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Clin Oncol 9: 311318 Parfrey N A, Doyle C T 1985 Elastosis in benign and malignant breast illness. Hum Pathol 16: 674676 Shivas A A, Douglas J G 1972 the prognostic significance of elastosis in breast carcinoma. J Pathol 151: 297303 Silverberg S G, Chitale A R 1973 Assessment of the importance of the proportion of intraductal and infiltrating tumor growth in ductal carcinoma of the breast. Cancer 32: 830837 Matsukuma A, Enjoji M, Toyoshima S 1991 Ductal carcinoma of the breast. Int J Radiation Oncol Biol Phys 17: 719725 Jacquemier J, Kurtz J M, Amalric R et al. Duraker N, Caynak Z C, T�rk�z K 2006 Perineural invasion has no prognostic value in patients with invasive breast carcinoma. Barbareschi M 1996 Prognostic worth of the immunohistochemi cal expression of p53 in breast carcinomas. Hilsenbeck S G, Osborne C K 2006 Is there a role for adjuvant tamoxifen in progesterone receptorpositive breast most cancers Allred D C 2008 Commentary: hormone receptor testing in breast cancer: a distress sign from Canada. Bird P A, Hill A G, Houssami N 2008 Poor hormone receptor expression in East African breast cancer: evidence of a biologically completely different illness Rhodes A, Jasani B 2009 the oestrogen receptor�negative/pro gesterone receptor�positive breast tumour: a biological entity or a technical artefact Jensen E V, Greene G L, De Sombre E R 1986 the estrogen receptor immunoassay in the prognosis and treatment of breast cancer. King W J, Greene G L 1984 Monoclonal antibodies localise oestrogen receptor in nuclei of goal cells. Rakha E A, ReisFilho J S, Ellis I O 2010 Combinatorial bio marker expression in breast most cancers. Adjuvant tamoxifen within the management of operable breast most cancers: the Scottish Trial. Murphy L C, Watson P 2002 Steroid receptors in human breast tumorigenesis and breast most cancers progression. Dunnwald L K, Rossing M A, Li C I 2007 Hormone receptor status, tumor characteristics, and prognosis: a prospective cohort of breast cancer sufferers. Badve S, Nakshatri H 2009 Oestrogenreceptor�positive breast most cancers: towards bridging histopathological and molecular classifi cations. Weigelt B, Baehner F L, ReisFilho J S 2010 the contribution of gene expression profiling to breast cancer classification, prognos tication and prediction: a retrospective of the final decade. Horwitz K B, Koseki Y, McGuire W L 1978 Estrogen control of progesterone receptor in human breast cancer: position of estradiol and antiestrogen. Horwitz K B, McGuire W L 1975 Specific progesterone receptors in human breast cancer. Clin Cancer Res 12: 46144618 sixteen Tumors of the Breast strategies using monoclonal antireceptor antibodies. Am J Clin Pathol 94: S35S40 Anderson J, Orntoft T, Skovgaard Poulson H 1986 Semiquanti tive oestrogen receptor assay in formalinfixed paraffin sections of human breast most cancers tissue using monoclonal antibodies. Br J Cancer 58: seventy seven 80 Poulson H S, Jensen J, Hermansen C 1981 Human breast cancer: heterogeneity of estrogen binding websites. Cancer forty three: 1791 Chiu K Y 1987 Use of microwave for fast immunoperoxidase staining of paraffin sections. Med Lab Sci 44: 35 Shi S R, Key M E, Kalra K L 1991 Antigen retrieval in formalin fixed, paraffin embedded tissues: an enhancement method for immunohistochemical staining based on microwave oven heating of tissue sections. J Clin Pathol 60: 299 302 Barnes D M, Millis R R 1995 Oestrogen receptors: the historical past, the relevance and the methods of analysis. Brown J, Jones M, Benson E A 1993 Confirmation of a longterm prognostic index in breast most cancers. Longacre T A, Bartow S A 1986 A correlative research of human breast and endometrium within the menstrual cycle. Tavassoli F A, Tienyeh I 1987 Lactational and clear cell modifications of the breast in non lactating, non pregnant girls. Watters A D, Bartlett J M 2002 Fluorescence in situ hybridization in paraffin tissue sections: pretreatment protocol. Rakha E, ReisFilho J S 2009 Basallike breast carcinoma: from expression profiling to routine practice. Rasbridge S A, Millis R R 1998 Adenomyoepithelioma of the breast with malignant options. Schurch W, Seemayer T A 1985 Malignant myoepithelioma (myoepithelial carcinoma) of the breast-an ultrastructural and immunohistochemical research. Moran C A, Suster S, Carter D 1990 Benign blended tumours (pleomorphic adenomas) of the breast. Smith B H, Taylor H B 1968 the incidence of bone and carti lage in mammary tumours. Quizilbash A H, Patterson M C, Oliveria K F 1977 Adenoid cystic carcinoma of the breast. Hanna W, Kahn H J 1985 Ultrastructural and immunohisto chemical characteristics of mucoepidermoid carcinoma of the breast. Covi J, Duong J D, Leffall L D 1981 High grade mucoepidermoid carcinoma of the breast. Vuitch M F, Rosen P P, Erlandson R 1986 A pseudoangiomatous hyperplasia of mammary stroma. Miettinen M, Lehto V P, Virtanen I 1983 Post mastectomy angio sarcoma (StewartTreves syndrome). Light microscopic, immuno histochemical and ultrastructural characteristics of two circumstances. McWilliam L J, Harris M 1985 Histogenesis of publish mastectomy angiosarcoma-an ultrastructural research. Hartveit F 1990 Attenuated cells in breast stroma: the lacking lymphatic system of the breast. Mammary and vaginal myofibroblastoma are genetically associated lesions: fluorescence in situ hybridization evaluation displaying deletion of 13q14 area. A Bcell spectrum together with the low grade Bcell lymphoma of mucosa associated lymphoid tissue. Lee A H 2007 the histological prognosis of metastases to the breast from extramammary malignancies. Table 17-1 lists probably the most frequent tumors arising within the sellar and parasellar area. The most typical tumors are, by far, the pituitary adenomas, benign epithelial tumors derived from cells of the adenohypophysis. In truth, pituitary adenomas characterize the third most common major intracranial tumor in neurosurgical follow, outnumbered only by gliomas and meningiomas. Pituitary adenomas predominantly affect females between the third and sixth decades; however, no age group is spared. In this chapter, solely the most typical and extra unique entities involving the sellar region might be mentioned. Anatomy and Histology of the Pituitary Gland the grownup human pituitary is a bean-shaped gland located inside a small bony box, the sella turcica, under the base of the mind. The adenohypophysis is epithelial in origin and arises from the Rathke pouch, an invagination within the oral ectoderm. The posterior pituitary is derived from neuroectoderm, arising as an outpouching from the floor of the third ventricle.

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The third variant shows growth into the connective tissue wall of the cyst, so-called intramural proliferation. It has an analogous prognosis to conventional ameloblastoma and requires similarly aggressive administration. Peripheral Ameloblastoma Very occasionally, ameloblastomas could come up from the oral epithelium of the gingiva or alveolus rather than inside bone. Part of the liner reveals features identifiable as ameloblastoma, however different areas are stratified squamous epithelium lacking ameloblastoma features. Squamous Odontogenic Tumor a sinister feature related to aggressive and possibly malignant behavior39,forty (see Malignant Ameloblastoma, later). This can pose diagnostic difficulty in some cases, particularly in small biopsies, and surgeons ought to all the time be inspired to biopsy solid or multicystic areas instead of extra thin-walled areas of a large cyst. Variation in nuclear shape exists between peripheral and central cells in epithelial nests, however variation in cell and nuclear dimension and staining depth is limited. If quite a lot of mitoses are seen, the potential of malignant ameloblastoma (see later discussion) ought to be considered. They are often handled by enucleation, and the prognosis is made subsequently by the pathologist. Unicystic ameloblastomas have the same website distribution as typical ameloblastomas but occur in a youthful age group, usually within the second decade. The first reveals a easy cystic lesion lined by ameloblastomatous epithelium, which can turn into flattened and resemble a easy squamous epithelial lining. In the second variant, intraluminal proliferations of ameloblastomatous epithelium may be seen. This intraluminal variant is normally plexiform42 (plexiform unicystic ameloblastoma), with strands of epithelium that typically lack apparent ameloblastomatous options. Distinguishing this from hyperplastic proliferation in a nonneoplastic cyst could also be difficult and is largely depending on the Clinical Features Squamous odontogenic tumor, derived from rest cells of Malassez, was described as a definite entity in 1975,forty three and only a small variety of circumstances have been recorded. It presents as an apparently cystic lesion in the alveolus adjoining to tooth roots, inflicting tooth mobility and displacement. Individual cell keratinization and small foci of keratin may be seen; cystic degeneration can happen throughout the epithelial islands. Differential Diagnosis the differential prognosis from ameloblastoma is made by the shortage of palisading of elongated cells at the periphery of the epithelial islands and the dearth of stellate reticulum areas. The necessary differential analysis from squamous cell carcinoma is made by the shortage of any cytologic features of malignancy within the squamous odontogenic tumor. Squamous odontogenic tumor-like proliferations have been described in affiliation with some odontogenic cysts,forty five but these appear to be of no prognostic relevance. The lesion is described later on this chapter within the part on odontogenic cysts (see p 265). Adenomatoid Odontogenic Tumor the adenomatoid odontogenic tumor,46 at one time designated adenoameloblastoma, is a benign lesion, but whether it should be categorized as a hamartoma or a benign neoplasm is still debated. Clinical Features these tumors most incessantly present in the second decade, virtually twice as typically within the maxilla as in the mandible. A useful radiographic function, strongly indicative of an odontogenic tumor, is the presence of radioopacities within a cyst cavity. Conservative surgical remedy is normally curative; recurrence, even after incomplete elimination, is very uncommon. Histologic Appearances Usually a well-circumscribed epithelial proliferation is seen, which can have a cystic component. Much of the epithelium consists of small polyhedral cells with little cytoplasm, present in strands, sheets, and whorled areas, not significantly suggestive of odontogenic origin. An additional variable characteristic is matrix formation within the type of small rounded acellular eosinophilic plenty, in all probability a form of enamel protein, or much less incessantly as bigger areas of dysplastic dentine that will calcify. Amyloid might sometimes be demonstrable,47 and melanin pigmentation is current on rare events. Calcifying Epithelial Odontogenic Tumor this is also called the Pindborg tumor, following its authentic description by that writer, first in 195849 and later in additional element. It may current as an ill-defined multilocular or unilocular radiolucency, however calcified materials is usually seen, and it could be associated with unerupted enamel. Occasional extraosseous lesions happen, but these are essentially benign and nondestructive. Calcifying epithelial odontogenic tumor has a local recurrence rate of 10% to 15%. Sheets and strands of polyhedral epithelial cells lie in a fibrous, typically hyalinized stroma, which can include in depth dystrophic or cementum-like calcifications. The epithelium regularly incorporates rounded masses of amyloid-like materials, which may calcify. A putting function, often current, is marked anisonucleosis, nuclear pleomorphism, and hyperchromasia. This offers a spurious impression of aggressiveness, but mitotic exercise is absent or minimal. Lesions presenting earlier than the age of about 20 years could additionally be a part of the spectrum of creating odontomas. However, some ameloblastic fibromas and ameloblastic fibrodentinomas presenting past that age behave as benign neoplasms. The presentation may be similar to that of ameloblastoma, however lesions are much less aggressive, slowly rising, and normally less than four cm in dimension. Recurrence of ameloblastic fibroma after conservative surgery could occur however is unusual. Histologic Appearances A combination of odontogenic mesenchyme and epithelium is seen. The mesenchyme is usually free or myxomatous with finely stellate or spindled fibroblasts giving an appearance similar to primitive dental pulp. The epithelium is arranged in small nests and branching strands resembling dental lamina, with small buds resembling the enamel organ. Ameloblastic fibromas have to be differentiated histologically from ameloblastomas to forestall the risk of inappropriately aggressive administration in a teenager. Focus showing marked cytologic atypia, however no mitotic activity in a clear cell variant. Odontoameloblastoma this very rare tumor exhibits odontoma formation in affiliation with an in any other case standard ameloblastoma. Odontogenic Ghost Cell Lesions Jaw lesions containing ghost cells are uncommon however well recognized. For a detailed discussion of this matter, readers are referred to specialist texts. Rare neoplastic variants are also acknowledged and have been designated calcifying cystic odontogenic tumor and dentinogenic ghost cell tumor for the cystic and strong variants, respectively. Histologic Appearances the characteristic function of this group of lesions is the presence of ghost cells.

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Metastases are generally seen to regional lymph nodes in a majority of patients (60%90%),253 in addition to to liver, lung, bone, and mind. Radiologically, the presence of stippled calcifications within the neoplasm is nearly pathognomonic of laryngeal cartilaginous tumors. The tumors present as onerous, smoothly lobulated submucosal lots which would possibly be nicely demarcated, grayish, and myxoid in look on reduce part. Degenerative changes may end in cyst formation, soft areas, and myxoid or gelatinous appearance. Histologically, the chondrocytes tend to cluster in a bluish chondroid and/or myxoid matrix. The tumor, with a blue-gray, myxoid minimize floor, arises from the cricoid cartilage and considerably narrows the subglottic lumen. Benign lesions of the larynx, with permission of the American Academy of Otolaryngology- Head and Neck Surgery Foundation, copyright � 1984. Low-power photomicrograph showing well-delineated cartilaginous nodule in submucosal laryngeal tissue. The majority of laryngeal chondrosarcomas are histologically low grade, which, compared with chondromas, show increased cellularity, nuclear hyperchromasia, nuclear pleomorphism, and binucleate or multinucleate cells. Chondrosarcomas are graded as low-grade or high-grade lesions on the premise of the degree of cellularity, pleomorphism, multinucleated cells, and mitoses. Applying typical diagnostic criteria for cartilaginous neoplasms of the bony skeleton, most laryngeal cartilaginous tumors can be categorised as low-grade chondrosarcomas (or chondrosarcomas grades 1 or 2). In addition to retaining the overall lobular configuration, high-grade chondrosarcomas are histologically readily obvious as malignant on the idea of the presence of hypercellularity, marked nuclear pleomorphism with bizarre cells, and presence of prominent nucleoli. In all histologic grades, metaplastic bone and foci of calcifications could be identified. Histologic subtypes might happen together with clear cell chondrosarcoma266 and dedifferentiated chondrosarcoma. Dedifferentiated chondrosarcoma is characterised by the presence of an admixture of well-differentiated chondrosarcoma with high-grade, noncartilaginous sarcoma. The therapy for laryngeal chondrosarcoma includes broad native (conservation) excision. The biologic behavior of laryngeal cartilaginous tumors is much less aggressive than that of chondrosarcomas in different websites. These are slowly rising neoplasms that have a tendency finally to recur locally if incompletely excised but very rarely metastasize. The presence of upper grade morphology and/or dedifferentiation is extra more probably to be (but not always) associated with metastasis. Fibrosarcoma was initially thought-about the commonest laryngeal malignant mesenchymal tumor271,272; nevertheless, the event of recent diagnostic techniques has resulted in a decreased incidence of the analysis of laryngeal fibrosarcoma. Other malignant mesenchymal neoplasms reported in the larynx (all rare occurrences) include rhabdomyosarcoma,271,273-275 so-called malignant fibrous histiocytoma,276 osteosarcoma,277,278 synovial sarcoma,272,279-281 liposarcoma (generally well differentiated within the larynx or hypopharynx and consequently usually troublesome to differentiate histologically from lipoma),282,283 malignant schwannoma,284 leiomyosarcoma,272,285 angiosarcoma,286,287 and extraskeletal Ewing sarcoma. Increased cellularity, nuclear pleomorphism, and binucleate chondrocytes are seen. They are reported most commonly to originate from cutaneous melanomas and renal cell carcinomas, but different websites of origin (breast, lung, prostate, colon, stomach) have been reported as nicely. Vocal Cord Polyps Vocal wire polyps are localized nonneoplastic swellings, thought to be induced by vocal abuse or "phonotrauma" and possibly by airborne irritants. They might happen anywhere along the vocal cord, however most happen on the free edge on the junction of the anterior and middle thirds. Because of their functionally important location on the true vocal cords, they cause symptoms of hoarseness or voice modifications ("breaking" of the voice), although they could be small. Clinicians distinguish between nodules and polyps on the premise of whether the lesion is sessile (nodule) or pedunculated (polyp). However, some authors maintain that the two represent essentially the identical lesion. Development may happen after voice abuse, an infection (laryngitis), alcohol, smoking, or endocrine dysfunction (hypothyroidism). Infrequently, hypothyroidism might cause vocal wire edema, which can progress to formation of a myxoid polyp. Histologic subtypes embody (1) edematous-myxoid, characterized by submucosal accumulation of pale blue to pink materials admixed with a sparsely mobile and variably vascularized stroma. For every kind the overlying epithelium may be atrophic, hyperplastic, and keratotic; hardly ever, dysplastic epithelium and/or invasive carcinoma could additionally be recognized. The commonest site of occurrence is the posterior aspect of one or both vocal cords, although it might uncommonly happen along the middle third or anterior portions of the true vocal cords. Ulcerated polypoid granulation tissue has capillaries oriented radially to the floor. Awareness that this may be a specific clinicopathologic entity will end in a selected diagnosis quite than a descriptive histopathologic diagnosis. A descriptive prognosis, though not technically incorrect, might not recommend that the lesion is normally caused by an extralaryngeal process that requires therapy. B, Vascular polyp containing outstanding vascular spaces and plentiful fibrinous material. Additional histologic findings could embrace the presence of scattered multinucleate large cells particularly slightly below the ulceration, marked vascular proliferation, and reactive fibroblastic proliferation. As a result of recurrent (chronic) disease the lesion might show hyperplastic epithelium with no ulcerative component or Laryngocele is an abnormal dilatation of the saccule (appendix of the ventricle) containing air and sustaining an open communication with the laryngeal lumen. The majority of cases are unilateral however could also be bilateral in as a lot as 25% of patients. Laryngoceles may present clinically with hoarseness or as a cystic neck mass which will fluctuate in measurement because of communication with the laryngeal lumen. These result from elevated intralaryngeal strain with relaxed supraglottic muscles against tightened lips, as in brass instrument players or glassblowers. Squamous metaplasia may be seen focally or, if infected, may fully substitute the respiratory epithelium; within the presence of infection, a persistent inflammatory cell infiltrate could additionally be seen within the wall of the cyst. Oncocytic metaplasia of the liner epithelium or minor salivary glands could additionally be seen. Complications related to laryngoceles embrace airway obstruction and an infection. Laryngeal Cysts Obstruction of the orifice of the laryngeal saccule or obstruction of the mucous gland ducts of the laryngeal saccule with subsequent accumulation of secretions results in cyst formation. The majority of cysts occur within the supraglottic larynx; less frequently, glottic and subglottic cysts occur. For ductal cysts the majority occur within the area of the true vocal cords but not in the region of the free margin, which lacks glands, with the next commonest site being the epiglottis.

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The histology is similar to that of mucoepidermoid carcinomas of more widespread locations (see Chapter 7) and consists of low-grade and high-grade tumors. A neck dissection is warranted for a diagnosis of high-grade mucoepidermoid carcinoma. The prognosis is similar to that of mucoepidermoid carcinomas of more usual sites. Low-grade tumors are inclined to have a better prognosis than high-grade lesions, with 5-year survival charges reported as 90% to 100 percent for low-grade tumors and about 50% for high-grade tumors, with a 77% to 80% 5-year survival reported for all laryngeal mucoepidermoid carcinomas. The tumors were predominantly supraglottic in location, typically within the arytenoid or aryepiglottic fold space. Grossly, laryngeal carcinoid seems as a submucosal nodular or polypoid mass with a tan-white look various in dimension from a few millimeters up to 3 cm in diameter. Histologically, carcinoid tumors are submucosal wellcircumscribed neoplasms composed of generally small uniform cells arranged in an organoid sample of nests, ribbons, trabeculae, and/or acini or gland-like buildings. Additional staining may be seen for neuron-specific enolase, Leu 7, neurofilament protein, epithelial membrane antigen, and carcinoembryonic antigen. Abundant neurosecretory granules (90230 nm), mobile junctional complexes, and intercellular and intracellular lumina are current on electron microscopy. Differential diagnostic considerations embody primarily paraganglioma and atypical carcinoids. The differential points between carcinoid tumor and paraganglioma embrace the absence of epithelial marker staining in paraganglioma and the presence of characteristic sustentacular cell pattern of S-100 protein staining. Carcinoid tumor has indolent biologic conduct and generally carries an excellent prognosis after excision. Metastasis occurs to liver and bone and usually happens late in the illness course. Patients characteristically are men in the sixth or seventh a long time, and most lesions are supraglottic. A paraneoplastic syndrome hardly ever occurs in association with atypical carcinoid tumor. Histologically, atypical carcinoid is a submucosal tumor arranged in nests, sheets, glands or acini, trabeculae, and ribbons, reflecting the "organoid" sample attribute of neuroendocrine tumors. Multiple patterns are characteristically present in a person neoplasm, and glandular buildings are virtually all the time in evidence. The nuclei are spherical to ovoid, with stippled chromatin, often with a quantity of nucleoli which are rarely prominent, and with occasional hyperchromasia. Immunohistochemical stain for chromogranin showing marked positivity of tumor cells. The neuroendocrine differentiation and calcitonin positivity may pose differential diagnostic issues with thyroid medullary carcinoma. Furthermore, patients with thyroid medullary thyroid carcinoma have elevated serum calcitonin stage, a discovering not associated with atypical carcinoid. A high incidence of cervical lymph node metastasis is seen, necessitating neck dissection even in clinically N0 necks. Survival rates are a 5-year survival fee of 48% and 10-year survival fee of 30%. The presence of metastatic illness (either at presentation or developing subsequently) is an ominous sign with demise at intervals ranging from 1 to 6 years. Size of the first tumor is four Tumors of the Upper Respiratory Tract 191 prognostically essential as tumors measuring larger than 1 cm have twice the mortality rate as tumors measuring lower than 1 cm. The histomorphology of laryngeal small cell carcinoma is analogous to that of its pulmonary counterpart. The tumor is composed of small cells organized in undifferentiated sheets and nests. Occasionally, ribbons of cells may be seen, as might rare neural rosette-like structures. The nuclear chromatin is stippled (so-called salt and pepper) in look with absence of nucleoli. Sheets of small undifferentiated tumor cells lie deep to the surface mucosal epithelium. Evidence of neuroendocrine differentiation is much less prominent than in the typical carcinoid and atypical carcinoid tumors and could also be troublesome to document. Tumor cells are solely rarely argyrophilic, and neurosecretory granules are sparse ultrastructurally. Immunohistochemical staining for neuroendocrine markers similar to synaptophysin, chromogranin, and neuron-specific enolase (the latter not completely specific for neuroendocrine cells) is often positive however will not be readily demonstrable in each case. Additional immunohistochemical staining includes cytokeratins and may also include Leu 7, neurofilament protein, epithelial membrane antigen, and carcinoembryonic antigen. The therapy of selection is nonsurgical and includes systemic chemotherapy and therapeutic irradiation. A, Undifferentiated small tumor cells with scant indistinct cytoplasm and nuclei with finely stippled chromatin and usually inconspicuous nucleoli. Possible causes of obstruction leading to saccular cysts embrace inflammation, trauma, or tumor. Glottic cysts may be as a outcome of vocal wire abuse; subglottic cysts could occur after intubation. Small laryngeal ductal cysts may come up on account of obstruction of the ducts of any of the quite a few seromucinous glands of the larynx. Other histologic cyst varieties are (1) tonsillar-type cyst resembling the palatine tonsillar crypt lined by stratified squamous epithelium with or without keratin-filled lumen and lymphoid follicles with germinal centers seen in cyst wall; (2) epithelial cyst lined by respiratory and/or squamous epithelium or flattened (attenuated) epithelium though the epithelial lining could additionally be papillary in architecture; (3) oncocytic cyst lined by oncocytic epithelium, which can have outstanding papillary architecture paying homage to a Warthin tumor of the parotid gland330,331. These have been called by varied names, including oncocytic cystadenoma, papillary cystadenoma, and oncocytic cyst. View of large multicystic lesion with focal invagination of papillary structures, lined by oncocytic epithelium. They happen predominantly in middle-aged to aged folks and are primarily innocuous curiosities unless they trigger signs by attaining considerable dimension. The term oncocytic cyst for such metaplastic or hyperplastic cystic lesions is most popular. Conservative management is usually advocated to include needle aspiration, deroofing of the cyst, laser marsupialization, or endoscopic removal, especially for infants and kids to avoid stenosis. Amyloidosis Amyloidosis represents idiopathic extracellular accumulation of fibrillar proteins (amyloid) recognized in a selection of medical settings and occurring in quite so much of tissue sites. Amyloidosis can have an effect on virtually every head and neck web site, however the most typical sites of prevalence include the larynx and tongue. The supraglottic larynx or false-cord space seems to be mostly affected,336,337 however the vocal cords and subglottic regions may be sites of amyloid deposition. Diffuse submucosal lesions could additionally be extra problematic and troublesome to eradicate, and really rare instances of diffuse tracheobronchial amyloidosis may be fatal, because of obstruction and repeated infections. An artifact of tissue processing typically produces small clefts separating masses of amyloid, resulting in a "cracked" look.

Diseases

• Fissured tongue
• Craniosynostosis arthrogryposis cleft palate
• Hereditary ceroid lipofuscinosis
• Osteoporosis macrocephaly mental retardation blindness
• Sinus cancer
• Cardiomelic syndrome Stratton Koehler type
• Marsden syndrome
• Anophthalmia esophageal atresia cryptorchidism
• Meningocele

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The differential diagnosis is with basal cell carcinoma, pityriasis versicolor, or disseminated superficial actinic porokeratosis. Multiple buds of monomorphous squamous epithelium related to keratinous cysts radiating from a central space which will connect with the floor. Rarely, different parts of the follicle, and even sebaceous components, are identified. Histologically, the differential analysis is with dilated pore, trichofolliculoma, and acrospiroma. Clinically, it often arises in older adults, however the age range varies from the second to the ninth decades. Individual lesions are usually dome-shaped, skin-colored papules lower than 5 mm in diameter. Most are situated on the face, significantly the nostril, but the eyelids, lips, and oral cavity additionally could additionally be affected. Architectural variations sometimes range from follicle-like, vertically oriented lesions, to lobular, bulbous, acrospiroma-like lesions that are devoid of ducts, and even verrucous lesions. Infundibular Cyst (Epidermoid Cyst) Infundibular cyst is the most typical kind of follicular cyst (approximately 80%). Clinically, it could be positioned on any area of furry pores and skin however is usually found on the pinnacle, neck, or trunk. The concomitant prevalence of multiple infundibular cysts with colonic polyps, desmoid tumors, and osteomas is called Gardner syndrome. It is lined by stratified squamous epithelium that matures by way of a granular layer and produces basket-weave and laminated flakes of orthokeratin similar to that of the epidermis. If the cyst wall ruptures, a foreign-body granulomatous response to keratin outcomes. Pigmented Follicular Cyst the pigmented follicular cyst392-396 is a uncommon stratified squamous-lined cyst that accommodates laminated keratin and numerous hair shafts. Clinically, it has been recognized on the top, neck, trunk, and, rarely, the limbs. It is often lower than 2 cm in diameter and usually has a darkish hue from the Tyndall impact. It is lined by stratified squamous epithelium that matures via a granular zone and accommodates laminated keratin and quite a few hairs inside the cyst cavity. Inconsistent findings are squamous eddies or orthokeratotic microcavities, just like those of inverted seborrheic keratosis. Desmoplastic tricholemmomata373 have an extensive quantity of stroma, peripherally rimmed with epithelium and incessantly positioned in the midst of the tumor nodule. This variant has a spindle cell element during which the tumor cells merge with the stroma, mimicking carcinoma. A variable fibrous stroma similar to the follicular sheath is seen; a mononuclear inflammatory infiltrate could also be present in some cases. Eruptive Vellus Hair Cyst the eruptive vellus hair cyst404-411 is a rare phenomenon consisting of a quantity of small cysts that usually appear rapidly, displaying infundibular, sebaceous duct, and focal isthmus-catagen maturation and containing vellus hairs. Some kindreds have been affected, which suggests a genetic association in some instances. Most lesions are recalcitrant to therapy, however limited success has been achieved with carbon dioxide laser416 and retinoic acid. Occasionally, telogen follicles and, rarely, sebaceous glands, smooth muscle, or each are seen. The histologic differential prognosis is with steatocystoma,418,419 infundibular cyst, and pigmented follicular cyst. Steatocystoma (Sebaceous Duct Cyst) Steatocystoma404,411,418,420-428 is a small cyst, the liner of which has similarities to the corrugated cuticle of the sebaceous duct. Clinically, these cysts arise usually within the second via the fourth a long time with an onset most often at or around puberty. They are usually skin coloured, to blue, to black papules that vary from a number of millimeters to several centimeters in measurement. The cysts are normally multiple (steatocystoma multiplex) however may be solitary (steatocystoma simplex). They are normally located on the chest, however they also can be discovered on the face, back, limbs, and, hardly ever, elsewhere. There is commonly an autosomal dominant pattern Tricholemmal (Pilar: Isthmus-Catagen) Cyst the tricholemmal cyst is the second most common type of follicular cyst (approximately 10%-15% of cases) and traditionally was referred to as a sebaceous cyst, although many terms were used uncritically for cysts of all histologic types up to now. Clinically, a tricholemmal cyst virtually at all times occurs on the scalp, but different sites on the trunk or extremities could also be affected. Histologically, the epithelial lining displays keratinocyte maturation although little, if any, granular layer. The lining cells are large and comprise plentiful cytoplasm toward the apical portions, just like the keratinization of the isthmic portion of the catagen hair follicle. Keratinization is abrupt and dense, in distinction to the laminated keratin of the infundibular cyst. In some, hyperplasia of the lining is seen, just like proliferative tricholemmal cysts (pilar tumor). This is similar to tricholemmal cyst, but the epithelium is advanced and situated within the mid and deep dermis. Therapy is normally unsuccessful, however isotretinoin429 and cryosurgery430 have been used with limited success. Histologically, an empty cyst with a serpiginous wall is lined by skinny squamous epithelium and surfaced by a corrugated cuticle. Sebaceous glands are generally adjacent to , or immediately contiguous with, the cyst wall. Clinically, most of those lesions are solitary nodules situated on the top, neck, or higher limb. They may be rubbery and pliable or onerous and faceted, and they often measure from 5 mm to 2 cm in diameter. Histologically, the hallmark is basaloid lobules contiguous with eosinophilic effete cells admixed with keratin; the latter are termed shadow or ghost cells. The basaloid cells are typically homogeneous and monomorphous, similar in size to the basaloid cells of basal cell carcinoma. The shadow cells are anucleate however retain the important morphology of the basaloid cells. Lesions that comprise a major number of basaloid cells may be cystic; lesions that are devoid of the basaloid cells are typically stable tumors of shadow cells, calcification, and large cell response. Matricoma lesions442 are most likely to be bigger and retain extra basaloid cells than typical pilomatricomas. Another variant, proliferative pilomatricoma, consists of enormous, lobular proliferations of basaloid cells with small to giant foci of shadow cells. Interestingly, pilomatricomas have recently been shown to consistently reveal trisomy 18. One tumor that accommodates totally different elements of the follicular apparatus is recognized as panfolliculoma.

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Microscopic Appearances Most cases exhibit irregular invasive borders, a minimal of focally. The tumor includes haphazardly dispersed mucin-filled cysts and tumor nests composed of mucous, squamoid (epidermoid), and nondescript intermediate cells in variable mixtures. The stroma is characteristically sclerotic and ample, with infiltrates of chronic inflammatory cells and occasional extravasated mucin swimming pools. Such stromal modifications are most regularly seen in low- and intermediate-grade mucoepidermoid carcinomas. Rarely, a really dense lymphoplasmacytic infiltrate could be discovered admixed with tumor islands, scattered multinucleate giant cells within the stroma, or melanin pigmentation. A, this illustration reveals the prototypic low-magnification look of this tumor: infiltrative borders, dense fibrous background with aggregates of continual inflammatory cells, cystic and strong islands of tumor cells, and presence of mucin. B, Solid and cystic tumor islands lying in a sclerotic stroma with persistent inflammatory cell aggregates are extremely attribute of this tumor type. A, the cells lining the cystic space embrace mucinous cells, intermediate cells (with less cytoplasm), and epidermoid cells (polygonal cells with a bigger amount of eosinophilic cytoplasm). B, the cyst is lined by mucinous cells supported by an underlying layer of intermediate cells. However, rounded or irregular-shaped stable epithelial islands are nearly at all times present. Mucous cells are massive, columnar, goblet-shaped or polygonal cells with copious mucin, imparting a frostedglass appearance to the cytoplasm. Mucous cells may form intently packed nests, line cystic structures, or be scattered among islands of squamoid cells. Another main cell kind is the intermediate cell, which is a small to medium-sized polygonal cell with a nondescript appearance. Characteristically, cystic tumor islands lie in a chronically inflamed fibrous stroma. Extravasation of mucin into the stroma is seen (left field); the irritation and fibrosis are most likely elicited by the extravasated mucin. The cells that line the cystic areas are sometimes mucinous cells with lightly basophilic cytoplasm. B, this cystic tumor island is fashioned by a mix of mucinous cells and epidermoid cells. The lumen is full of mucus, by which are suspended exfoliated tumor cells and histiocytes. A, the tumor grows in anastomosing, irregular strong islands with few interspersed cystic areas. B, Higher magnification exhibits epidermoid cells exhibiting average nuclear pleomorphism. They have a stratified appearance, however intercellular bridges are often inconspicuous. Mucin-containing cysts could rupture, permitting escape of mucus into the stroma, eliciting an inflammatory response and subsequently sclerosis. The lymphoid infiltrate can be exuberant and accompanied by lymphoid follicles and thus may impart an faulty impression of metastatic deposit in lymph node. High-Grade Mucoepidermoid Carcinoma High-grade mucoepidermoid carcinoma reveals extra strong areas and few cystic areas. The strong areas are shaped by massive polygonal squamoid (epidermoid) cells with pale to eosinophilic cytoplasm and distinct cell borders, as well as nondescript intermediate cells. Squamous options are often higher developed in contrast with low-grade tumors-intercellular bridges and even individual cell keratinization may be seen, but keratin pearls are uncommon. Cellular pleomorphism, nuclear hyperchromasia, and mitotic figures are extra impressive, and areas of coagulative necrosis could additionally be current. Mucous cells are normally sparse, such that staining for mucin may be required to determine them. In basic, much less fibrous stroma or continual inflammatory infiltrate is present compared with that in lowgrade tumors. Sometimes a part of low-grade mucoepidermoid carcinoma is present, suggesting that the high-grade tumor arises via progressive lack of differentiation. Intermediate-Grade Mucoepidermoid Carcinoma the intermediate-grade tumors lie histologically between the low- and high-grade tumors. Invasion of the stroma within the form of irregular small islands is an important antagonistic parameter in the histologic grading of mucoepidermoid carcinoma. Variants of Mucoepidermoid Carcinoma Large polygonal clear cells with discrete cell membrane, ample water-clear cytoplasm, and eccentric nuclei are a minor part of many mucoepidermoid carcinomas. Occasionally clear cells represent a significant portion of the tumor, rendering distinction from other clear cell tumors problematic. The cells positioned within the peripheral parts of the clear cell islands are sometimes much smaller, with eosinophilic cytoplasm and a squamoid high quality. A, the intermediate-grade mucoepidermoid carcinoma as seen in the best field includes stable and cystic tumor islands infiltrating a fibrous stroma. Compared with the low-grade element in the left subject, cystic areas represent a less outstanding component. B, Comparison of cytologic features exhibits that the tumor cells are bland looking in the low-grade element (left) and mildly atypical with bigger nuclei within the intermediate-grade part (right). A, Single or teams of clear cells with distinct cell membranes and water-clear cytoplasm are interspersed inside the tumor islands. Focal spindle cell growth and oncocytic change are unusual patterns observed in some mucoepidermoid carcinomas. The uncommon oncocytic variant (oncocytes accounting for >60% of the cell population) can potentially be confused with oncocytoma or oncocytic carcinoma. Because of the paucity of tumor islands, which are often confined to the peripheral zone, this variant could also be mistaken for an inflammatory lesion. Most tumor cells have a squamoid appearance, and focal keratinization can be current. This parotid tumor includes islands and trabeculae of squamoid cells that infiltrate a sclerotic stroma rich in eosinophils. Admixed mucinous epithelial cells and glandular structures merge with the squamoid islands or kind discrete tubules. Median survival for fusion-positive patients exceeds 10 years, whereas that for fusion-negative sufferers is only one. This gene fusion is equally related to favorable clinicopathologic options. The behavior is strongly correlated with the clinical stage and histologic grade, although these components turn out to be much less necessary if radical surgery is performed. In a retrospective evaluation of archival circumstances originally identified as mucoepidermoid carcinoma, the prognosis needed to be revised in about half of the instances, mostly from high-grade mucoepidermoid carcinoma to adenosquamous carcinoma, squamous cell carcinoma, or salivary duct carcinoma.

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B, Rarely, coalescence of the tubules result in formation of cribriform buildings, mimicking adenoid cystic carcinoma. The recommended therapy consists of complete surgical excision, neck dissection, and postoperative radiotherapy. Pathologic Features the tumor is poorly circumscribed, predominantly stable, and tan coloured. Gross extension of tumor beyond the salivary gland is noted in about 70% of instances. The intraductallike component exhibits cribriform, papillary-cystic, or strong patterns, usually with prominent comedo necrosis. The clearly infiltrative element consists of cords, nests, small glands, and single cells. The neoplastic cells in each parts have a similar apocrine look, with abundant eosinophilic cytoplasm, large pleomorphic vesicular nuclei, and prominent nucleoli. Vascular invasion, perineural invasion, intravascular tumor emboli, and invasion of adjacent constructions are common. The sarcomatoid element comprises anaplastic spindle cells, weird multinucleate large cells, rhabdoid cells, and, not often, osteosarcomatous cells. This variant options areas of mucinous/colloid carcinoma by which clusters of carcinoma cells with or without cytoplasmic mucin float in mucin swimming pools. The tumor (left field) infiltrates the parotid parenchyma (right field) and is accompanied by a desmoplastic stroma. A, the large cribriform tumor units with comedo necrosis resemble high-grade intraductal carcinoma of the breast, however most of them are actually invasive islands. B, Immunostaining for p63 reveals that some tumor islands within the left area are surrounded by p63+ myoepithelium and thus represent an intraductal component. The islands in the best and lower fields lack p63+ myoepithelium and thus symbolize invasive islands. C, Lymph node might include metastatic tumor islands reminiscent of the structure of intraductal carcinoma. This variant features oncocytic modifications in some areas of the tumor, mimicking oncocytic carcinoma. The tumor cells have plentiful eosinophilic granular cytoplasm and are strongly immunoreactive with antimitochondrial antibody. Prognostic Factors Previous research recommend that tumor dimension smaller than 3 cm is related to a more favorable prognosis,431,438 however this was not confirmed by the Mayo Clinic collection. Almost all cases express androgen receptor, a attribute, but not particular, feature of this tumor sort, whereas estrogen and progesterone receptors are normally unfavorable. A, the cribriform tumor island comprises massive cells with vital nuclear pleomorphism. C, In areas, the tumor cells infiltrate the fibrous stroma in the type of trabeculae and irregular islands, resembling odd infiltrative ductal carcinoma of breast. The standard salivary duct carcinoma part is seen in the left upper area. The sarcomatous element is shaped by spindle and stellate cells with pleomorphic nuclei. Genetic Features Frequent loss of heterozygosity has been detected in chromosome 9p21, 6q, 16q, 17p, 17q regions. A scientific history of breast carcinoma, constructive estrogen/progesterone receptor, and unfavorable androgen receptor strongly favor a prognosis of metastatic mammary carcinoma. Oncocytic carcinoma is characterized by large tumor cells with granular eosinophilic cytoplasm filled with mitochondria. Both oncocytic carcinoma and cystadenocarcinoma lack the comedo necrosis and intraductal-like pattern sometimes seen in salivary duct carcinoma. The uncommon intraductal carcinoma should not be mistaken for salivary duct carcinoma due to the significantly better prognosis. These observations could be attributable to the indiscriminate use of the term intraductal, which, by definition, ought to require the presence of an intact myoepithelial layer as in mammary intraductal carcinoma. Strictly defined as such, intraductal carcinoma represents a tumor of low malignant potential, with habits much like that of the mammary counterpart. Some other specific carcinoma types may also have an intraductal growth element focally, corresponding to acinic cell carcinoma. Clinical Features Similar to salivary duct carcinoma, this tumor most regularly impacts the parotid gland of the aged, with a slight feminine predilection. It is characterized by pure intraductal proliferation of tumor cells and probably represents the precursor of salivary duct carcinoma. A, the dilated duct shows a micropapillary and Roman-bridge sample of mobile proliferation, similar to that in mammary intraductal carcinoma. Other incidental findings are hyalinized pleomorphic adenoma within the left subject and intercalated duct hyperplasia in the right higher subject. B, the proliferated cells show reasonable nuclear pleomorphism and apocrine cytoplasm. Roman-bridge patterns, similar to the architectural patterns observed in atypical ductal hyperplasia or intraductal carcinoma of the breast. The stroma is sclerotic and should exhibit secondary modifications corresponding to hemorrhage, persistent inflammatory infiltrate, and dystrophic calcification. Prerequisites of Diagnosis A analysis of intraductal carcinoma could be confidently made solely when an invasive element has been ruled out after full sampling. It is also imperative to carry out immunostaining to show an intact myoepithelial layer around each tumor island. This precaution in diagnosis is important as a end result of the alternative interpretation is salivary duct carcinoma, which is a extremely aggressive neoplasm. A, the discrete islands of proliferated cells are harking back to atypical ductal hyperplasia or intraductal carcinoma of the breast. B, Immunostaining for muscle-specific actin shows intact myoepithelial cells across the cell islands, confirming the in situ nature of the tumor process. It is a analysis of exclusion, in that features attribute of other neoplasms (most notably epithelial-myoepithelial carcinoma, clear cell oncocytoma, mucoepidermoid carcinoma, acinic cell carcinoma, clear cell myoepithelial tumor, sebaceous carcinoma, and metastatic renal cell carcinoma) should be absent. Most reported cases come up from the minor salivary glands of the oral cavity as a painless slow-growing mass, and some might ulcerate or trigger fixation to adjoining tissues. It is a low-grade, domestically invasive tumor, with a bent for locoregional recurrence. It consists of sheets, streaming columns, nests, and cords of huge, monomorphic clear cells that show mild variation in size. The nuclei are centrally or eccentrically positioned and have finely granular chromatin and inconspicuous nucleoli.

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Attempts have been made to enhance biologic and clini cal significance of histologic grading by subclassification of grade 2 tumors into two distinct subclasses: a grade 1�like subgroup, which has an excellent end result and should not require adjuvant chemotherapy, and a grade 3�like subgroup, which includes tumors that behave in a method similar to that of highgrade cancers and need extra aggressive systemic treatment. One potential drawback with the point scoring system for the evaluation of tubules and nuclear pleomorphism lies in the tendency of inexperienced observers, when confronted with a alternative of 1 to 3, to "play secure" and go for the center. This can be obviated by making an initial determination to cut back the out there options to two. Thus in a tumor with a big tubular element the score can only be 1 or 2; the rating of 3 is eliminated. Similarly, when assessing nuclear pleomorphism, the presence of enormous, irregular nuclei greater than twice the scale of two. Some degree of variation in appearance from one part of a tumor to one other undoubtedly happens; that is notably true of tumors of blended kind and is considered one of the major reasons for inspecting multiple blocks. Assessment of tubular differentiation is made on the general appearances of the tumor, and so account is taken of any variation. Nuclear appearances are evaluated at the periphery of the tumor to obviate variations between the rising edge and the less lively heart. Unless otherwise indicated, grading is restricted to the invasive compo nent of the tumors. Lymphovascular invasion is taken into account as an important step in breast cancer metastasis and the primary explanation for morbidity and mortality from the disease. Detection of vascular invasion in the major tumor is a marker of metastatic potential and of prognos tic significance, significantly within the lymph node�negative group. The reported vary extends from 10% to 54%, and the percentage is positively correlated with lymph node stage. In the Not tingham collection, vascular invasion was detected in 19% of lymph node�negative and in 49% of lymph node�positive cohorts,510 although lower figures have been reported (5%10%) of lymph node�negative instances. This subject, several millimeters from the primary tumor nodule, reveals a half of a traditional breast lobule (left) and a vessel (center), lined by flattened endothelial cells, containing a tumor embolus. Moreover, we discovered that the result of patients with lymph node�negative tumors but with vascular invasion is similar to the result of those with one node�positive tumors. Finally, the presence of vascular invasion is amongst the most essential elements in the prediction of local recurrence after conservation therapy463,529,533535 and flap recurrence after mastectomy. The presence of foci of necrosis in invasive breast carcinomas is a relatively widespread phenomenon, sometimes visible macroscopically as a sharply demar cated area of dullness, normally centrally positioned. Micro scopically necrotic tumor is characterised, as in any tissue, by the nuclear changes of karyorrhexis, pyknosis, and karyolysis with lack of cytoplasmic detail. When tumor necrosis has been current for a adequate size of time it may be accompanied by substitute fibrosis. Carter and colleagues553 gave a determine of 40%, compared with 60% estimated by Fisher and coworkers. The worth of tumor necrosis as a potential prognostic factor has been evaluated in a number of research. Carter and colleagues553 confirmed decreased 10year survival in sufferers with tumor necrosis, and Fisher and coworkers437 discovered that the presence of necrosis was related to early therapy failure. Parham and colleagues,554 in a comparatively small morphometric research, discovered a powerful cor relation between in depth necrosis and poor survival. Unfortunately, in none of those studies is a exact defini tion given of terms such as "extensive" necrosis, which limits their worth. Parham and associates555 subsequently proposed a simplified methodology for grading breast most cancers by combining mitotic counts with tumor necrosis. The authors declare an excellent correlation with survival, but it has been pointed out that few numeric information were supplied, particularly regarding the diagnostic standards used, and for that reason the method lacks sensible utility. In abstract, some proof exists that the presence of necrotic tumor is a poor prognostic characteristic, however more detailed research are required to generate reproducible estimates of the extent of necrosis, and its correlation with other prognostic variables, specifically histologic grade. Considerable variation occurs within the quantity of stromal connective tissue within invasive breast carcinomas. Immunohisto chemical studies using lymphatic and vascular endothelial particular markers have demonstrated that nearly all of vascular invasion in breast most cancers is lymphatic vessel, somewhat than blood vessel, invasion. The determination of vascular invasion should be made only in tissue adjoining to the tumor mass and never within it. Tumor emboli should be seen inside areas having a clear lining of endothelial cells. In routine apply, however, we only use these markers in histologically equivocal instances. The reproducibility of the histologic evaluation of vascular invasion has been shown to be passable in several studies,437,531 and, even where this has been questioned,545 full agreement was obtained between three observers in almost 90% of circumstances. Vascular invasion correlates very carefully with locore gional lymph node involvement,535537,546 and, possibly because of this association, it has been claimed that it might possibly present prognostic data as powerful as lymph 1112 sixteen Tumors of the Breast this finding is unsure, with conflicting revealed data. Thus, in subjective or semiquantitative research, stromal fibrosis has been related variably with a favorable prognosis557 and poorer survival558 and has been shown to make no distinction in a comparison of brief and long run survivors. A additional variable component of the stroma of breast carcinomas is elastic tissue. As is the case with stromal fibrosis, information are conflicting on the relation ship between elastosis and prognosis. Some studies have suggested that the presence of elastosis is related to an excellent prognosis,560,561 but this has not been confirmed by others. Millis and colleagues567 have also shown that within the majority of circumstances the grades of the in situ and invasive components correspond. Several other conven tional clinicopathologic factors have been assessed as potential prognostic indicators in breast cancer. Among these are affected person age, household history, tumor detection method (symptomatic vs. Younger age, optimistic family historical past, symptomatic pre sentation, and presence of skin infiltration are associated with adverse prognosis, whereas the presence of a promi nent lymphoplasmacytic infiltrate and fibrotic foci are associated with good prognosis. Increased microvessel density in breast most cancers is reported to be associated with lymph node metastasis and decreased survival in lymph node� unfavorable breast cancer. Counting of apoptotic index could be carried out on H&E sections in the same means as the mitotic index or may be carried out through the use of immunocytochemical markers. It could also be as a outcome of intratumoral hypoxia leading to clonal heterogeneity of tumor cells. Fibrotic foci are asso ciated with basal subtype, an expansive growth pattern, hypoxia and angiogenesis, activated woundhealing sig nature and a poor prognosis 76gene signature,588 and poor prognosis. However, an overlap exists between prognostic and predictive factors, and any given variable could show either or both features. Con versely those with a poor prognosis could profit from an aggressive adjuvant approach.

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