervicovaginal smears from women with squamous intraepithelial lesions (SILs) were independently evaluated on two separate occasions by four cytopathologists using a binary classification system (the Bethesda system). Smears were categorized as low-grade (LSIL) or high-grade (HSIL) using previously published criteria. All women had subsequent cervical biopsies containing human papillomavirus (HPV) DNA amplified with the polymerase chain reaction and typed by restriction fragment polymorphism analysis. Three or more observers agreed on classification in 49 of 55 cases (87%); unanimous diagnoses were rendered in 31 cases (56%). Interobserver and intraobserver reproducibility ranged from fair to near-excellent (kappa values 0.40 to 0.63; 0.63 to 0.74, respectively). HPV types included HPV 16 (27%), 18 (7%), 31 (9%), 35 (4%), 39 (4%), 6 (10%), 11 (2%), novel types (30%), and multiple types (4%). High-risk HPV types (16, 18, 31, 35, and 39) were significantly associated (P = .03) with consensus HSIL diagnoses (agreement of three or more observers). This was primarily because of the strong association of HPV 16 with HSIL (P = .001). After excluding HPV 16, the other high-risk HPV types (18, 31, 35, and 39) were no longer significantly associated with consensus HSIL diagnoses (P > .5). Conversely, LSIL diagnoses were significantly associated with non-high-risk HPV types (all HPV types except 16, 18, 31, 35, and 39; P = .006). Binary cytological classification of cervicovaginal SILs is reproducible among cytopathologists. Such classification correlates well with most low-risk HPV types and with the prototypic high-risk HPV 16 but not with other high-risk HPV types.

Female↗

Pseudobowenoid change of the vulva: a histologic variant of untreated condylata acuminatum.

Vulvar condylomata are distinguished from vulvar intraepithelial neoplasia by orderly maturation, a low mitotic index, and the absence of nuclear atypia in the lower epithelial layers. Podophyllin therapy might produce changes in condylomata mimicking vulvar intraepithelial neoplasia but can be distinguished, particularly with a recent history of podophyllin use. This report describes five patients with vulvar condylomata that morphologically resemble both podophyllin effect and vulvar intraepithelial neoplasia. The mean age was 30.5 years. All lesions exhibited superficial keratinocytes in various stages of apoptosis, with a spectrum of nuclear degenerative changes characterized by absence of the nuclear membrane and dispersed nuclear chromatin. The characteristic finding was a perichromatin halo delineated by a rim of dense cytoplasm, beyond which a second zone of uniform clearing was observed, similar to changes noted in vulvar intraepithelial neoplasia. There was an absence, however, of either nuclear atypia in the lower cell layers or apoptosis and mitotic arrest observed in vulvar intraepithelial neoplasia and podophyllin therapy. Two (50%) of four lesions tested positive for human papillomavirus nuclei acids, one by polymerase chain reaction and the other by DNA-DNA in situ hybridization. No common human papillomavirus types were found. Pseudobowenoid change might represents a distinct type of vulvar condyloma, perhaps related to an unusual human papillomavirus.

Adult↗

Prevalence of human papillomaviruses (HPV) in benign and malignant tumors of the upper respiratory tract.

The role for human papillomavirus (HPV) in head and neck tumors is not established. To evaluate the possible role of HPV in head and neck neoplasms, 22 cases of laryngeal squamous papilloma (LP), 32 cases of laryngeal squamous cell carcinoma (LSCC), 40 cases of nasal inverted papilloma (NIP), 14 cases of nasal squamous cell carcinoma (NSCC), and 40 cases of nasopharyngeal carcinoma (NPC) were evaluated for the presence of HPV DNA using the polymerase chain reaction (PCR) with two sets of primers in separate reactions: HPV-L1 consensus primers, HPV16 and HPV18 E7 primers for HPV nucleic acid detection. Restriction fragment length polymorphism of L1 PCR product was used for typing of HPV. Overall, HPV DNA was detected in 18 of 22 cases (81.8%) of LP, 3 of 32 cases (9.4%) of LSCC, 17 of 40 cases (42.5%) of NIP, 3 of 14 cases of NSCC (21.4%), and none of 40 cases of NPC. HPV6 was found more frequently in LP and HPV11 in NIP (P < 0.001). In the three HPV positive LSCCs, two cases had previous LP and were HPV6 and HPV11 positive, as were the prior papillomas. One other case was HPV18 positive. Only HPV16 was found in the NSCC patients. There was no significant difference in the index of HPV positivity between the NSCC cases associated with (16.7%) and without NIP (25.6%). Our results suggest that HPV plays a role in the development of both LP and NIP, and that similar viral types (i.e., HPV6 and HPV11) may exhibit relative differences in their tissue specificity. HPV appears to be of limited importance as a co-factor in LSCC and NPC lesions, indicating differences in the pathogenesis between papillomas and carcinomas in the upper respiratory tract.

Adolescent↗