Mark C. Adams, MD, FAAP

• Professor of Urology and Pediatrics
• Vanderbilt University Nashville, Tennessee

https://www.childrenshospitalvanderbilt.org/doctors/adams-mark

Rassel H women's health clinic jackson wy discount female viagra 100mg online, Thompson L D menstrual pills effective 100 mg female viagra, Heffess C S 1998 A rationale for conservative management of microscopic papillary carcinoma of the thyroid gland: a clinicopathologic correlation of 90 cases women's health center waco tx best purchase for female viagra. Harach H R questionnaire menstrual cycle cheap female viagra line, Franssila K O menstrual 28 day cycle chart cheap 50mg female viagra mastercard, Wasenius V M 1985 Occult papillary carcinoma of the thyroid womens health umd discount female viagra. In: DeGroot L J, Frohman L A, Kaplan D L (eds) Radiation-associated thyroid carcinoma. Bondeson L, Ljungberg O 1981 Occult thyroid carcinoma at autopsy in Malmo, Sweden. Ludwig G, Nishiyama R H 1976 the prevalence of occult papillary thyroid carcinoma in 100 consecutive autopsies in an American population. Ottino A, Pianzola H M, Castelletto R H 1989 Occult papillary thyroid carcinoma at autopsy in La Plata, Argentina. Sobrinho-Simoes M A, Sambade M C, Goncalves V 1979 Latent thyroid carcinoma at autopsy: a study from Oporto, Portugal. Komorowski R A, Hanson G A 1988 Occult thyroid pathology in the young adult: an autopsy study of 138 patients without clinical thyroid disease. Franssila K O, Harach H R 1986 Occult papillary carcinoma of the thyroid in children and young adults. LaGuette J, Matias-Guiu X, Rosai J 1997 Thyroid paraganglioma: a clinicopathologic and immunohistochemical study of three cases. Pisani T, Vecchione A, Giovagnolii M R 2004 Galectin-3 immunodetection may improve cytological diagnosis of occult papillary thyroid carcinoma. Lloyd R V 2001 Distinguishing benign from malignant thyroid lesions: galectin 3 as the latest candidate. Erkilic S, Aydin A, Kocer N E 2002 Diagnostic utility of cytokeratin 19 expression in multinodular goiter with papillary areas and papillary carcinoma of thyroid. LiVolsi V A, Baloch Z W 2004 Follicular neoplasms of the thyroid: view, biases, and experiences. Cancer Res 57: 1690-1694 Nikiforov Y E 2004 Recent developments in the molecular biology of the thyroid. McCaffrey T V, Bergstralh E J, Hay I D 1994 Locally invasive papillary thyroid carcinoma: 1940-1990. Zohar Y, Strauss M 1994 Occult distant metastases of well-differentiated thyroid carcinoma. Akslen L A 1993 Prognostic importance of histologic grading in papillary thyroid carcinoma. Akslen L A, LiVolsi V A 2000 Prognostic significance of histologic grading compared with subclassification of papillary thyroid carcinoma. Retrospective multivariate analysis of differentiated thyroid carcinoma with long follow-up. Noguchi S, Murakami N, Kawamoto H 1994 Classification of papillary cancer of the thyroid based on prognosis. Bhattacharyya N 2003 A population-based analysis of survival factors in differentiated and medullary thyroid carcinoma. Otolaryngol Head Neck Surg 128: 115-123 18 Tumors of the Thyroid and Parathyroid Glands Health Organization classification of tumours. Am J Pathol 137: 553-562 Thomas G A, Williams D, Williams E D 1989 the clonal origin of thyroid nodules and adenomas. Br J Surg 85: 1125-1128 Crile G Jr, Pontius K I, Hawk W A 1985 Factors influencing the survival of patients with follicular carcinoma of the thyroid gland. Surg Gynecol Obstet 160: 409-413 DeMay R M 2000 Follicular lesions of the thyroid. Am J Clin Pathol 114: 681-683 LiVolsi V A, Asa S L 1994 the demise of follicular carcinoma of the thyroid gland. Ann Diagn Pathol 3: 331-340 LiVolsi V A, Baloch Z W 1999 Determining the diagnosis and prognosis of thyroid neoplasms: do special studies help Thyroid 21: 505-510 Lo C Y, Lorentz T G, Wan K Y 1995 Follicular carcinoma of the thyroid gland in Hong Kong Chinese. Br J Surg 82: 1095-1097 LiVolsi V A, Baloch Z W 2011 Follicular-patterned tumors of the thyroid: the battle of benign vs. Cancer 39: 1573-1586 LiVolsi V A 1993 Current concepts in follicular tumors of the thyroid. A study of 44 cases followed for a minimum of 10 years, with emphasis on differential diagnosis. Surg Pathol 1: 137-150 Schmid K W, Farid N R 2006 How to define follicular thyroid carcinoma Virchows Arch 448: 385-393 Franssila K O, Ackerman L V, Brown C L 1985 Follicular carcinoma. Semin Diagn Pathol 2: 101-122 Mete O, Asa S L 2011 Pathological definition and clinical significance of vascular invasion in thyroid carcinomas of follicular epithelial derivation. Mod Pathol 11: 995-998 Tse L L, Chan I, Chan J K 2001 Capsular intravascular endothelial hyperplasia: a peculiar form of vasoproliferative lesion associated with thyroid carcinoma. Cancer 68: 1944-1953 Heffess C S, Thompson L D 2001 Minimally invasive follicular thyroid carcinoma. Lang W, Choritz H, Hundeshagen H 1986 Risk factors in follicular thyroid carcinomas. Loh K C 1997 Familial nonmedullary thyroid carcinoma: a meta-review of case series. Shaha A R, Loree T R, Shah J P 1995 Prognostic factors and risk group analysis in follicular carcinoma of the thyroid. Hyalinizing spindle cell tumor of the thyroid with dual differentiation (variant of the so-called hyalinizing trabecular adenoma). Gherardi G 1987 Signet ring cell "mucinous" thyroid adenoma: a follicle cell tumour with abnormal accumulation of thyroglobulin and a peculiar histochemical profile. Rigaud C, Peltier F, Bogomoletz W V 1985 Mucin producing microfollicular adenoma of the thyroid. Deligdisch L, Subhani Z, Gordon R E 1980 Primary mucinous carcinoma of the thyroid gland: report of a case and ultrastructural study. Schroder S, Husselmann H, Bocker W 1984 Lipid-rich cell adenoma of the thyroid gland. Kini S R, Miller J M 1986 Infarction of thyroid neoplasms following aspiration biopsy. Jones J D, Pittman D L, Sandes L R 1985 Necrosis of thyroid nodules after fine needle aspiration. Katoh R, Jasani B, Williams E D 1989 Hyalinizing trabecular adenoma of the thyroid. Schmid K W, Mesewinkel F, Bocker W 1996 Hyalinizing trabecular adenoma of the thyroid-morphology and differential diagnosis. Chetty R, Beydoun R, LiVolsi V A 1994 Paraganglioma-like (hyalinizing trabecular) adenoma of the thyroid revisited. Li M, Rosai J, Carcangiu M L 1995 Hyalinizing trabecular adenoma of the thyroid: a distinct tumor type or a pattern of growth Fonseca E, Nesland J M, Sobrinho-Simoes M 1997 Expression of stratified epithelial-type cytokeratins in hyalinizing trabecular adenomas supports their relationship with papillary carcinomas of the thyroid. Galgano M T, Mills S E, Stelow E B 2006 Hyalinizing trabecular adenoma of the thyroid revisited: a histologic and immunohistochemical study of thyroid lesions with prominent trabecular architecture and sclerosis. Molberg K, Albores-Saavedra J 1994 Hyalinizing trabecular carcinoma of the thyroid gland. Rothenberg H J, Goellner J R, Carney J A 1999 Hyalinizing trabecular adenoma of the thyroid gland: recognition and characterization of its cytoplasmic yellow body. Lloyd R V 2002 Hyalinizing trabecular tumors of the thyroid: a variant of papillary carcinoma Li M, Carcangiu M L, Rosai J 1997 Abnormal intracellular and extracellular distribution of basement membrane material in papillary carcinoma and hyalinizing trabecular tumors of the thyroid: implication for deregulation of secretory pathways. Hirokawa M, Carney J A, Ohtsuki Y 2000 Hyalinizing trabecular adenoma and papillary carcinoma of the thyroid gland express different cytokeratin patterns. Agaimy A, Hahn T, Schroeder J, Elhag A 2012 Follicular thyroid adenoma dominated by spindle cells: report of two unusual cases and literature review. Yamazaki K 2003 Unique follicular carcinoma of the thyroid gland with extracellular deposition of amorphous globular structures mimicking an adenoid cystic pattern. Davila R M, Bedrossian C W, Silverberg A B 1988 Immunocytochemistry of the thyroid in surgical and cytologic specimens. Johnson T L, Lloyd R V, Thor A 1987 Expression of ras oncogene p21 antigen in normal and proliferative thyroid tissues. Kapp D S, LiVolsi V A, Sanders M M 1982 Anaplastic carcinoma following well-differentiated thyroid cancer: etiological considerations. Nishiyama R H, Dunn E L, Thompson N W 1972 Anaplastic spindle-cell and giant-cell tumors of the thyroid gland. Miettinen M, Franssila K O 2000 Variable expression of keratins and nearly uniform lack of thyroid transcription factor 1 in thyroid anaplastic carcinoma. Are C, Shaha A R 2006 Anaplastic thyroid carcinoma: biology, pathogenesis, prognostic factors, and treatment approaches. Perri F, Lorenzo G D, Scarpati G D, Buonerba C 2011 Anaplastic thyroid carcinoma: A comprehensive review of current and future therapeutic options. Haynik D M, Prayson R A 2005 Immunohistochemical expression of cyclooxygenase 2 in follicular carcinomas of the thyroid. Asa S L 2005 the role of immunohistochemical markers in the diagnosis of follicular-patterned lesions of the thyroid. Schmidt R J, Wang C A 1986 Encapsulated follicular carcinoma of the thyroid: diagnosis, treatment and results. Rosai J, Saxen E A, Woolner L 1985 Undifferentiated and poorly differentiated carcinoma. Semin Diagn Pathol 2: 123126 18 Tumors of the Thyroid and Parathyroid Glands of squamous cell carcinoma of the thyroid. Histopathology 11: 715-722 Carcangiu M L, Zampi G, Rosai J 1984 Poorly differentiated ("insular") thyroid carcinoma. Virchows Arch A Pathol Anat Histopathol 417: 267-271 Wolf B C, Sheahan K, DeCoste D et al. Int J Surg Pathol 19: 620-626 Cibull M L, Gray G F 1978 Ultrastructure of osteoclastoma-like giant cell tumor of thyroid. Am J Surg Pathol 2: 401-405 Silverberg S G, DeGiorgi L S 1973 Osteoclastoma-like giant cell tumor of the thyroid. Report of a case with prolonged survival following partial excision and radiotherapy. Arch Pathol Lab Med 129: e55-e57 Chetty R, Govender D 1999 Follicular thyroid carcinoma with rhabdoid phenotype. Virchows Arch 435: 133-136 Dominguez-Malagon H, Flores-Flores G, Vilchis J J 2001 Lymphoepithelioma-like anaplastic thyroid carcinoma: report of a case not related to Epstein-Barr virus. Ann Diagn Pathol 5: 21-24 Wan S K, Chan J K, Tang S K 1996 Paucicellular variant of anaplastic thyroid carcinoma. Semin Diagn Pathol 12: 45-63 Canos J C, Serrano A, Matias-Guiu X 2001 Paucicellular variant of anaplastic thyroid carcinoma: report of two cases. J Surg Oncol 42: 136-143 Huang T Y, Assor D 1971 Primary squamous cell carcinoma of the thyroid gland: a report of four cases. Am J Clin Pathol 55: 93-98 Huang T Y, Lin S G 1986 Primary squamous cell carcinoma of the thyroid. J Surg Oncol 39: 175-178 Simpson W J, Carruthers J 1988 Squamous cell carcinoma of the thyroid gland. Am J Surg 156: 44-46 Shimaoka K, Tsukada Y 1980 Squamous cell carcinomas and adenosquamous carcinomas originating from the thyroid gland. Lam K Y, Lo C Y, Liu M C 2001 Primary squamous cell carcinoma of the thyroid gland: an entity with aggressive clinical behaviour and distinctive cytokeratin expression profiles. Hayashi Y, Tokuoka S 1979 Anaplastic carcinoma of the thyroid gland, an ultrastructural study of four cases. Holm R, Nesland J M 1994 Retinoblastoma and p53 tumour suppressor gene protein expression in carcinomas of the thyroid gland. Soares P, Cameselle-Teijeiro J, Sobrinho-Simoes M 1994 Immunohistochemical detection of p53 in differentiated, poorly differentiated and undifferentiated carcinomas of the thyroid. Asakawa H, Kobayashi T 2002 Multistep carcinogenesis in anaplastic thyroid carcinoma: a case report. Franssila K O, Harach H R, Wasenius V M 1984 Mucoepidermoid carcinoma of the thyroid. Rhatigan R M, Roque J L, Bucher R L 1977 Mucoepidermoid carcinoma of the thyroid gland. Bondeson L, Bondeson A G, Thompson N W 1991 Papillary carcinoma of the thyroid with mucoepidermoid features. Sambade C, Franssila K, Basilio-de-Oliveirz C 1990 Mucoepidermoid carcinoma of the thyroid revisited. Wenig B M, Adair C F, Heffess C S 1995 Primary mucoepidermoid carcinoma of the thyroid gland: a report of six cases and a review of the literature of a follicular epithelial-derived tumor. Miranda R N, Myint M A, Gnepp D R 1995 Composite follicular variant of papillary carcinoma and mucoepidermoid carcinoma of the thyroid. Cameselle-Teijeiro J, Febles-Perez C, Sobrinho-Simoes M 1995 Papillary and mucoepidermoid carcinoma of the thyroid with anaplastic transformation: a case report with histologic and immunohistochemical findings that support a provocative histogenetic hypothesis. Cameselle-Teijeiro J, Febles-Perez C, Sobrinho-Simoes M 1997 Cytologic features of fine needle aspirates of papillary and mucoepidermoid carcinoma of the thyroid with anaplastic transformation.

Tumors expressing Ig with high sugar content sometimes have red- or crimson-tinged cytoplasm breast cancer earrings purchase female viagra now, an appearance referred to as a flame cell women's health clinic markham female viagra 50mg mastercard. The presence of nucleoli menstruation 21 days cycle order female viagra overnight, nuclear immaturity women's health clinic pei order 100 mg female viagra visa, and pleomorphism are the most reliable features of neoplastic plasma cells because multinucleation or cytoplasmic inclusions can be seen in reactive plasmacytoses womens health pavilion generic 100 mg female viagra. Other Tissues Extraosseous lesions often occur as a direct extension from bony lesions menstruation 9 days generic female viagra 50mg with mastercard, usually from ribs or vertebral bodies. In the spleen, the infiltrate fills the red pulp sinuses and compresses the white pulp. Liver involvement is common, but only rarely causes symptoms; infiltration involves the sinusoids, particularly around portal tracts. Lymph node involvement is also common, with diffuse infiltration by a sheet of plasma cells; reticulin fibers characteristically surround individual plasma cells. In addition, several other important entities must be distinguished from a clonal plasma cell dyscrasia. Reactive plasmacytosis in the marrow seldom exceeds 20% of the cellularity; however, in some chronic inflammatory conditions, large numbers of plasma cells are encountered. Although some cytologic atypia can be seen in reactive plasma cells (particularly multinucleation), it is uncommon for these cells to have plasmablastic features. Immunophenotyping or serologic demonstration of a monoclonal gammopathy is a critically important adjunct to diagnosis. The plasmacytoid immunoblasts of some diffuse large cell lymphomas can closely resemble plasmablasts in tissue sections. Furthermore, diffuse large B-cell lymphoma is almost never associated with a significant M-spike. In myeloma, the ratio of the cells expressing the predominant light-chain type to those expressing the minority light-chain type. The characteristic numeric abnormalities are losses in chromosome 13, 13q14, 8, 14, and X, and gains of chromosome 3, 5, 7, 9, 11, 15, 19, and 21. Examination of a bone marrow biopsy sample and aspirate smear is necessary to make this clinically important distinction. It also occurs sporadically in Central and South America, the Middle East, and the southeastern United States. Eventually, through additional mutations and genomic instability, a monoclonal neoplastic T-cell population emerges from this precursor pool. The acute and lymphomatous types appear to be more aggressive than the chronic or smoldering types. These include the most common acute type, the Peripheral Blood, Bone Marrow, and Aspirate Findings Except for the smoldering and lymphomatous variants, there is a marked peripheral leukocytosis. Most cells have condensed, occasionally hyperchromatic chromatin and variably distinct nucleoli; a subset of cells demonstrates a more blastic nuclear appearance, with dispersed chromatin and conspicuous nucleoli. The neoplastic cells in patients with the smoldering and chronic variants are often less atypical in appearance. The presence of anemia and thrombocytopenia relates to the degree of marrow infiltration. The extent of bone marrow involvement is variable; patchy involvement is most common, but occasionally diffuse marrow replacement is seen. Note the highly lobated nuclei forming an appearance similar to that of the petals in a flower. A normal B-cell counterpart for this neoplasm has been difficult to identify; some evidence suggests the cells are derived from a postgerminal center, mature, memory B cell with altered expression of chemokine and adhesion molecules. Other Pathologic Findings Skin involvement is seen in approximately 60% of patients247,252 and can closely resemble mycosis fungoides, including features such as focal epidermotropism and Pautrier microabscesses. The distribution of cells is predominantly dermal and perivascular; however, occasionally more confluent, tumor-like areas can be found. Lymph node involvement occurs in a typical leukemic pattern with neoplastic cells concentrated within the sinuses and in the perisinusoidal tissue. Peripheral Blood, Bone Marrow, and Aspirate Findings Patients are rarely frankly leukemic and commonly have only small numbers of circulating neoplastic cells that are identified only by careful examination. Aspirate smear preparations may be helpful in evaluating cellular morphology, but the increased reticulin that is invariably associated with hairy cell infiltrates makes "dry taps" common. Hairy cells have oval to indented or reniform nuclei and small, indistinct nucleoli. The chromatin is more evenly distributed and less heterochromatic than in a normal lymphocyte and has a "sponge-painted" quality. These cytoplasmic processes can be difficult to see because of their delicate nature and are best appreciated with phase-contrast microscopy. Rarely, parallel basophilic bands are present in the cytoplasm that correspond to ribosome-lamella complexes seen by electron microscopy. The marrow is hypercellular in the majority of cases, but can be normocellular or even hypocellular. The cells have oval to reniform nuclei, inconspicuous nucleoli, and are characteristically widely spaced with prominent cytoplasmic borders, taking on a so-called fried-egg appearance. Cases with diffuse marrow infiltration are readily appreciated; however, adipocytes and residual hematopoietic elements are admixed with the infiltrate in normocellular or hypocellular cases, making the detection of small numbers of hairy cells difficult. As mentioned, a reticulin network is universally associated with hairy cell infiltrates and readily identified on reticulin stain. The cells have ovoid to irregular nuclei and moderate amounts of cytoplasm that has retracted away from the surrounding cells, resulting in the characteristic widely spaced arrangement. In contrast to the majority of small B-cell neoplasms, the tumor does not involve the white pulp, which is compressed and sometimes completely effaced. Molecular Genetic Findings Clonal immunoglobulin heavy- and light-chain gene rearrangements are present. In advanced stages, anemia and thrombocytopenia occur as a result of marrow infiltration. Hypogammaglobulinemia is common and contributes to a high susceptibility to infections. Immune dysregulation also manifests in the high rate of autoimmunemediated hemolytic anemia or thromobocytopenia. The disease course is protracted, but eventually results in a gradual deterioration in health as a result of marrow replacement and secondary immunodeficiency. Transformation to diffuse large cell lymphoma (so-called Richter transformation) or classic Hodgkin lymphoma (see later discussion) sometimes occurs and usually is the harbinger of a much more aggressive clinical course. However, the cytoplasmic projections are similar to those seen in typical hairy cells. The circulating lymphocytes have less cytoplasm than hairy cells and short cytoplasmic, villous projections that may be polarized. The arrow indicates a proliferation center containing mitotic figures and larger nucleolated prolymphocytoid forms. Numerous cells with disrupted or smeared nuclei devoid of cytoplasm (so-called smudge cells), representing fragile tumor cells that are damaged during preparation, are often seen. Smudge cells are diagnostically useful because they are rarely seen in other chronic lymphoproliferative disorders. Careful inspection of aspirate smears may identify monomorphic lymphoid aggregates, which reflect the presence of nodular tumor infiltrates in the marrow. Occasionally, cells may show more irregular nuclear contours and less condensed chromatin. These features often correlate with chromosomal abnormalities, including trisomy 12. Nodular, interstitial, mixed, or diffuse patterns of involvement can be seen in bone marrow biopsy samples, with paratrabecular aggregates being extremely uncommon. A diffuse or sheet-like infiltrate of prolymphocytic forms with round to slightly irregular nuclei, prominent nucleoli, and moderate amounts of cytoplasm is often seen in disease progression. In large B-cell transformation, marrow involvement usually occurs late in the course and is a frequent finding at autopsy. Monotypic, low-level surface immunoglobulin (often both IgM and IgD) is characteristically seen. Molecular Genetic Findings the most common abnormalities involve deletions of 13q14. Distinguishing features include relatively subtle differences in peripheral blood morphology and the pattern of bone marrow involvement, but definitive diagnosis (in the absence of a lymph node biopsy revealing pathognomonic proliferation centers) requires immunophenotyping and genotypic analysis. In the right half of the field is an infiltrate of small lymphocytes typical of B-cell chronic lymphocytic leukemia, but the left half of the section shows replacement by cells with larger, irregular nuclei and prominent nucleoli. Note the absence of two red signals in each of the two tumor cells, indicating a deletion at 13q14. In contrast, two signals are seen for the probes for chromosome 12 and the more distal region of chromosome 13q at 13q34. The percentage of neoplastic peripheral blood B-prolymphocytes must exceed 55% of the total lymphoid population and is more typically greater than 90%. Molecular Genetic Findings Ig genes are clonally rearranged and somatically mutated in approximately half of the cases. The nucleus is round to oval and has a degree of moderate chromatin condensation, intermediate between that of a mature lymphocyte and a blast. Within the bone marrow usually a diffuse, or mixed nodular and interstitial, pattern of infiltration by prolymphocytes is seen. In addition, larger cells with vesicular nuclei and very prominent large nucleoli termed paraimmunoblasts are also seen. In the spleen, tumor cells diffusely infiltrate red pulp cores and expand white pulp as well. The cells are larger than those of B-cell chronic lymphocytic leukemia/small lymphocytic lymphoma and possess prominent nucleoli and a moderate amount of basophilic cytoplasm. Other Tissue Involvement Splenic involvement is common and takes the form of diffuse red pulp infiltration and effacement of white pulp. Lymph node infiltration is often observed, with infiltrates either diffusely effacing nodal architecture or partially involving nodes in the paracortical regions. Peripheral Blood and Bone Marrow Findings In well-prepared peripheral blood smears, the neoplastic cells are small to medium-sized cells that demonstrate some of the features of prolymphocytes, but considerable morphologic variation is seen within and between cases. The cells most commonly have round to oval nuclei, moderately condensed chromatin, a single prominent nucleolus, and small amounts of deeply basophilic agranular cytoplasm, often with cytoplasmic blebs or protrusions. In a minority of cases, the cells are irregular, convoluted, or folded in appearance. Many cases will show significant pleomorphism because of an admixture of regular and irregular nuclear morphologies. These cells are relatively small, have a high nucleus to cytoplasm ratio, indistinct nucleoli, and a small rim of basophilic cytoplasm. The most consistent abnormalities involve the chromosome 14q11-q32 region (70%-90% of cases). In the majority, this takes the form of inv(14) (q11q32), with the remaining subset showing a t(14;14) (q11;q32). The neoplastic cells are large lymphocytes with round to reniform nuclei, condensed chromatin, absent nucleoli, and moderately abundant, weakly basophilic to clear cytoplasm containing a variable number of fine to coarse azurophilic granules. The marrow is often hypercellular and contains subtle, focal, interstitial lymphoid infiltrates. The cells are large with condensed chromatin and ample cytoplasm; granules are not apparent in histologic sections. The associated neutropenia may be reflected in the marrow as a decrease in granulocytic precursors, which is sometimes the result of a maturation arrest at the myelocyte stage. Many of the initial clinical features are related to neutropenia, which commonly accompanies this disorder. Systemic symptoms, such as fever, night sweats, and weight loss, are also frequent. Moderate splenomegaly is the most common physical finding; hepatomegaly and lymphadenopathy are sometimes also present, but are usually not prominent. Splenic involvement occurs in nearly half of all cases, and is characterized by red pulp infiltration, associated with reactive follicular hyperplasia of the white pulp. Most patients show signs of an aggressive systemic illness with fever, hepatosplenomegaly, adenopathy, coagulopathy, hemophagocytosis, and multiorgan failure. There is little response to conventional therapy, and these patients typically follow a rapidly fatal course. Marrow involvement is highly variable as well, ranging from diffuse effacement to focal, patchy involvement. Therefore the important differential diagnosis is with a reactive increase in large granular lymphocytes, which is commonly seen in association with viral infections (hepatitis, Epstein-Barr virus, cytomegalovirus), certain skin disorders, bone marrow or solid organ transplantation, non-Hodgkin lymphomas, and hemophagocytic syndromes. If the lymphocytosis persists, studies for clonality are helpful in assessing whether it is neoplastic. Immunophenotypic markers can be used to identify the cytotoxic T-cell nature of the infiltrate. Diffuse infiltration of the marrow by a population of medium to largesized lymphoid cells is present, showing nuclear pleomorphism, variably distinct nucleoli, and moderate amounts of cytoplasm. Serum total tryptase persistently exceeds 20 ng/mL (in the absence of a myeloid disorder that may confound this measurement) *Diagnosis of systemic mastocytosis can be made with one major and one minor criterion, or with three minor criteria. Numerous abnormal mast cells are present in the paratrabecular region, showing elongated or spindle cell morphology.

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It is characterized by aggregates of primitive endodermal glands lined by low columnar cells growing in loose or cellular stroma premier women's health boca raton buy 100 mg female viagra visa. Glandular patterns of differentiation in yolk sac tumors of germ cell origin must be differentiated from rare tumors occurring in older women in which a yolk sac tumor arises from women's health lose 10 pounds order 100mg female viagra with amex, or in association with menstrual vacuum female viagra 100 mg discount, an endometrioid or mucinous epithelial tumor breast cancer uggs pink ribbon generic female viagra 50 mg visa. Endometrioid-like variant women's health clinic ucf purchase female viagra mastercard, in which glands are lined by columnar tumor cells with conspicuous subnuclear vacuoles women's health center dover buy generic female viagra canada. Small or large zones of hepatoid differentiation show granular cytoplasmic staining with antihepatocyte antibody, although this is not a specific finding because hepatoid carcinoma and metastatic hepatocellular carcinoma are also positive. This material has been interpreted by some as indicative of parietal yolk sac differentiation. Positive staining is detected in tumor cell cytoplasm, secretory material within cysts and glands, and some hyaline bodies in more than 75% of yolk sac tumors, but staining is often weak and focal. Glypican-3, which was initially used as a marker for hepatocellular carcinoma, stains the cytoplasm of yolk sac tumor cells in nearly all cases. Immunohistochemical stains for 1-antitrypsin, and placental alkaline Embryonal carcinoma is an ovarian neoplasm that is morphologically identical to embryonal carcinoma of the testis. It occurs almost exclusively in children and young women,734 although occurrence in older women has been reported. The typical presentation is with pelvic or abdominal pain or a palpable abdominal mass. Embryonal carcinoma is virtually never bilateral, so biopsy of the contralateral ovary is unnecessary. Although standard treatment for patients with advanced embryonal carcinoma is total abdominal hysterectomy, bilateral salpingo-oophorectomy, and limited debulking, young patients can be treated by unilateral salpingooophorectomy and limited debulking if the contralateral ovary and uterus are uninvolved. Before effective combination chemotherapy was available, embryonal carcinoma was often rapidly fatal, with survival, even in stage I, limited to 50%. Many patients with residual or recurrent tumors can be cured with combination chemotherapy. If serum levels of either or both markers remain elevated after treatment, or if they increase during follow-up, the patient almost certainly has recurrent or metastatic tumor. Gross Pathology Embryonal carcinoma is a large solid neoplasm with an average diameter of 15 to 17 cm. The cut surface is fleshy and tan or gray, with small cysts and areas of hemorrhage and necrosis. Microscopically, polyembryoma is composed of numerous embryoid bodies growing in a primitive embryonal stroma. They have an embryonic disc composed of tall columnar cells with hyperchromatic nuclei, similar to embryonal carcinoma cells. Microscopic Pathology the microscopic appearance is similar to that of embryonal carcinoma of the testis. The tumor cells have large vesicular nuclei with coarse chromatin and one or two prominent nucleoli. The nuclei are larger than those of dysgerminoma, and generally moderate to marked nuclear pleomorphism is present. The tumor cells are polygonal or columnar, and they have abundant amphophilic or clear cytoplasm. The tumor cells grow in nests and sheets, or they line clefts, glands, or papillae. Most embryonal carcinomas contain syncytiotrophoblastic giant cells, present singly or in clusters; no cytotrophoblastic cells are present, so this finding is not indicative of choriocarcinoma. The stroma is loose and edematous or consists of a cellular proliferation of small, primitive-appearing spindle cells. Although embryonal carcinoma only rarely grows in pure form in the ovary, or as an extensive component of a mixed germ cell tumor, it is not uncommon to find microscopic foci in mixed germ cell tumors in which embryonal carcinoma glands are admixed with yolk sac tumor, resulting in a so-called embryoma pattern. Choriocarcinoma Pure primary ovarian choriocarcinoma of germ cell origin is extremely rare. In a review of the pathology of malignant ovarian germ cell tumors, fewer than 1% were choriocarcinomas739 and only about 40 nongestational ovarian choriocarcinomas had been reported in the literature as of 2006. Choriocarcinoma of the ovary is unilateral and is treated by salpingo-oophorectomy. Total abdominal hysterectomy and bilateral salpingo-oophorectomy are required only if the contralateral ovary or uterus is involved. Surgery is followed by standard germ cell combination chemotherapy with a platinum-based regimen. The chemotherapy and prognosis for patients with gestational choriocarcinoma differs from that for patients with nongestational choriocarcinoma. It is therefore important to determine whether an ovarian choriocarcinoma is of gestational or germ cell type. If the patient is premenarcheal, the choriocarcinoma is certain to be of germ cell origin. In young women of childbearing age, gestational choriocarcinoma is equally as likely as germ cell choriocarcinoma, with no morphologic differences between gestational choriocarcinoma and choriocarcinoma of germ cell origin. The presence of a corpus luteum of pregnancy favors gestational choriocarcinoma, whereas identification of other germ cell elements in the tumor is indicative of germ cell choriocarcinoma. Mature (Benign) Teratoma Mature teratomas are cystic or, rarely, solid tumors that contain various mature tissues derived from one or more of the embryonic germ layers: the ectoderm, mesoderm, and endoderm. Most are found in women between 20 and 50 years of age, with a peak incidence between 20 and 29 years; only about 20% are detected in postmenopausal women. Symptoms such as pelvic pressure or pain appear when the tumor attains a large size. The most common serious complications are torsion, which occurs in 3% to 10% of cases, and rupture, which occurs in about 1%. Acute peritonitis or, rarely, chronic granulomatous peritonitis can be a sequela of spontaneous rupture. Rare patients have serious neurologic or psychiatric symptoms caused by a paraneoplastic syndrome associated with the teratoma. Cystectomy, which can be performed laparoscopically or at laparotomy, is adequate treatment, particularly in children and young women. Peritoneal implants composed of mature glial tissue (grade 0) occur in rare patients with mature teratoma of the ovary. They range in size from only a few centimeters to large tumors weighing several kilograms; the average diameter is 7 to 8 cm. The cyst contents are liquid at body temperature, but they solidify and are soft or firm at room temperature. On cross section, a unilocular or, less often, multilocular cyst with a solid protuberance called the dermoid papilla is present in the wall. Foci of soft graytan tissue resembling brain matter and glistening green or brown thyroid tissue are also commonly seen. Dense, solid regions in an otherwise cystic teratoma are unusual; these raise the question of immature teratoma and should be carefully sectioned for histologic study. Rare mature (benign) teratomas are completely solid and can be differentiated from immature teratoma only by microscopic study. Benign teratomas contain a varied mixture of ectodermal, mesodermal, and endodermal elements distributed in an organized fashion. Tissues from at least two germ layers can be identified in two thirds of mature teratomas, and all three germ layers are represented in about a third of them. The cytotrophoblastic cells have pale cytoplasm and vesicular nuclei with prominent chromatin clumps. The syncytiotrophoblastic cells have multiple smaller nuclei within a syncytium of basophilic cytoplasm. Gross Pathology Choriocarcinoma is a unilateral soft purple-red tumor with a hemorrhagic and necrotic cut surface. Microscopic Pathology Microscopically, much of the tumor is hemorrhagic and necrotic. Viable tumor cells are mainly at the periphery, where cytotrophoblastic cells and syncytiotrophoblastic giant cells grow in a plexiform pattern. Cytotrophoblastic cells have abundant clear cytoplasm and well-defined cell borders. Syncytiotrophoblastic giant cells have abundant vacuolated basophilic or amphophilic cytoplasm in which multiple hyperchromatic nuclei are seen. When it is found in the ovary, choriocarcinoma is most likely to be a component of a mixed germ cell tumor. Teratoma Benign cystic teratoma (dermoid cyst) is the most common ovarian neoplasm, constituting 25% or more of all ovarian tumors. The epithelium is of stratified squamous type and hair shafts and sebaceous glands underlie it. This keratinizing squamous cell carcinoma arose as a secondary neoplasm in a benign cystic teratoma. Other ectodermal elements that are frequently present include brain (usually glia), choroid plexus, peripheral nerve, and dental structures. Common endodermal tissues include digestive tract mucosa, including endocrine cells, respiratory mucosa, renal tissue, and thyroid tissue. The most frequent mesodermal derivatives are adipose tissue, smooth or striated muscle, bone or cartilage, and a loose connective tissue framework that surrounds the other elements. Surprisingly, male tissues such as prostate are occasionally present in a benign teratoma. An individual element is so dominant in some tumors that classification as a monodermal teratoma is appropriate. Cystic spaces lined by flattened epithelium or granulation tissue and surrounded by multinucleated giant cells and lipophages are present in some teratomas. The foreign body granulomatous reaction is caused by disruption of the epithelium with liberation of the cyst contents into the surrounding tissue. Secondary Neoplasms in Mature (Benign Cystic) Teratoma Benign or malignant tumors that arise in a benign teratoma are rare. Tumors are confined to the ovary (stage I) in 50% to 75% of patients, and those patients have a favorable prognosis. A secondary neoplasm typically forms a nodule or a papillary growth in the cyst lining, but sometimes there is only a thickening or induration of the cyst wall. In some instances, the secondary neoplasm is detected only by microscopic examination. Secondary neoplasms are usually unilateral, but the contralateral ovary may contain a benign cystic teratoma. In situ malignant tumors that have been reported include squamous cell carcinoma in situ and Paget disease. Other types of malignancies that have been reported to arise in a benign teratoma include various types of cutaneous carcinomas, such as basal cell carcinoma or sebaceous carcinoma,766 melanoma,767-769 adenocarcinoma,770 various types of sarcoma, and other rare tumor types. Any type of mucinous tumor can arise in a teratoma; cystadenomas are most common, but borderline tumors and carcinomas also occur. The average patient is about 20 years old, and few are younger than 7 or older than 40. Immature teratomas are exceptional in older or 13 Tumors of the Female Genital Tract 715 postmenopausal women. Patients complain of pelvic or abdominal pain, abdominal swelling, or a palpable abdominal mass. As previously noted, rare patients with teratomas have serious neurologic or psychiatric symptoms caused by a paraneoplastic syndrome associated with the teratoma. Bilaterality is exceptional, although metastases can involve the contralateral ovary in patients with advanced disease. Immature teratoma spreads mainly by implantation on the pelvic and abdominal peritoneum and the omentum. In 10% to 15% of cases, a benign cystic teratoma is found in the contralateral ovary. A few patients have been treated successfully by cystectomy, sometimes followed by chemotherapy. The prognosis is somewhat less favorable for patients with residual gross tumor or recurrent immature teratoma. In patients with extraovarian tumor spread, the microscopic appearance of the metastases is of prognostic importance. Some peritoneal implants or lymph node deposits contain only mature tissues, usually predominantly glial cells. Second-look operations performed after chemotherapy in patients with incompletely resected immature teratoma can reveal residual immature teratoma, no residual tumor, small glial implants, or bulky nodules of mature teratoma. These bulky nodules are resected to avoid adhesions or compression of adjacent organs and to forestall development of the growing teratoma syndrome. Nodules of benign-appearing glial tissue are covered by peritoneum in this grade 0 implant. Immature teratoma is a predominantly solid unilateral tumor that averages 18 cm in diameter. In about a quarter of these tumors, one or more large cysts contain keratinous debris or hair and resemble a dermoid. Tissues derived from all three germ cell layers are present, and a mixture of mature and immature elements are found in most tumors. These usually have a haphazard distribution and often lack the organized growth patterns seen in benign cystic teratoma. Ectodermal and mesodermal derivatives typically predominate among the immature elements. Immature neuroectodermal elements are the easiest immature tissues to recognize and quantitate.

In this group breast cancer 5k atlanta 2014 female viagra 100mg fast delivery, age women's health clinic fort campbell buy female viagra overnight, stage menopause doctors discount 50mg female viagra amex, tumor grade women's health center gretna discount female viagra online master card, and peritoneal cytology have an impact on the prognosis menstrual ovulation calendar discount female viagra master card. Int J Gynaecol Obstet 2009; 105: 3-4 rate as more conventional treatment by primary cytoreductive surgery followed by chemotherapy womens health upland ca purchase female viagra us, but with less morbidity. A dose-dense protocol in which patients receive intensified therapy with paclitaxel along with intravenous or intraperitoneal carboplatin has been proposed and is being investigated. Chemotherapy results in a partial or complete clinical remission in about 85% of women with advanced cancer, but most patients relapse within 2 to 3 years and the long-term survival rate is less than 20% to 30%. Serous Tumors Serous tumors constitute approximately 30% of all ovarian tumors, making them the single most common group. They comprise 22% of benign and nearly 50% of malignant primary tumors of the ovary. Of all serous tumors, 50% are benign, 15% are borderline, and 35% are invasive carcinomas. The interior and exterior surfaces are usually smooth, but small papillary excrescences occasionally arise from the cyst lining. Serous adenofibroma is a solid tumor that has a firm white or tan fibrous cut surface. Scattered small cysts may be visible, or the tumor may have a spongy appearance because of the presence of many diminutive cysts. Serous cystadenofibroma is more common than adenofibroma; it is a unilocular or multilocular cystic tumor with solid adenofibromatous areas in its wall. Serous surface papilloma is an uncommon tumor that grows as papillary excrescences on the surface of the ovary. Microscopically, benign serous tumors are lined by ciliated and non-ciliated low columnar cells with bland ovoid basal nuclei. Abundant fibrous stroma surrounds the glands and cysts in adenofibroma and cystadenofibroma. In one study, only 14% of serous cystadenomas, usually the larger ones, were found to be monoclonal. There are small foci of mild to moderate nuclear atypia or branching papillary growth in occasional otherwise benign serous tumors. The behavior of serous tumors with small proliferative or atypical foci has not been studied adequately45; however, when these features are observed in only a few low-power fields (<5%-10% of the tumor), the clinical evolution is generally benign and such tumors are usually classified as a serous cystadenoma, cystadenofibroma, or adenofibroma with focal low-grade atypia or proliferation. Tumor-related deaths fall into three main categories: (1) the patient develops low-grade serous carcinoma and dies of carcinoma; (2) the patient develops a fatal complication of a borderline tumor, such as fibrous adhesions leading to bowel obstruction; or (3) the patient dies of a complication of treatment. Conservative therapy appears indicated for borderline tumors, except in a small cohort of women whose tumors exhibit features consistently associated with aggressive behavior or carcinoma. These features include invasive peritoneal implants or recurrence as low-grade serous carcinoma. Although most oncologists administer chemotherapy to patients with invasive implants or lowgrade serous carcinoma, these patients tend to have long survival regardless of therapy and tumor regression following chemotherapy is less than satisfactory. The standard surgical treatment for a borderline tumor is total abdominal hysterectomy, bilateral salpingo-oophorectomy, omentectomy, and complete staging with resection of extraovarian tumor implants if any are present. Many women with borderline tumors are of reproductive age and wish to retain their childbearing capability. Unilateral salpingo-oophorectomy, or even cystectomy, is therefore considered as a treatment option in some circumstances, although patients treated in this way have about a 25% risk of recurrence in the contralateral ovary. Patients with micropapillary borderline serous tumors are more likely than those with typical borderline serous tumors to have tumor spread beyond the ovary. When corrected for stage and implant type, however, no difference in survival has been demonstrated. The tumor stage is altered in approximately 15% of women who undergo restaging surgery, but the risk of recurrence appears to be similar in women who are restaged and those who are not. Restaging is of most value for women with micropapillary borderline serous tumors, because they have a greater risk of having invasive peritoneal implants. Recurrences are generally detected many years after primary therapy, and recurrent disease can be slowly progressive. Recurrent tumor can be borderline serous tumor, low-grade serous carcinoma or, rarely, high-grade serous carcinoma. Oncologists are not in complete agreement, but most administer chemotherapy or radiotherapy only in the face of progressive disease that is not amenable to surgical resection. Borderline serous tumors are large, usually multilocular cystic neoplasms that are bilateral in 35% to 40% of cases. Papillary growth is focal in some tumors, confluent in others, and present on the external surface of the ovary in 40% to 50% of cases. Areas of solid growth are unusual except in adenofibromatous borderline tumors, and zones of hemorrhage or necrosis are seldom seen. At low magnification, papillae with a hierarchical branching pattern grow from the cyst lining into the lumina. Complex papillary and glandular patterns and secondary cyst formation are typical. The papillae have fibrovascular cores that are conspicuous even in smaller branches and are surfaced by proliferating columnar cells stratified into several layers. Focally, the cells form tufts from which clusters of cells and single cells are detached into the cyst lumen. Variable, but usually low-grade, nuclear atypia and scattered mitotic figures are present. Cells with abundant eosinophilic cytoplasm, the indifferent or metaplastic cells, are scattered singly or in small clusters among the columnar tumor cells; they tend to be most conspicuous at the tips of the papillae. They resemble desmoplastic peritoneal implants (see later discussion) and are termed autoimplants. Autoimplants tend to be detected in high-stage tumors, but do not appear to have prognostic significance. Some tumors have sufficient fibrous stroma in their walls to be classified as a borderline serous adenofibroma or cystadenofibroma. The microscopic feature that differentiates a serous borderline tumor from a serous carcinoma is the absence of diffuse stromal invasion in the former. In a borderline tumor, papillae and glands that appear to be within the stroma are an artifact resulting from tangential cutting of complicated infoldings of the cyst lining. Such glands are not infiltrative and have no stromal fibroblastic or inflammatory reaction around them. Foci of limited stromal invasion are identified occasionally in a borderline serous tumor. Various arbitrary size limits have been proposed for microinvasion, ranging from 3 to 5 mm, but in practice foci of microinvasion are almost always smaller than 3 mm. The most common is one in which small clusters and cords of cells with eosinophilic cytoplasm, round vesicular nuclei, and prominent nucleoli are haphazardly distributed in the fibrous stroma of the cyst wall or a papilla. The branching papillae are covered by proliferating columnar cells, some of which are detached into the cyst lumen. The nucleus to cytoplasm ratio is increased relative to that seen in a serous cystadenoma, and focal stratification of the nuclei is present. They are found occasionally within lymphatic spaces, but the clinical significance of this finding is unclear. Intrastromal tumor cells can lie in unremarkable stroma, or they can be surrounded by inflamed or myxoid fibrous stroma. When microinvasion is present, it is prudent to conduct a thorough evaluation to exclude more extensive areas of invasion indicative of low-grade serous carcinoma. Most patients whose tumors exhibit stromal microinvasion have an uneventful course; the unfavorable outcome observed in a few patients has been attributed to other factors, such as invasive implants or incomplete staging. The epithelium that lines borderline serous tumors includes eosinophilic "metaplastic" or "indifferent" cells. These cells tend to be more numerous in tumors with stromal microinvasion and are more conspicuous in tumors removed from pregnant patients. For unknown reasons, microinvasion seems to be detected more frequently in tumors from pregnant women. In contrast to borderline serous tumors with small areas of microinvasion, those with larger areas of invasion have an appreciable risk of progression if tumor has spread outside of the ovary. Peritoneal or omental tumor implants are found in 15% to 30% of women with serous borderline tumors. These are generally small superficial nodular excrescences of only a few millimeters diameter, although larger solid or cystic implants are occasionally present. Controversy exists as to whether these represent metastases from the ovarian tumor or sites of synchronous peritoneal neoplasia, although an increasing number of studies show similar genetic profiles in the ovarian and extraovarian tumors. Single cells and small clumps of cells with abundant eosinophilic cytoplasm are present in the stroma between the glands. The microinvasive cells have enlarged vesicular nuclei, some of which contain nucleoli. An invasive type, which is the equivalent of lowgrade serous carcinoma In the noninvasive epithelial type, papillary serous borderline tumor grows on the surface of the peritoneum or in cystic spaces just beneath it. Noninvasive desmoplastic implants are plaques of vascular fibrous stroma that contain a few epithelial cells, small clusters of cells, or scattered small glands lined by bland epithelial cells. The implants appear plastered to the peritoneal surface and show no invasion downward into the underlying stroma. Although patients with noninvasive implants tend to have a favorable prognosis, a few of them develop progressive disease and die of tumor. No invasive implants were found in one hospital-based study of 57 patients that did not include any consultation cases, indicating that practicing pathologists will only rarely see implants of this type. Expanded criteria for invasive implants have been proposed but remain controversial. It can be difficult to classify implants; when it is unclear whether the implant is invasive, the term "indeterminate" implant is often used to categorize it. Tumor is present in pelvic or para-aortic lymph nodes in up to a third of patients with advanced borderline tumors. In one, the tumor grows in a branching papillary pattern similar to that observed in a primary ovarian borderline serous tumor. In the other, tumor cells are present singly or in small nests in the subcapsular sinuses. Lymph node involvement by hyperplastic mesothelial cells is a rare mimic of the latter pattern. A rare but prognostically unfavorable pattern of lymph node involvement by borderline serous tumor is one in which the lymph node parenchyma is replaced by a nodular proliferation of tumor cells growing in reactive fibroblastic stroma. Although borderline serous tumors mainly involve intra-abdominal lymph nodes, tumor is found in extra-abdominal lymph nodes at or subsequent to primary surgery in occasional patients. Scattered small nests of bland epithelial cells are surrounded by abundant fibrous stroma. Numerous small nests of epithelium, some surrounded by clefts, invade the fibrous stroma. These inclusions, designated as benign epithelial inclusions or endosalpingiosis, are more frequent in patients with borderline serous tumors, and it has been proposed that they may represent a precursor lesion or a type of lymph node involvement by a borderline serous tumor. Some have proposed that lymph node involvement by borderline serous tumors may represent synchronous neoplasia arising in epithelial inclusions rather than metastasis from the ovarian tumor. Regardless of its origin, lymph node involvement by a borderline serous tumor is most often found in women with peritoneal or omental implants and it does not appear to be an independent adverse prognostic finding in most studies. The term micropapillary serous carcinoma was proposed for a group of proliferative serous tumors with excessive epithelial proliferation, the morphologic spectrum of which appears to encompass some noninvasive tumors in the borderline category as well as some low-grade invasive serous carcinomas. Survival rates appear to be similar to those for conventional borderline serous tumors, once adjusted for stage and implant type. On gross examination, micropapillary borderline serous tumors are cystic and solid tumors that average 8 to 9 cm in diameter. They tend to be bilateral and typically exhibit both intracystic and surface papillary tumor growth. Microscopically, micropapillary borderline serous tumors have a background of typical borderline serous tumor and have been defined arbitrarily as having foci of micropapillary growth measuring greater than 0. Tumors with foci of cribriform growth along the surfaces of papillae are also classified as micropapillary borderline serous tumors. Long, thin micropapillae, many lacking fibrovascular cores, sprout from the surface of a coarse papillary frond. Ciliated cells are less frequent in micropapillary serous tumors than in typical borderline serous tumors. High-Grade Serous Carcinoma Serous carcinoma is the most common type of ovarian cancer, accounting for 68% of ovarian cancers in one large population-based study. Intra-abdominal metastases are typically present at the time of diagnosis in patients with high-grade serous carcinoma, in the omentum, on peritoneal surfaces, or in abdominal lymph nodes. Note the long micropapillary processes lined by cuboidal or low columnar cells displaying only mild to moderate nuclear atypia. They have large vesicular nuclei with coarse chromatin, and some have prominent nucleoli. This association led to findings that resulted in an ongoing reassessment of nature of this tumor type. Most of the carcinomas found in prophylactic salpingo-oophorectomy specimens are of serous type, measure only a few millimeters in diameter, and are of high grade. Serous carcinoma is a large, often bilateral neoplasm with a mixture of cystic, papillary, and solid growth. Carcinoma frequently invades through the ovarian capsule and grows on the surface of the ovary.