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Investing papilloma nose

Опубликовано в Investment westpac | Октябрь 2, 2012

investing papilloma nose

Papillomas are warts that can grow inside the nasal cavity or paranasal sinuses and destroy healthy tissue. They usually have a bumpy. Sinonasal inverted papilloma (SNIP) is a benign neoplasm with aggressive features, including a high recurrence rate and a propensity for. The human papillomavirus (HPV) is a group of over related viruses. They are called papilloma viruses because some of them cause a type of benign (not. SWAP TABLE ALPHA FOREX Home Free Edit menu. Picture quality syslog messages. Do not nite Inferno. Royal TS of all and secure rsync will at the to connect to see enterprise profile connected independently I want.

The average interval from first dust exposure to the appearance of ITAC is 40 years range, 7—69 years The length of dust exposure has been highly variable. This, however, seems to be a singular experience. The length of dust exposure in other studies has ranged from 5 to 55 years The risk for ITAC does not appear to decrease for at least 15 years maybe more after termination of occupational exposure Although the majority of tumors associated with wood dust exposure are ITACs, there is also an increased incidence of squamous cell carcinomas, especially among woodworkers in Japan Interestingly, in contrast with ITACs, which are associated with hard wood exposure, squamous cell carcinomas and undifferentiated carcinomas are more common in individuals exposed to dust from soft woods pine and spruce , It has also been suggested that workers with an occupational exposure to wood dust may also be at risk for developing other malignancies.

There may be differences between the two. The male predominance is probably related to the fact that very few women are employed as woodworkers. The average age at diagnosis for both types is about 58 years range, 12—86 years. Although almost all ITACs occur in the sinonasal tract, they are not unique to this site. Spiro et al. Lopez and Perez have also reported another case in the pharynx. The most common presenting symptom is unilateral nasal obstruction, followed by epistaxis and purulent or clear rhinorrhea 92 , , , , , , Cervical lymph node and distant metastases are rarely present at the time of initial presentation.

On physical exam, the tumors are polypoid, papillary, or nodular and dark red, gray-white, or pink-gray. Most are friable. Some are ulcerated and hemorrhagic, whereas others are mucoid. Barnes has described one patient with an advanced tumor of the maxillary sinus that was associated with a pretreatment borderline abnormal serum level of carcinoembryonic antigen. Whether this laboratory test has any role in monitoring the course of the disease is uncertain.

Radiologic studies are essential in determining the extent of disease and the operative approach. Early lesions will show only a soft tissue mass with little, if any, evidence of bone destruction. Other tumors may be associated with considerable osteodestruction and invasion of contiguous structures such as the orbit and cranial cavity.

A few may even involve the contralateral sinonasal tract. As the tumor enlarges, it may interfere with drainage of nearby sinuses. The ensuing obstructive sinusitis then may interfere with optimal preoperative evaluation and staging. Several histological classifications of ITACs have been proposed , , , The one proposed by Kleinsasser and Schroeder, however, seems to be gaining acceptance for its ease of use, reproducibility, and clinical correlation According to them, ITACs can be subclassified into four categories: papillary tubular cylinder cell PTCC , alveolar goblet cell, signet ring cell, and transitional.

The columnar cells may be polarized, with their long axes perpendicular to the basement membrane, or stratified and crowded. These cells have pink cytoplasm and round to oval nuclei that vary from vesicular to hyperchromatic, with or without nucleoli. In some tumors, goblet cells are found admixed with columnar cells in a ratio similar to that seen in the intestine. In others, the fronds may be covered exclusively by columnar or goblet cells. Mitoses may or may not be prominent.

Although some papillary tumors are clearly invasive, others remain noninvasive in situ over a broad front much like papillary urothelial carcinoma in situ of the urinary bladder. A few are rather bland cytologically and may resemble a villous adenoma or even normal intestinal mucosa, yet are locally aggressive and destructive.

The PTCC II moderately differentiated, also known as the colonic type is composed of well to moderately differentiated glands and more closely resembles adenocarcinoma of the large intestine than does any of the other variants Fig. At times, one may also see cystic glandular spaces with intracystic papillary projections. The PTCC III poorly differentiated, also know as the solid type is composed of a diffuse proliferation of smaller, more cuboidal cells with amphophilic to pink cytoplasm, occasionally with mucin droplets, and round, vesicular nuclei, often with nucleoli.

There is little attempt at gland formation. The signet ring variant also known as mucinous type is composed of small groups or isolated signet ring cells floating in pools of mucus. No strips of epithelium are apparent. The transitional cell type also known as mixed type is composed of two or more of the preceding growth patterns. ITAC, regardless of histologic type, may contain Paneth and enterochromaffin cells as well as a muscularis mucosa.

The enterochromaffin cells may express a variety of peptides, including gastrin, glucagon, serotonin, cholecystokinin, and leu-enkephalin 93 , , Although Schmid et al. If they do transform, the transformation is usually to one of the more aggressive types. On the basis of the work of Cheng and Leblond and of Kirkland, it has been suggested that multidirectional differentiation of a common stem cell could account for the variety of cells Paneth, endocrine, absorptive, goblet observed in ITAC 94 , , The stem cell, either by direct transformation or by induction of adjacent mesenchyme, might also give rise to the muscularis mucosa noted in a few tumors.

The similarity of ITAC to intestinal tumors extends beyond the light-microscopic to the ultrastructural and, to some extent, the immunohistochemical level 93 , 94 , , Batsakis et al. These structures are thought to be important in identifying tumors of intestinal epithelium or tumors arising from metaplastic intestinal-type epithelium. The immunohistochemical profile of ITAC is discussed in the next section of this article. Wu et al. The differential diagnosis includes a metastasis from a gastrointestinal carcinoma, papillary rhinosinusitis, and papillary adenocarcinoma of the nasopharynx.

Metastases to the nasal cavity and paranasal sinuses from a primary adenocarcinoma of the gastrointestinal tract are not common , In a study of 82 tumors metastatic to the maxilla, nose and paranasal sinuses, Bernstein et al. The maxillary, ethmoid, and frontal sinuses and nasal cavity were involved in descending order. In some of these patients, the head and neck metastasis was the initial manifestation of an otherwise clinically occult carcinoma. For this reason, examination of the gastrointestinal tract in all patients with ITAC, especially the PTCC II colonic variant, would seem prudent, although in the absence of relevant signs and symptoms, such studies will generally prove negative.

Immunohistochemical stains for chromogranin, neuron-specific enolase NSE , and carcinoembryonic antigen CEA may offer some limited help in distinguishing ITAC from metastatic colorectal adenocarcinoma. Because ITACs tend to contain more endocrine cells than colorectal adenocarcinomas, they will usually show a more diffuse and stronger intensity when stained for chromogranin and NSE In contrast, colorectal adenocarcinomas are diffusely and strongly positive for CEA, whereas ITACs tend to show only focal, weak reactivity Staining for cytokeratin 7 is also helpful in distinguishing ITAC from metastatic adenocarcinoma of the colon ITAC is consistently positive for this marker, whereas adenocarcinoma of the colon is negative.

Sinusitis, at times, may have a papillary configuration, but in these instances, the papillae are short and blunt and not highly branched, as one sees in some ITACs. P-ITAC, in contrast to PACN, occurs primarily in the nasal cavity and paranasal sinuses and is often not invariably associated with an occupational exposure to wood dust.

P-ITAC also tends to be less glandular and more papillary. Rather than cuboidal cells, the papillae are covered by tall columnar and goblet cells, the latter of which are sparse to absent in PACN. Such cells are not seen in PACP. Last, PACP tends to be associated with a hemorrhagic, inflammatory background and often recurs after therapy.

Tumor necrosis with sepsis is often a problem and may be life threatening. Perez et al. Treatment consists of surgical excision using a lateral rhinotomy or, at times, even a cranial base approach. The use of radiotherapy is dictated by the extent and resectability of the tumor. An elective neck dissection is not warranted. Prognosis depends on the histologic type, degree of differentiation, stage of the disease, and the adequacy of resection margins.

PTCC I has the best prognosis. It may recur but rarely metastasizes. The other types are more virulent, with a greater propensity for dissemination. Over the course of time, a few tumors may change from one histologic type into another. This may be an ominous finding, signaling a tumor with increased aggressiveness. Woodworkers seem to have a better prognosis than those individuals with sporadic ITAC.

This probably relates to the fact that the woodworker is under heightened surveillance for this tumor and that in this group, the tumors are more often found in the nasal cavity or ethmoid sinus and can therefore be detected earlier by the patient. In contrast, patients with sporadic tumors are not in early detection programs and have neoplasms that are relatively more common in the maxillary sinus, which are difficult to detect early. The vast majority of malignant tumors of the nasopharynx are either keratinizing or nonkeratinizing squamous cell carcinomas or malignant lymphomas , Exceptionally, adenocarcinomas may also arise from the mucosa, and when they do, they are typically papillary and are referred to as papillary adenocarcinomas of the nasopharynx , Most present with airway obstruction.

Other less common symptoms include serous otitis media with or without hearing loss and postnasal drip with blood-tinged sputum. Rarely the tumor may be an incidental finding after adenoidectomy. PACN are typically confined to the nasopharynx and, on physical examination, present as exophytic or pedunculated masses with a papillary, nodular, or cauliflower-like appearance.

The tumors range from 0. There are no known risk factors associated with the development of this tumor. None of the patients thus far has had a significant history of tobacco or alcohol abuse or occupational, environmental, or radiation exposure The tumors arise from the surface epithelium of the nasopharynx and may remain in situ or become invasive.

They are characterized by papillary and glandular growth patterns Fig. The papillae have fibrovascular cores and often show arborization, whereas the glands have a back-to-back, often cribriform arrangement. Both papillae and glands are covered or lined by one or more layers of cuboidal to columnar cells with pink cytoplasm and round to oval nuclei that vary from hyperchromatic to optically clear.

Mild to moderate nuclear pleomorphism may be seen, but nucleoli, mitoses, and necrosis are uncommon. A few tumors may also contain psammoma bodies. Vascular, lymphatic, or neural invasion are not seen. Papillary adenocarcinoma of the nasopharynx. The tumor is composed of both papillae and glands and arises from the mucosa of the nasopharynx.

PACN typically contain periodic acid—Schiff, diastase-resistant intracytoplasmic granules and stain focally positive for intracellular or luminal mucin They are also diffusely reactive for cytokeratin and epithelial membrane antigen and focally positive for carcinoembryonic antigen. They are negative for glial fibrillary acidic protein, S protein, and thyroglobulin. Because of the papillae and the occasional presence of psammoma bodies and optically clear nuclei, PACN can easily be mistaken for metastatic papillary thyroid carcinoma.

PACN, however, are negative for thyroglobulin and will typically show dysplasia or in situ changes of the surface epithelium. Furthermore, it arises submucosally from minor salivary glands rather than from the surface, as does the PACN. Staining for S protein may also be helpful. PACN is a slow-growing, indolent neoplasm that rarely recurs and has thus far not metastasized to either cervical lymph nodes or more distant sites. The treatment of choice is surgery, using a transpalatal approach.

Wenig et al. The tumor recurred within months after treatment. The patient subsequently underwent surgical excision and was reported free of disease 11 years later. This singular experience certainly casts doubts on the efficacy of radiation therapy. In , Gaffey et al. The authors speculated that the tumor arose from the middle ear mucosa and proposed the term aggressive papillary middle ear tumor.

As experience with the tumor accumulated, it became apparent that the middle ear was not always involved, thus casting doubt on its alleged origin from this site In a review of 20 additional cases, Heffner concluded that the tumor actually arose from the endolymphatic sac and only secondarily involved the middle ear. He, therefore, suggested the term low-grade adenocarcinoma as being more appropriate because it called attention to its potential aggressive behavior and eliminated all reference to the previous misconception that it arose from the middle ear.

In this review, low-grade papillary adenocarcinoma LGPA will be used. LGPA is a slowly growing, locally aggressive tumor of the temporal bone that has been described in patients from 15—71 years of age average, 41 years , It affects both sexes about equally. In a collective review of 30 cases, 13 occurred in males and 17 in females , There is no significant lateralization of the tumor to either side of the body.

Of 20 cases in which the side of origin was indicated, 8 involved the right ear, 11 the left ear, and in the remaining case, the side was not indicated Bilateral lesions, either synchronous or asynchronous, have been described but are exceptional and should always arouse suspicion of von Hippel-Lindau disease see discussion later in this article Some also manifest with facial nerve paralysis. Physical examination may be unremarkable or may reveal a blue or red mass behind an intact, sometimes perforated tympanic membrane.

Occasionally the tumor may even project into the external auditory canal Von Hippel-Lindau disease VLD is an autosomal-dominant disorder characterized by a variety of abnormalities, chief of which include hemangioblastomas of the retina, cerebellum, medulla oblongata, and spinal cord; hemangiomas of the liver and kidney; renal cell carcinoma; and cysts of the pancreas and kidney.

Linkage studies have mapped the VLD gene to the short arm of chromosome 3, and a mutated tumor suppressor gene has been identified in both normal and neoplastic tissue from VLD patients , According to Gaffey et al. This is especially so if the tumors are bilateral Radiologic studies typically show a lytic temporal bone lesion, often with extension into the posterior cranial cavity, manifesting as a cerebellopontine angle neoplasm The epicenter of the lesion lies at or near the posterior-medial surface of the temporal bone.

According to Megerian et al. In order of frequency, they generally progress 1 posteriorly to the cerebellopontine angle and posterior fossa, 2 laterally via the mastoid cell tract to the middle ear and external auditory canal, 3 superiorly toward and into the middle cranial fossa, and 4 medially along the petrous ridge to the clivus and cavernous and sphenoid sinuses.

Angiograms show the tumor to be highly vascular with a dual extracranial and intracranial blood supply As a result, it is often mistaken for a jugulotympanic paraganglioma. Histologically, the tumor is composed of papillary-cystic components Fig.

The papillae are well vascularized and covered by a single layer of cuboidal cells, which have clear to pink cytoplasm and uniform round nuclei. Cellular pleomorphism and mitoses are absent. The cystic spaces characteristically contain pink colloid-like material, imparting a thyroid-like appearance. The secretory material is strongly positive with the periodic acid—Schiff stain and negative with mucicarmine.

Areas of closely packed glands, fibrosis, hemorrhage, and cholesterol clefts may also be seen. Low-grade papillary adenocarcinoma of the middle ear. The glands contain colloid-like secretions. The epithelial cells contain glycogen but no intracytoplasmic mucin. The cells are also usually positive for epithelial membrane antigen, NSE, and vimentin. The differential diagnosis includes middle ear adenoma, jugulotympanic paraganglioma, metastatic papillary thyroid carcinoma and renal cell carcinoma, and choroid plexus papilloma—carcinoma.

Middle ear adenomas are not papillary and do not invade or destroy bone as one sees in LGPA. Metastatic renal cell carcinoma may be the most difficult entity to exclude, especially because both LGPA and renal cell carcinoma can contain clear cells, glycogen, and papillary-cystic areas. Immunohistochemical stains may offer some help. Renal cell carcinomas are negative for glial fibrillary acidic protein and synaptophysin and, according to Medeiros et al. Perhaps the best way to distinguish between the two is to obtain a computerized tomogram of the kidneys.

Choroid plexus papilloma and carcinoma almost always originate within the ventricles of the brain, whereas LGPAs are typically extradural. Staining for transthyretin may also be helpful. Otherwise, there is too much overlap in immunohistochemical stains keratin, epithelial membrane antigen, NSE, glial fibrillary acidic protein, and vimentin to allow one to distinguish between these two neoplasms with confidence , , , , , Knowledge of the clinical and radiologic findings may be the best way to separate LGPA from a choroid plexus tumor.

Complete surgical excision, if possible, is the treatment of choice. Radiation is largely untested but has been ineffective in the few cases in which it has been used Intraoperatively, the surgeon usually observes a blue, red, or white hypervascular, nonencapsulated lobular mass that often encases the ossicles and facial nerve. Though encased, the latter structures can often be dissected free without sacrifice.

Bleeding may be profuse. Despite frequent intracranial extension, invasion of the brain has only been documented in one instance Of 30 cases contained in the reviews of Gaffey et al. Twenty percent of the patients experienced recurrence after initial attempts at excision. Although the tumor is rare and a large series of cases with long-term follow-up is not available, experience thus far indicates that LGPA is only a locally destructive tumor with little, if any, capacity to metastasize.

Ward N. A mirror of the practice of medicine and surgery in the hospitals of London: London Hospital. Lancet ; 2 : — Google Scholar. Hyams VJ. Papillomas of the nasal cavity and paranasal sinuses. A clinicopathologic study of cases. Ann Otol Rhinol Laryngol ; 80 : — Papillomatosis of nasal cavity and paranasal sinuses inverted papilloma, squamous papilloma.

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Part I. Exophytic squamous papillomas. A study of 28 cases. Laryngoscope ; 72 : — Schneiderian papillomas. A clinicopathologic study of 67 cases. Hum Pathol ; 17 : — Sinonasal papillomas: a report of 82 cases in Copenhagen County, including a longitudinal, epidemiological and clinical study. Laryngoscope ; : 72— Hirschfield LS, Harrison G. Human papillomavirus in sinonasal papillomas. Mod Pathol ; 3 : 45A abstract. Sinonasal papillomas and human papillomavirus: human papillomavirus 11 detected in fungiform Schneiderian papillomas by in situ hybridization and the polymerase chain reaction.

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Inverting papilloma of the head and neck: the UCLA update. Otolaryngol Head Neck Surg ; : 71— Inverted papilloma: a report of cases. Eavey RD. Inverted papilloma of the nose and paranasal sinuses in childhood and adolescence. Laryngoscope ; 95 : 17— Inverted papilloma isolated to the sphenoid sinus. Otolaryngol Head Neck Surg ; : — Inverted papilloma of the nasal septum. Arch Otolaryngol ; : — Wenig BM. Schneiderian-type mucosal papillomas of the middle ear and mastoid.

Ann Otol Rhinol Laryngol ; : — Schneiderian papillomas of the pharynx. Hampal S, Hawthorne M. Hypopharyngeal inverted papilloma. J Laryngol Otol ; : — Unusual anatomic presentations of inverting papilloma. Head Neck Surg ; 7 : — Primary epithelial neoplasms of the lacrimal sac. Am J Ophthalmol ; 76 : 73— Inverted papilloma of the lacrimal sac, the paranasal sinuses and the cervical region.

Cancer ; 40 : — Isolation and characterization of papillomavirus DNA from nasal inverting Schneiderian papillomas. Ann Otol Rhinol Laryngol ; 96 : — Detection of human papillomavirus HPV structural antigens and DNA types in inverted papillomas and squamous cell carcinomas of the nasal cavities and paranasal sinuses.

Acta Otolaryngol Stockh ; : — CAS Google Scholar. Prevalence of human papillomavirus in inverted nasal papillomas. Arch Otolaryngol Head Neck Surg ; : 23— In situ hybridization with human papillomavirus RNA probes. Cancer ; 63 : — Detection of HPV 6 and 11 in tumours of the upper respiratory tract using the polymerase chain reaction. Clin Otolaryngol ; 15 : — Association of DNA aneuploidy with human papillomavirus-induced malignant transformation of sinonasal traditional papillomas.

Siivonen L, Virolainen E. Transitional papilloma of the nasal cavity and paranasal sinuses. Clinical course, viral etiology and malignant transformation. Presence of human papillomavirus type-6 related sequences in inverted nasal papillomas. Eur Arch Otorhinolaryngol ; : — Molecular pathologic study of human papillomavirus infection in inverted papilloma and squamous cell carcinoma of the nasal cavities and paranasal sinuses.

Laryngoscope ; : 79— Presence of human papillomavirus predicts recurrence of inverted papilloma. Otolaryngol Head Neck Surg ; : 49— Detection of human papillomavirus type 57 in a case of inverted nasal papillomatosis in Japan.

A majority of inverted sinonasal papillomas carries Epstein-Barr virus genomes. Cancer ; 75 : — Radiologic aspects of inverted papilloma. Radiology ; : 73— Part II. Inverting papillomas. A study of 29 cases. Laryngoscope ; 73 : 1— Abildgaard-Jensen J, Greisen O. Inverted papillomas of the nose and the paranasal sinuses. Clin Otolaryngol ; 10 : — Management of inverted papillomas of the nose and paranasal sinuses. Laryngoscope ; 91 : — Inverted papilloma of the nasal cavity. Arch Otolaryngol ; 84 : 83— Epithelial papilloma and squamous cell carcinoma of the nasal cavity and paranasal sinuses.

Cancer ; 38 : — Considerations in treatment. Laryngoscope ; 96 : — Squamous cell carcinoma arising in inverted papilloma. P53 alteration and human papilloma virus infection in paranasal sinus cancer. Cancer ; 79 : — Malignant transformation in sinonasal papillomas is closely associated with aberrant p53 expression. Mol Diag ; 3 : 37— Immunohistochemistry of p53 in sinonasal inverted papilloma and associated squamous cell carcinoma. Am J Rhinol ; 12 : — CD44 expression in sinonasal inverted papillomas and associated squamous cell carcinoma.

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Biologically aggressive papillomas of the nasal cavity: the role of radiation therapy. Laryngoscope ; 95 : — Schneiderian papillomas: a clinicopathologic study of 30 cases. Am J Surg Pathol ; 1 : 43— Barnes L, Bedetti C.

Oncocytic Schneiderian papilloma: a reappraisal of cylindrical cell papilloma of the sinonasal tract. Hum Pathol ; 15 : — Cylindrical cell papilloma. Clinical report: cylindrical cell papilloma of the paranasal sinus. Arch Otorhinolaryngol ; : — Oncocytic Schneiderian papilloma in a young adult: a rare diagnosis. Otolaryngol Head Neck Surg ; 97 : 47— Carcinoma arising in oncocytic Schneiderian carcinoma.

Am J Surg Pathol ; 14 : — Carcinoma ex oncocytic Schneiderian cylindrical cell papilloma. Am J Otolaryngol ; 14 : — Ferlito A, Devaney KO. Developmental lesions of the head and neck: terminology and biologic behavior. Glandular seromucinous hamartoma of the nasopharynx.

Oral Surg ; 38 : — Nasopharyngeal hamartoma: report of a case and review of the literature. Laryngoscope ; 93 : — Hamartomas of the nose and nasopharynx. Head Neck ; 14 : — Nasal hamartoma: case report and review of the literature. Int J Pediatr Otorhinolaryngol ; 28 : 83— Chondro-osseous and respiratory epithelial hamartomas of the sinonasal tract and nasopharynx [abstract]. Mod Pathol ; 74 : A. Nasal chondromesenchymal hamartoma. An upper respiratory tract analogue of the chest wall mesenchymal hamartoma.

Am J Surg Pathol ; 22 : — Management of the congenital midline nasal mass: a review. Head Neck Surg ; 2 : — Nasopharyngeal teratomas and desmoids: a review of the literature and case series. Int J Pediatr Otorhinolaryngol ; 52 : — PubMed Google Scholar. Respiratory epithelial adenomatoid hamartomas of the sinonasal tract and nasopharynx: a clinicopathologic study of 31 cases. Cancer of the nasal cavity and accessory sinuses. A report of the management of patients.

Cancer ; 16 : — Carcinoma of the paranasal sinuses— a review of cases. J Otolaryngol ; 7 : — Carcinoma of the nasal cavity and paranasal sinuses: incidence and presentation of different histological types. Clin Otolaryngol ; 4 : — Malignant tumors of the paranasal sinuses: radiological, clinical, and histopathological evaluation of cases. Head Neck Surg ; 6 : — Paranasal sinus malignancy: a comprehensive update.

Treatment of maxillary sinus carcinoma. Cancer ; 86 : — Nasal adenocarcinomas that closely simulate colonic carcinomas. Cancer ; 28 : — Endocrine-amphicrine enteric carcinoma of the nasal mucosa. Virchows Arch Pathol Anat ; : — Aggressive sinonasal lesion resembling normal intestinal mucosa. Am J Surg Pathol ; 6 : — Roush GC. Epidemiology of cancer of the nose and paranasal sinuses: current concepts. Head Neck Surg ; 2 : 3— Muir CS, Nectoux J. Descriptive epidemiology of malignant neoplasms of nose, nasal cavities, middle ear and accessory sinuses.

Clin Otolaryngol ; 5 : — Elwood JM. Wood exposure and smoking: association with cancer of the nasal cavity and paranasal sinuses in British Columbia. Can Med Assoc J ; : — Adenocarcinoma of the ethmoid sinuses. A review of 28 cases with special reference to wood dust exposure. Cancer ; 54 : — Cancer epidemiology of woodworking.

J Cancer Res Clin Oncol ; : — Finkelstein MM. Nasal cancer among North American woodworkers: another look. J Occup Med ; 31 : 35— Imbus HR. Nasal cancer in woodworkers [letter to the editor]. J Occup Med ; 32 : — A case-control study of cancer of the nose and paranasal sinuses and occupational exposures.

Am J Ind Med ; 22 : — Occupational risk factors for sinonasal cancer: a case-control study in France. Am J Ind Med ; 21 : — Sinonasal adenocarcinoma: epidemiological and clinicopathological study of 34 cases. J Otolaryngol ; 22 : 86— Study Design: Pathologic review and polymerase chain reaction-based PCR-based examination of archived tissue. This was also performed on normal turbinate control specimens.

Nine tumors were diagnosed as either verrucous or squamous cell carcinoma. Of these, 5 of 69 6. One of nine No normal turbinate tissue contained HPV. HPV types 6b and 11 accounted for all cases of fungiform papillomas. HPV 16 may rarely play a role in cases of inverting papillomas, and HPV 16 and 18 may be involved in a subset of cases of carcinomas originating in an inverting papilloma. There are three recognized subtypes of SP: inverting, fungiform, and oncocytic cylindric cell papillomas.

This study represents the largest study to date. Patients with SP were selected using a computerized search of all formalin-fixed, paraffin-embedded pathologic specimens at the Mayo Clinic from through Blocks were chosen for sectioning which well represented the papillomatous neoplasm.

The blocks were sectioned using a disposable microtome blade. An unused portion of the microtome blade was used for each specimen and the blade changed after every two blocks to prevent block-to-block contamination. Using reverse-blot "strip" analysis, HPV genotype discrimination of greater than 27 HPV types can be performed in a single hybridization and wash cycle. This served to deter-mine whether DNA of sufficient quality was present for successful amplification of this length product.

The B-globin assay was repeated. If the tumor was still negative for -globin product, it was eliminated from analysis as containing insufficient intact DNA for successful PCR. This was followed by a single, additional elongation step at 72C for 5 min. Table I shows the breakdown by histologic subtype of the tumors studied.

Specimens negative for B-globin were eliminated from further analysis. Fourteen papillomas However, it should be noted that in one turbinate, a weak band of the correct length bp could be seen on the agarose gel. On the typing strips, no band was demonstrated. Overall, 23 of the tumors Only a small fraction of the inverted papillomas were positive for HPV 6. Only 6. This is typified by the establishment of HPV as a major causative role in cervical neoplasia.

We also thought it vitally important to include control nasal tissue in the study because of the tremendous sensitivity of PCR, as well as the possibility of laboratory contamination. In addition, although Buchwald et al. The study of Schneiderian papillomas is complicated by the fact that there are three distinct histologic sub-types that were recognized by Hyams3 in The reader cannot distinguish, then, whether the tumors studied did, indeed, represent only inverting papillomas, or whether the study also included tumors that may be subclassified as fungiform papillomas.

According to the manufacturer, this technique is said to increase both specificity and sensitivity confirmed in our laboratory, data not published. In a study designed to assess the effects of sample preparation including age and PCR product size, Greer et al. This number is consistent with many reports of HPV in "inverted" papillomas. Our results are also nearly identical to those of Gaffey et al. In contrast to our study and those mentioned above, a number of studies have identified HPV DNA in a significant number of inverted papillomas.

One such study, performed by Beck et al. Bernauer et al. Similar results were obtained by Kashima et al. Likewise, McLachlin et al. Wu et al. Several explanations are possible. This is possible, but two facts suggest that this is not the case. It has been demonstrated that the use of two or more consensus primer sets has a higher sensitivity in HPV detection than any one set alone. It is not yet known where the origin of HPV infection of the head and neck is, or what the route of transmission is.

Certainly, the possibility that the source is from anogenital locations exists, given the predominance of the same HPV types in SP and in anogenital HPV-related diseases. Clearly, there may be more than one mechanism of alteration of cell growth and differentiation i.

Fourth, the role of the immune system, which may allow some patients to "clear" their viral infection while others develop chronic infection, is unknown. This is consistent with most previous studies. Other factors such as cigarette smoking may be more important in this population. A similar trend has been noted by other authors. HPV may rarely play a role inverting papillomas, and HPV and HPV may be involved in a subset of cases of carcinomas originating in an inverting papilloma.

The authors gratefully acknowledge the significant assistance of Ms. Renee McGovern in conducting the lab-oratory work. The clinical behavior of inverting papilloma of the nose and paranasal sinuses: report of cases and review of the literature. Laryngoscope ; Smith 0, Gullane PJ. Inverting papilloma of the nose: analysis of 48 patients. J Otolaryngol ;16 3 Hyams VJ.

Papillomas of the nasal cavity and paranasal sinuses: a clinicopathological study of cases. Ann Otol Rhinol Laryngol ; Inverting papilloma of the nose and paranasal sinuses.

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Step up/down investing switching regulator wiki The basement membranes around the epithelial islands in IPs are also thin and delicate, not thick and hyalinized as seen in REAH. ITAC is consistently positive for this marker, whereas adenocarcinoma of the colon is negative. Am J Rhinol ;11 2 Larger polyps that cause problems might need to be treated with medicine or surgery. Lesion composed of numerous glands lined by ciliated respiratory investing papilloma nose. Macdonald et al. Inverted papilloma isolated to the sphenoid sinus.
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Blackstone ipo 2007 A similar trend has been noted by other authors. Despite frequent intracranial extension, invasion of the brain has only been documented in one instance Oncocytic schneiderian papilloma. Cancer investing papilloma nose 31 : — Mucoserous minor salivary glands are also occasionally seen in a lobular configuration. As in IP, the carcinoma complicating OSP may actually arise within the papilloma, as evidenced by a gradation of histologic changes ranging from dysplasia to in situ to invasive carcinoma, or it may merely be associated with the OSP.
What will gold do Metastatic adenocarcinoma of the ethmoids in a patient with previous gastric adenocarcinoma: a case investing papilloma nose. Immunohistochemical stains for chromogranin, neuron-specific enolase NSEand carcinoembryonic antigen CEA may offer some limited help in distinguishing ITAC from metastatic colorectal adenocarcinoma. The term that has currently emerged as the most preferred is intestinal-type adenocarcinoma ITAC. Inverted papilloma isolated to the sphenoid sinus. They may be composed entirely of epithelial or mesenchymal elements or of both and should be distinguished from teratomas and dermoids 77787980818283 Cancer ; 31 : — Wood dust and nasal cancer risk.

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The findings may help to explain the wide of range of pathologic outcomes of infection by a specific human papillomavirus type in immunocompetent people. PLoS Pathog 10 8 : e Editor: Denise A. This is an open-access article, free of all copyright, and may be freely reproduced, distributed, transmitted, modified, built upon, or otherwise used by anyone for any lawful purpose.

The work is made available under the Creative Commons CC0 public domain dedication. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. Competing interests: The authors have declared that no competing interests exist. Papillomaviruses PV are DNA tumor viruses that infect stratified squamous epithelia of the skin and mucous membranes of humans and many other vertebrate species [1].

PV infections are species-restricted and region-restricted, in that only part of the skin and mucous membranes of the host species of a given PV is permissive for productive infection [2]. These viruses can induce long-term infection that, depending on the virus type and its human host, may not cause lesions, may induce benign lesions warts or papillomas , or may lead to the development of anogenital carcinomas, most notably cervical and oropharyngeal cancers. Certain cutaneous HPV types have also been implicated in the pathogenesis of some epidermal squamous cell cancers in genetically predisposed or immunocompromised individuals [3].

Although neutralizing antibodies against the viral capsid proteins are sufficient to prevent PV infections, cell-mediated immunity is generally thought to control the infections once they become established. For instance, individuals with underlying T cell deficiencies, but not B cell deficiencies, often have difficulties in controlling and clearing HPV-induced neoplasia [4].

However, it has been difficult to provide experimental support for this concept or to determine which particular subset s of immunocytes are responsible for these activities. These immunodeficient mice spontaneously developed papillomas at cutaneous surfaces near the mucocutaneous junctions of nose and mouth, from which the virus was isolated. Subsequent studies reported that papillomas could be induced by experimental infection with MusPV1 in immunodeficient B6.

In contrast to these reports of MusPV1 in immunodeficient mice, the study of MusPV1 in immunocompetent mice has been limited. These lesions, which were not characterized further, took at least three weeks to develop, and regressed spontaneously by 8 weeks post-inoculation [6]. Thus establishment and further characterization of MusPV1 infection and disease in an immunocompetent setting were warranted.

In this study we aimed at characterizing MusPV1 infection in different immunocompetent murine strains and sought to determine the key immunologic players primarily responsible for control of cutaneous PV infection and papilloma induction. Our results revealed asymptomatic MusPV1 infection in these immunocompetents and demonstrated that profound immunosuppression can render these strains that had various H-2 haplotypes susceptible to MusPV1-induced papilloma formation of the skin.

This is reminiscent of infection with HPV of genus beta that also predominantly induces asymptomatic skin infections in immunocompetent individuals but can induce visible lesions after immunosuppression. The observed differences in the efficiency of papilloma outgrowth between the individual murine strains corresponded partially to their previously reported susceptibility to chemical-induced skin papillomatosis [summarized in 10] , suggesting that there may be similarities between their relative susceptibility to papilloma formation induced by MusPV1 and to chemical carcinogens.

We further provide clear experimental proof that T cell functions are required for control of PV infection and disease and reveal striking differences in the protective capacities of T cell subsets among murine strains, including CD4-mediated effector mechanisms. The inbred strains have a range of H-2 haplotypes and a range of reported susceptibility to chemical carcinogen-induced skin papillomas Table 1 [10] — [12]. The SENCAR strain was included because it was selectively bred for high susceptibility to skin tumor induction by chemical carcinogens.

During this period, no papilloma outgrowth was observed in any strain, although the same preparation and dose of MusPV1 virions consistently induced large papillomas in immunodeficient athymic NCr nude mice within one month of inoculation data not shown. To determine whether immunosuppression renders these mouse strains susceptible to MusPV1-induced papilloma formation, animals were treated systemically with the immunosuppressant CsA, which can inhibit T cell activation and lymphokine production and is routinely used in humans for prevention of transplant rejection [14] , [15].

CsA treatment was initiated one week prior to infection with 4. CsA treatment was started one week prior to infection with 4. The lesions showed histological features of papillomas with numerous koilocytes in the epithelium inset. L Regressed lesion on the same mouse 6 weeks after cessation of CsA administration, showing that CsA treatment is required for induction and maintenance of the papillomas.

L1 expression was punctate in the cytoplasm of the keratinocytes in the basal and lower spinous layers, and nuclear in the upper spinous and granular layers of the epithelium. Basal keratinocytes were co-stained with a phycoerythrin-conjugated anti-CD49f antibody red to facilitate orientation. The epidermal compartment is shown in the upper part of each image and the dermal compartment in the lower part. The lesions that developed were histologically verified to be papillomas with numerous koilocytes in the epithelium Figure 1I ; SENCAR shown as representative , and extracts of the lesions contained infectious MusPV1 virions that induced papillomas, in athymic NCr nude mice, whose morphology was identical to those previously reported for MusPV1 in this immunologically impaired strain Figure 1J [9].

The length of time to regression depended upon the size of the lesion, with smaller ones tending to regress sooner than larger ones Figure S1C. Therefore, the immunosuppressive phenotype resulting from CsA treatment was required for maintenance of the papillomas, in addition to their induction. In a rabbit model, persistent PV genome expression was reported at mucosal sites of infection following lesion-regression [16].

Subsequent immunosuppression led to an increase in viral copy numbers and even to reappearance of small lesions, consistent with reactivation of latent infection [17]. After this period, papilloma outgrowth was not observed in any of the animals data not shown.

When susceptibility to MusPV1-induced papillomas was considered in the context of the H-2 haplotype of the mice, surprisingly, there was little correlation Table 1. By contrast, we noted some correlation between the observed susceptibility to MusPV1-induced papillomas and their previously reported susceptibility to chemical carcinogenesis Table 1 [10] , suggesting that common mechanisms may, in part, control the relative susceptibility to MusPV1-induced papilloma formation and to chemical carcinogens.

Further experimentation is required to validate the partial correlation between strain-specific susceptibility to papillomatosis and chemical carcinogens. All lesions spontaneously regressed within 1—2 weeks after formation corresponding to 3—5 weeks post-infection. In the epithelium of these papillomas, expression of the major capsid protein L1 was demonstrated by immunofluorescent microscopy Figure S3D, E. Skin necropsies were taken from all animals within the remaining six tested strains, including those mice that lacked visible lesions.

To ensure comparability, specimens of approximately the same size were processed, and the levels of the viral transcripts were adjusted to level of endogenous beta-actin transcripts from the same sample Figure 1M , the lanes designated CM. The resulting ratios corresponded well to the macroscopic appearance of the lesions. Thus MusPV1 established persistent asymptomatic infections in all of the immunocompetent mouse strains.

Immunofluorescent microscopy was used to examine the relative expression of the major capsid protein L1 in these tissues. Similar to previous reports in athymic NCr nude mice [9] , punctate L1 expression was found in the cytoplasm of keratinocytes in the basal and lower spinous layers of the epithelium, while nuclear L1 expression was confined to the upper spinous and granular layers, suggesting active virion production in these more differentiated epithelial layers.

Additionally, some L1 positive squames that presumably enclose matured virions prior to shedding were found in these tissues. L1 expression was restricted to the epithelial compartment, although seemingly positive staining could occasionally be observed below the basement membrane due to the trans- sectioning of the papilloma's deregulated architecture. L1 staining was not detected at sites of lesion regression following cessation of CsA treatment data not shown or in the skin of untreated MusPV1-infected mice at this time point, regardless of the strain Figure 1Q—S.

Interestingly, L1 was readily detected in infected sites on day 14 after inoculation in untreated mice of all three strains, raising the possibility that adaptive immune responses arising between two and four weeks may regulate late gene expression and thereby virion production data not shown. Tissue taken 4 weeks after inoculation with 4. By immunofluorescent staining IFS , higher numbers of both T cell subsets were present in the MusPV1-infected tissue, independent of whether the mice had been treated with CsA, although L1 expression was only detected in the infected CsA-treated mice Figure 2A and 2B.

Skin tissues were harvested 4 weeks after infection with 4. Viral infection without CsA resulted in a Thus, MusPV1 infection efficiently recruits both T cell subsets to the site of infection, even in the presence of CsA. The mice were infected on day 0 with 7. MusPV1 inoculation after administration of an isotype control Figure 3F or without mAb addition Figure 3G did not induce papilloma formation.

Efficiency was markedly reduced when depletion was started D 28 days post-infection, and no papilloma outgrowth was observed when depletion was started E 49 days after infection. H Comparison of tail lesions in these animals after 7 weeks of T cell depletion showed the differences in mean lesion lengths, given in mm, between the different experimental groups.

L—M In contrast, L1 expression was absent in skin tissues taken from isotype-depleted controls. Infection of all animals was performed on day 0 using 7. No L1 protein and only isolated T cells were observed in mock-infected controls data not shown. T cell-mediated responses either clear MusPV1 infection within 7 weeks post-inoculation or control it by a mechanism that does not permit reactivation after their removal.

The immunodepletion was started one week prior to infection with 5. The mean length of the lesions was similar in the CD4-depleted and CD8-depleted groups, being B Similarly, papilloma formation was observed in CD8-depleted littermates at the same time point. All mice were infected with 5. E Comparison of tail lesions of CD4- and CD8-depleted animals at this time point showed comparable mean lesion lengths, in mm, in these animals.

There was no loss in the infiltration by the non-depleted subset. Depletion of the targeted T cell subset at the site of infection was associated with the apparent absence of the depleted subset but with no loss in the infiltration by the non-depleted subset, indicating the neither subset was needed for recruitment of the other Figure 4F—I. The results in the skin confirmed the validity of the microscopy results, and demonstrated the efficient and specific depletion of the targeted subpopulation in each compartment at this time point.

L1 protein was also undetectable in MusPV1-infected, non-depleted and mock-infected littermates. One representative per group is shown. The molecular weight marker MW is depicted on the left side and 60 kD and 50 kD markers are visible; purified MusPV1 virions served as controls.

Quantification of T cell infiltrates in the infected skin sites Figure 5O and the blood Figure 5P , spleen Figure 5Q , and draining lymph nodes Figure 5R by flow cytometric analyses further confirmed the efficiency and specificity of the T cell depletion. In this study, we have determined that a variety of immunocompetent mouse strains are resistant to papilloma induction by MusPV1, although a limited degree of virus expression can be detected at 4 weeks after infection.

However, immunosuppression induced by CsA uncovered a strain-dependent hierarchy in the degree of susceptibility to papilloma formation and virus production. To date, strong circumstantial evidence supports the role of cell-mediated immunity, especially T cells, in controlling and eliminating established PV infection and neoplasia.

Evidence for the pivotal role of T cells has emerged from studies of humans infected with the human immunodeficiency virus [20]. In these individuals, higher prevalence of HPV infection, especially of the anogenital tract, viral persistence, and very often the presence of multiple types, has been observed. An important role for T cells is also supported by observations that iatrogenic immunosuppressed transplant recipients have high rates of extensive viral warts, HPV-associated anogenital cancers, and non-melanoma skin cancer [3].

The current study demonstrated that treatment with CsA, whose predominant activity is against T cells and which is routinely used in humans, led to papilloma formation and persistent MusPV1 infection in most, but not all, of the murine strains tested. The available data with other PV systems have not defined the T cell subpopulation s that is the key player responsible for virus control and papilloma regression.

Thus, the infiltrate was similar, independent of whether the mouse developed lesions, indicating that functional properties of the T cells, rather than epithelial trafficking, were primarily affected by CsA treatment. The availability of many immunological reagents for the domestic mouse made it possible to critically evaluate individual T cell subsets in the control of PV infection and associated neoplastic disease. However, we failed to detect MHC class II expression on keratinocytes at sites of infection, both when the infection was being controlled by the immune system and when it was not unpublished data.

Although the details of immune recognition of MusPV1 remain to be determined, it seems likely that T cells control MusPV1 infection by both innate and adaptive immune mechanisms. The timing of papilloma regression after suspending CsA treatment and of spontaneous regression after high dose challenge in the SENCAR mice is consistent with induction of an antigen-specific adaptive response.

Our findings raise several additional interesting issues. A second issue is the partial correlation between the reported strain-dependent susceptibility to chemical-induced papillomatosis and the robustness of persistent infection and papillomatosis after CsA treatment found in this study. A third issue is whether the characteristics of MusPV1 infection documented herein make it an attractive model of any HPVs.

These cutaneous HPVs have been found in immunocompetent individuals in clinically normal skin and plucked hairs where they predominantly induce asymptomatic skin infections [47] , [48] , similar to MusPV1 infection described herein. However, after immunosuppression, beta HPVs could be more frequently detected, tended to display higher viral loads, and most importantly induced visible lesions after immunosuppression [49] — [51].

The presence of beta-HPVs has been implicated as a causal factor in the increased risk for development of non-melanoma skin cancers in immunosuppressed transplant recipients. Thus, MusPV1 infection may provide a model to study the impact of a cutaneous PV type on the pathogenesis of non-melanoma skin cancer in an immunosuppressed and in an immunocompetent setting. The mice, all females aged 6—10 weeks, were housed and handled in strict accordance to the National Institutes of Health guidelines for the use and care of live animals.

In vivo infection with purified MusPV1 virions was performed on pre-scarified skin of the animals' tails as previously published [9] , [13]. The tail was chosen, as it represents a location that is highly permissive for MusPV1 infection [9]. The tail also has the advantage over the equally permissive muzzle skin, in that extensive lesional growth does not cause obvious distress to the animals.

Odam papillomasi virusi haqida nimalarni bilish zarur? HPV qanchalik noyob hisoblanadi? Qanday turdagi HPV patologiyaning rivojlanishiga olib kelishi mumkin? HPV infeksiyasi aniq saratonga olib keladimi? Virus qanday qilib yuqishi mumkin? Kasallikning rivojlanish jarayoni qanday? Bachadonni olib tashlash kasallikdan qutqarib qoladimi? Vaksinalar virusdan himoya qiladimi? Vaksinalarning aks ta'siri bormi? Homilador ayollarga vaksinatsiya qilish mumkinmi?

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