Human Papillomavirus in Squamous Cell Carcinoma, Leukoplakia, Lichen Planus, and Clinically Normal Epithelium of the Oral Cavity

Kashima, Haskins K.; Levin, L. Stefan; Kutcher, Mark J.; Villiers, E.-M. de; Kessis, Ted; Shah, Keerti V.

doi:10.1177/000348949009900110

Cited by 114 publications

(44 citation statements)

References 13 publications

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“…Some investigators either failed to identify HPV DNA in none of oral cavity VC, 18 or identified HPV DNA in a very limited number of cases. [19][20][21] Perhaps these discrepancies relate to the difficulties in the interpretation of ISH studies. This may be complicated by problems of non-specific staining or sensitivity of detection and it is unclear that VC has been separated reliably (During our analysıs we have utlızed Internatınal Unıon Agaınst Cancer -TNM stagıng system.…”

Section: Discussionmentioning

confidence: 99%

Investigation of HPV Infection and P53 Expression in Laryngeal Verrucous Carcinoma

Tunçbilek¹,

Çallı²,

Öncel³

et al. 2010

Turkiye Klinikleri J Med Sci

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A AB BS S T TR RA AC CT T O Ob bj je ec ct ti iv ve e: : Ver ru co us car ci no ma is an un com mon, well-dif fe ren ti a ted va ri ant of squ a mo us cell car ci no ma that is re gar ded as a low gra de, lo cally in va si ve ma lig nant tu mor with ra re po ten ti al for dis tant me tas ta sis. Alt ho ugh the pat ho ge ne sis of ver ru co us car ci no ma is unk nown, many pos sib le ca u ses ha ve been pro po sed. The le a ding the o ri es inc lu de hu man pa pil lo ma vi rus (HPV) in fec ti on and che mi cal car ci noge ne sis. The aim of this study is to analy se the sta tus of the p53 ge ne and hu man pa pil lo ma vi rus (HPV) in fec ti on in ver ru co us car ci no ma of larynx, and to in ves ti ga te the cor re la ti on of p53 ex pres si on and HPV in fec ti on in ver ru co us car ci no ma of the larynx. M Ma a t te e r ri i a al l a an nd d M Me et t h ho od ds s: : A ret ros pec ti ve study has be en per for med bet we en the ye ars of 1994 and 2004, com pri sing 21 con se cu ti ve pa ti ents with ver ru co us carci no ma of larynx. De ta i led cli ni cal pa ra me ters ha ve al so be en re vi e wed. HPV iden ti fi ca ti on was ac complis hed with poly me ra se cha in re ac ti on. p53 im mu no his toc he mistry was per for med on 21 ver ru co us car ci no ma using poly clo nal se rum CM-1. R Re e s su ul lt ts s: : The HPV in fec ti on has be en de tec ted in in all of the twenty-one ca ses of ver ru co us car ci no mas. p53 im mu no his toc he mistry was per for med on 21 HPV conta i ning ver ru co us car ci no mas and sho wed the ex pres si on of p53 in 14 ca ses. No sta tis ti cally sig ni fi cant dif fe ren ces we re fo und bet we en p53 ex pres si on and sta ge. C Co on nc c l lu u s si i o on n: : The da ta in di ca te that HPV and the in cre a sed ex pres si on of p53 can co e xist in ver ru co us car ci no mas. Our study sug gests that verrucous carcinomas of the larynx may ari se thro ugh a still unk nown mec ha nism which ca u ses p53 inac ti va ti on or HPV in fec ti on.We think that p53 ove rex pres si on and on co ge nic HPV in fec ti on may co o pe ra te in the estab lish ment of ma lig nant cells in ver ru co us car ci no ma of the larynx. The in te rac ti on bet we en the HPV in fec ti on and cer ta in cel lu lar on co ge nes such as p53 ne eds furt her studies.K Ke ey y W Wo or rd ds s: : Car ci no ma, ver ru co us; larynx; p53 pro te in, hu man; pa pil lo ma vi rus in fec ti ons Ö ÖZ ZE ET T A Am ma aç ç: : Na dir me tas taz po tan si ye li bu lu nan dü şük de re ce li lo kal in va ziv ma lign tü mör ola rak bi linen ver rü köz kar si nom, sku a möz hüc re li kar si no mun iyi di fe ran si ye bir var yan tı dır. Ver rü köz kar si nomun pa to ge ne zi bi lin me se de ba zı ola sı ne den ler öne sü rül müş tür. Bun la rın ba şın da hu man pa pil lo ma vi rus enfeksiyonu ve kim ya sal kar si no ge nez gel mek te dir. Ça lış ma mı zın ama cı la rink sin ver rü köz kar sinom la rın da p53 gen ve hu man pa pil lo ma vi rus en fek si yo nu nun ana li zi ve p53 eks pres yo nu ile hu man papil lo ...

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Section: Discussionmentioning

confidence: 99%

Investigation of HPV Infection and P53 Expression in Laryngeal Verrucous Carcinoma

Tunçbilek¹,

Çallı²,

Öncel³

et al. 2010

Turkiye Klinikleri J Med Sci

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“…Human papillomaviruses (HPV) have been found in lesions of LP (Maitland et al, 1987;Jontell et al, 1990;Kashima et al, 1990) (Walsh et al, 1990a,b). Interestingly, humoral responses to EBV appear to be altered in OLP (Pedersen, 1996).…”

Section: (3) Drugsmentioning

confidence: 99%

Update On Oral Lichen Planus: Etiopathogenesis and Management

Scully

Beyli²,

Ferreiro

et al. 1998

Critical Reviews in Oral Biology & Medicine

475

461

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Lichen planus (LP) is a relatively common disorder of the stratified squamous epithelia, which is, in many ways, an enigma. This paper is the consensus outcome of a workshop held in Switzerland in 1995, involving a selection of clinicians and scientists with an interest in the condition and its management. The oral (OLP) eruptions usually have a distinct clinical morphology and characteristic distribution, but OLP may also present a confusing array of patterns and forms, and other disorders may clinically simulate OLP. Lesions may affect other mucosae and/or skin. Lichen planus is probably of multifactorial origin, sometimes induced by drugs or dental materials, often idiopathic, and with an immunopathogenesis involving T-cells in particular. The etiopathogenesis appears to be complex, with interactions between and among genetic, environmental, and lifestyle factors, but much has now been clarified about the mechanisms involved, and interesting new associations, such as with liver disease, have emerged. The management of lichen planus is still not totally satisfactory, and there is as yet no definitive treatment, but there have been advances in the control of the condition. There is no curative treatment available; immunomodulation, however, can control the condition. Based on the observed increased risk of malignant development, OLP patients should be offered regular follow-up examination from two to four times annually and asked to report any changes in their lesions and/or symptoms. Follow-up may be particularly important in patients with atrophic/ulcerative/erosive affections of the tongue, the gingiva, or the buccal mucosa. Much more research is required into the genetic and environmental aspects of lichen planus, into the premalignant potential, and into the possible associations with chronic liver, and other, disorders. More clinical studies are required into the possible efficacy of immunomodulatory drugs such as pentoxifylline and thalidomide.

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“…HPV infection has also been detected in pre-malignant and in transfected immortalized oral keratinocytes (Kashima et al, 1990;Shah and Howley, 1990;Tyan et al, 1993;Miller et al, 1994). Many of these lesions also express the HPV proteins E6 and E7.…”

Section: (D) the Use Of Archival Biopsy Materialsmentioning

confidence: 99%

Biomarkers and Molecular Epidemiology and Chemoprevention of Oral Carcinogenesis

Schwartz

2000

Critical Reviews in Oral Biology & Medicine

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Chemopreventives are chemicals that prevent the formation of cancers such as oral cancer. They can take the form of nutrients or synthetic molecules, and their fundamental characteristic is that they do not produce disease processes that would result in debilitating symptoms. Current evidence indicates that they function by modifying the oxidative state of transforming cells. Biomarkers can take the form of genetic and molecular indicators, which characterize the function of chemopreventives and cancer processes such as oral carcinogenesis. Biomarkers cannot provide all the required information for risk assessment or possible activity of the chemopreventives. Other methods, such as epidemiological analyses and techniques, must be used to enhance our understanding of the risk for oral cancer in human populations. One common epidemiologic method, the questionnaire, helps to determine the use and carcinogenic potential of tobacco and alcohol during oral carcinogenesis. Genetic and molecular changes in human patient populations may result in a reduction in the number and function of tumor suppressor genes. If these changes are to be assessed, the tissues (e.g., buccal mucosa) must be accessible and harvested in a reliable and consistent manner for the acquisition of DNA, mRNA, and protein. Oral tissues provide sufficient quantities of these molecules and, under stringent conditions, the quality required for the isolation of these molecular constituents. In conjunction with epidemiologic techniques, various genotypic polymorphisms, such as glutathione-S-transferase (GSTM 1) or cytochrome P450 (CYP450Al), have indicated a loss in carcinogen detoxification or the processing of internal growth control signals. Biomarkers are composed of a large diverse group of genetic and molecular structures. Some of these biomarkers are indicators for programmed cell death (PCD), while others describe malignant tumor growth. Many of these classes of molecules are oxidative-responsive (e.g., tumor suppressor p53, Bcl-2, growth factors, immune-derived proteins, and death-inducing molecules) and induce PCD by triggering a cascade of cysteine proteases and regulators (e.g., caspases, death receptors). This pathway results in cell-cycle alterations and DNA fragmentation. It is hoped that a detailed knowledge of the processes involved in malignant transformation will better define the biomarker-screening tools for oral cancer. These tools will enhance our ability to predict the incidence of cancer, detect early malignant change, and quantitate chemoprevention during oral carcinogenesis. Chemopreventives such as the retinoids have already demonstrated their ability to suppress potential malignant changes in pre-malignant oral leukoplakias and decrease the incidence of second head-and-neck cancer primaries. It is our hope that this review will increase investigators' interest in developing new screening and detection systems for oral cancer.

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Human Papillomavirus in Squamous Cell Carcinoma, Leukoplakia, Lichen Planus, and Clinically Normal Epithelium of the Oral Cavity

Cited by 114 publications

References 13 publications

Investigation of HPV Infection and P53 Expression in Laryngeal Verrucous Carcinoma

Investigation of HPV Infection and P53 Expression in Laryngeal Verrucous Carcinoma

Update On Oral Lichen Planus: Etiopathogenesis and Management

Biomarkers and Molecular Epidemiology and Chemoprevention of Oral Carcinogenesis

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