Lymph Node برای بزرگنمایی عکسها کلیک را روی ان نگه دارید..... Figure 37.1 Normal Lymph Node. A, The morphologic differences among the various nodal compartments are particularly evident in mesenteric lymph nodes, of which this is an example. B, Secondary lymphoid follicle with obvious polarity of the germinal center Figure 37.2 Appearance of Various Lymph Node Diseases as Seen in Fine Needle Aspiration Specimens. A, follicular hyperplasia; B, Hodgkin lymphoma (Reed-Sternberg cell); C, small lymphocytic lymphoma/chronic lymphocytic leukemia; D, follicular lymphoma, grade 3; E, lymphoblastic lymphoma; F, metastatic pulmonary small cell carcinoma; G, metastatic alveolar rhabdomyosarcoma; H, same case as G immunostained for desmin. (Courtesy of L. Alasio, Milan, Italy.) Figure 37.3 Schematic representation of an immunoglobulin gene rearrangement, in this case the kappa (IGK) gene. The germline configuration of the kappa light chain gene (upper line) consists of numerous variable gene segments (V-kappa, 1-n), five joining gene segments (J-kappa, 1-5), and a single constant region gene segment (C-kappa). To assemble a functional light chain gene (lower line), select V and J segments are juxtaposed with each other by deletion of the intervening DNA. The deletion reconfigures restriction enzyme cutting sites upstream of J-kappa, changing the size of the BamH1 fragment detected with a C-kappa hybridization probe (12 kb germline vs. 10 kb rearranged in figure) when examined by Southern blot analysis. Current polymerase chain reaction method target detection of the rearranged product (lower line). (From Warnke RA, Weiss LM, Chan JKC, et al. Tumors of the Lymph Nodes and Spleen. Atlas of Tumor Pathology, series 3, fascicle 14. Washington, DC: Armed Forces Institute of Pathology; 1995.) Figure 37.4 Follicular Hyperplasia. A, Low-power view showing marked differences in size of germinal centers, their well-circumscribed character, and the fact that they are surrounded by a well-defined mantle. B, High- power view showing numerous "tingible body" macrophages Figure 37.5 Progressively Transformed Germinal Centers. A, Low-power view showing that this formation is larger and less well defined than the adjacent hyperplastic follicles. B, High-power view showing cytologic composition not too dissimilar from that of ordinary hyperplastic follicles. C, CD21 staining highlights the expanded and disrupted follicular dendritic cell network of follicle. D, IgD staining shows preserved mantle zones with infiltration into the transformed germinal center Figure 37.6 Paracortical hyperplasia, identified by the prominence of postcapillary venules Figure 37.7 Sinus Hyperplasia. The cells present in the sinus represent an admixture of histiocytes and sinus lining cells Figure 37.8 Monocytoid B-Cell Hyperplasia in a Case of Toxoplasmic Lymphadenitis. Clusters of small to medium-sized cells are present with clear cytoplasm. Note the presence of admixed neutrophils and nuclear remnants, a feature of reactive monocytoid B-cells Figure 37.9 Plasmacytoid monocytes as seen on low (A) and high power (B) Figure 37.10 So-Called Polykaryocytes. These cells are characterized by numerous clustered nuclei Figure 37.11 Necrotizing Lymphadenitis (Kikuchi-Fujimoto Disease). A, The most common pattern shows necrosis with karyorrhexis/pyknosis with nuclear debris but no neutrophils. B, Other cases show a more mononuclear infiltrate with debris without zonal necrosis. C, Increased numbers of CD123-positive cells, and D, myeloperoxidase positive histiocytes, support the diagnosis Figure 37.12 Large adherent tuberculous lymph nodes containing extensive foci of caseation necrosis Figure 37.13 Numerous confluent non-necrotizing granulomas mainly composed of epithelioid cells in a lymph node affected by sarcoidosis Figure 37.14 Asteroid body in the cytoplasm of a multinucleated giant cell in sarcoidosis Figure 37.15 Hamazaki-Wesenberg bodies in a lymph node with sarcoidosis, as shown in (A) hematoxylin-eosin, (B) periodic acid-Schiff, and (C) Gomori methenamine-silver stains Figure 37.16 Numerous Histoplasma organisms in the cytoplasm of histiocytes Figure 37.17 Toxoplasmosis of Lymph Node. A, Small noncaseating granulomas composed of epithelioid cells are located at the periphery of a hyperplastic follicle. This picture is almost pathognomonic of this disease. B, An area of massive monocytoid B-cell hyperplasia Figure 37.18 Toxoplasma cyst as seen in a microscopic section, (A) and a touch preparation (B). This is a very unusual finding in lymph nodes affected by the disease Figure 37.19 Syphilis of Lymph Node. A, Follicular hyperplasia associated with striking pericapsular inflammation and fibrosis. B, The prominent vasculitis seen in this field is an important clue to the diagnosis Figure 37.20 A and B, Lymph node involvement by lepromatous leprosy. The sinuses are massively dilated as a result of the accumulation of foamy histiocytes Figure 37.21 Lymph Node Involved by Cat-Scratch Disease Figure 37.22 Cat-scratch disease with an area of stellate necrosis with neutrophils surrounded by histiocytes Figure 37.23 Necrotizing granuloma in a lymph node affected by lymphogranuloma venereum, showing features similar, if not identical, to cat-scratch disease Figure 37.24 Low-power (A) and high-power (B) microscopic views of AIDS-related lymphadenopathy. The depicted germinal center shows disruption of its architecture by intrusion of small lymphocytes from the mantle zone. This is a common but not pathognomonic feature of this disease Figure 37.25 Lymph Node Involved by Infectious Mononucleosis. There is a marked effacement of the architecture by a polymorphic lymphoid infiltrate Figure 37.26 Various types of immunoblast seen in a lymph node involved by infectious mononucleosis. The binucleated form (shown in the fourth image) can simulate Reed-Stemberg cells. Note the basophilic character of the nucleus and the presence of a paranuclear hof. Also note the variability in size of background lymphocytes that also demonstrate a plasmacytoid appearance. This variability is characteristic of infectious mononucleosis Figure 37.27 Demonstration of EBV EBER by in situ hybridization in a case of infectious mononucleosis. Note that both large and small cells are positive, in contrast to EBV+ Hodgkin lymphoma in which the EBV is primarily in large cells Figure 37.28 Viral lymphadenitis showing scattered immunoblasts resulting in a "salt-and-pepper" appearance Figure 37.29 Large accumulations of DNA-containing basophilic material in the subcapsular region of a lymph node in a patient with systemic lupus erythematosus Figure 37.30 Castleman Disease of Hyaline Vascular Type. There is prominent germinal center showing well-developed changes Figure 37.31 Castleman Disease of Plasma Cell Type. A, Low-power view showing follicular hyperplasia without hyaline vascular changes. B, High-power view of the interfollicular region showing a massive infiltration by plasma cells. Some of these plasma cells show multinucleation and mild nuclear atypia Figure 37.32 Gross appearance of Castleman disease of the hyaline vascular type Figure 37.33 Prominent network of CD21-positive dendritic follicular cells in the abnormal germinal center of Castleman disease Figure 37.34 "Dysplasia" of Reticular/Dendritic Cells in Castleman Disease. These cells were immunoreactive for desmin Figure 37.35 Castleman disease of hyaline vascular type with a prominent stromal component which is richly vascularized ("stroma-rich" variant) Figure 37.36 Castleman disease associated with vascular proliferation in the surrounding soft tissues. (Courtesy of Dr. Pietro Muretto, Pesaro, Italy.) Figure 37.37 Castleman Disease Complicated by the Development of Sarcoma. A, Gross appearance of a case located in the perirenal region. B, Microscopic appearance of another case. The tumor has a vaguely hemangiopericytomatous quality. C, High-power view Figure 37.38 Dermatopathic Lymphadenitis. A, Massive expansion of the paracortical region, resulting in a wide, pale area between the capsule and the lymphoid follicles. B, High-power view of the paracortical region showing numerous cells with oval vesicular nuclei, which correspond to an admixture of interdigitating dendritic cells and Langerhans cells with nuclear grooves. Scattered cells containing pigment are also present Figure 37.39 Rosai-Dorfman Disease. Low-power view showing massive distension of the sinuses by the histiocytic infiltrate Figure 37.40 Rosai-Dorfman Disease. High-power view showing lymphocytophagocytosis by the sinus histiocytes Figure 37.41 Rosai-Dorfman Disease. Oil red O stain showing abundant neutral lipid in the cytoplasm of the histiocytes Figure 37.42 Strong immunoreactivity of the sinus histiocytes for S100 protein in Rosai-Dorfman disease Figure 37.43 A and B, Lymph node involvement by Kimura disease. There is follicular hyperplasia and massive perinodal inflammation, which is predominantly composed of eosinophils. (Courtesy of Dr. T.-T. Kuo, Taipei, Taiwan.) Figure 37.44 Lymph Node Containing Lipophagic Granulomas. The change is manifested by the presence of mononuclear and multinucleated histiocytes located in the sinuses and containing large cytoplasmic vacuoles Figure 37.45 Presence of the EBV in a the neoplastic cells of Hodgkin lymphoma as demonstrated immunohistochemically by the detection of LMP1 antigen Figure 37.46 A and B, Gross appearance of lymph nodes involved by Hodgkin lymphoma. Note nodularity and sclerosis Figure 37.47 Spectacular example of a Reed-Sternberg cell. (Courtesy of Dr. Fabio Facchetti, Brescia, Italy.) Figure 37.48 Various Appearances of Reed-Sternberg Cells. The cell located at the bottom right has a "mummified" appearance Figure 37.49 Reed-Sternberg-like cells in malignant melanoma (A), and osteoblastoma (B) Figure 37.50 Membrane and Golgi-type immunoreactivity for CD30 in a Reed-Sternberg cell. (Courtesy of Dr. Fabio Facchetti, Brescia, Italy.) Figure 37.51 A Typical Case of Nodular Sclerosis Hodgkin Lymphoma. The lymphoid nodule is encased in dense fibrohyaline tissue Figure 37.52 Various appearances of lacunar cells in nodular sclerosis Hodgkin lymphoma Figure 37.53 Mixed Cellularity Hodgkin Lymphoma. Several diagnostic Reed-Sternberg cells are seen admixed with a polymorphic lymphoid infiltrate rich in eosinophils Figure 37.54 Lymphocyte Depletion Type of Hodgkin Lymphoma. Numerous atypical cells are present in a densely fibrotic stroma. Lym- phocytes are scanty Figure 37.55 Hodgkin Lymphoma Accompanied by Numerous Sarcoid-Like Granulomas. The presence of this component can obscure the basic nature of the disease Figure 37.56 Blood Vessel Invasion in Hodgkin Lymphoma Figure 37.57 Lymphocyte Predominant Hodgkin Lymphoma. A, Low-power view showing a mottled appearance of the node. B, High-power view showing the lymphocytic and/or histiocytic (L&H) type of cell ("popcorn" cell) that is characteristic of this condition Figure 37.58 Lymphoblastic Lymphoma. The immature lymphoma cells have fine nuclear chromatin more characteristic of blasts over large mature B cells Figure 37.59 Low-Power View of Small Lymphocytic Lymphoma. A proliferation of small lymphocytes effaces the architecture of the node Figure 37.60 High-Power View of Small Lymphocytic Lymphoma. There is some variability in cell size. The nuclear contours are regular, the chromatin is clumped, and nucleoli are inconspicuous Figure 37.61 So-called proliferation center in a lymph node involved by small lymphocytic lymphoma Figure 37.62 Gross appearance of lymph nodes involved by chronic lymphocytic leukemia/small lymphocytic lymphoma with anaplastic transformation (so-called Richter syndrome) Figure 37.63 Various morphologic types of lymph node involvement by chronic lymphocytic leukemia/ small lymphocytic lymphoma: A, monotonous infiltrate of small mature lymphocytes; B, increased pro- lymphocytes, with slightly larger nuclei and more open chromatin; C, large pleomorphic tumor cells (so-called Richter syndrome) Figure 37.64 Intranuclear immunoglobulin inclusions (Dutcher bodies) in a lymph node affected by lymphoplasmacytoid lymphoma as seen after hematoxylin-eosin (A) and PAS stains (B) Figure 37.65 Malignant lymphoma composed of lymphocytes and immature plasmacytoid forms (so-called pleomorphic immunocytoma) Figure 37.66 Lymph node involvement by marginal zone B-cell lymphoma with a prominent perifollicular or marginal zone pattern. There are numerous residual, non-neoplastic germinal centers Figure 37.67 Lymph node involvement by marginal zone B-cell lymphoma with small lymphoma cells with clear cytoplasm. This tumor also affected the thymus gland. (Courtesy of Dr. John Chan, Hong Kong.) Figure 37.68 Gross Appearance of a Lymph Node Affected by Follicular Lymphoma. The neoplastic nodules bulge onto the surface. (Courtesy of Dr. R. A. Cooke, Brisbane, Australia; from Cooke RA, Stewart B. Colour Atlas of Anatomical Pathology. Edinburgh: Churchill Livingstone; 2004.) Figure 37.69 Even distribution of neoplastic follicles in follicular lymphoma (B), as opposed to the pre- dominantly cortical distribution typical of follicular hyperplasia (A) Figure 37.70 Fuzzy edge of neoplastic nodule of follicular lymphoma (B), as opposed to sharp edge bound by the mantle zone in follicular hyperplasia (A) Figure 37.71 Homogeneous population of small cleaved cells in follicular lymphoma (B), as opposed to the polymorphic composition seen in follicular hyperplasia, including the presence of tingible-body macrophages (A) Figure 37.72 Marked contrast between the cleaved cells of follicular lymphoma (B) and the regular mature lymphocytes of small lymphocytic lymphoma (A) Figure 37.73 Follicular Lymphoma. A, CD20 stain decorates the neoplastic nodule and identifies the cells as of B-cell nature. B, CD3 stain shows a rim of non-neoplastic T cells around the follicles. C, CD21 stain shows a large number of dendritic follicular cells within the neoplastic follicle. D, BCL2 stains the B cells within the germinal centers. (Courtesy of Dr. Glauco Frizzera, New York, NY, USA.) Figure 37.74 Blood smear from a patient with follicular lymphoma showing a so-called notched nucleus cell or buttock cell Figure 37.75 A and B, Follicular lymphoma with deposition of protein-aceous material among the tumor cells. Ultrastructurally, some of this material was found to be within the cytoplasm of dendritic follicular cells Figure 37.76 Follicular lymphoma featuring signet ring changes in some of the tumor cells Figure 37.77 So-called floral variant of follicular lymphoma which refers to the flower-like pattern of the expanded, disrupted neoplastic follicles Figure 37.78 Follicular lymphoma showing rosette formation by some of the lymphoid cells Figure 37.79 Mantle cell lymphoma surrounding a small residual germinal center Figure 37.80 High-Power View of Mantle Cell Lymphoma. There are subtle abnormalities of the nuclear contours, the appearance being intermediate between that seen in small cleaved follicular lymphoma and that of small lymphocytic lymphoma. Note the individual epithelioid histiocytes that are characteristically associated with this disorder Figure 37.81 So-Called Blastoid Variant of Mantle Cell Lymphoma. A, Hematoxylin-eosin-stained section showing high mitotic activity. B, A high percentage of the tumor cells show nuclear immunoreactivity for MIB-1 Figure 37.82 Immunoreactivity for cyclin D1 in mantle zone lymphoma Figure 37.83 Gross appearance of lymph nodes involved by non-Hodgkin lymphoma of diffuse large B-cell type. The nodes are enlarged and show a homogeneous tan cut surface Figure 37.84 Medium- (A) and high-power (B) views of diffuse large B-cell lymphoma with large cleaved cells Figure 37.85 Medium- (A) and high-power (B) views of diffuse large B-cell lymphoma with immunoblastic features Figure 37.86 Marked sclerosis and hyalinization in diffuse large B-cell lymphoma Figure 37.87 Myxoid stromal change in diffuse large B-cell lymphoma. This is an exceptional occurrence Figure 37.88 A and B, Large B-cell lymphoma with a sinus pattern of growth that simulates a metastatic tumor Figure 37.89 T-Cell/Histiocyte-Rich Large B-Cell Lymphoma. A, hematoxylin-eosin; B, membrane and Golgi-type immunoreactivity for CD20 in the large tumor cells Figure 37.90 The neoplastic cells of this case of plasmablastic lymphoma have fairly fine nuclear chromatin with abundant eosinophilic cytoplasm and a high mitotic rate Figure 37.91 ALK-Positive Large B Cell Lymphoma. A, The large atypical cells cluster and may mimic metastatic carcinoma. B, the neoplastic cells demonstrate ALK expression Figure 37.92 HHV+ DLBCL, NOS Arising in a Patient With Castleman Disease. A, The lymphoma cells surround the upper left portion of the typical Castleman germinal center. B, The cells have morphologic features similar to plasmablastic lymphoma but were HHV8 positive and EBV negative. C, The lymph node capsule also showed a focus of Kaposi sarcoma Figure 37.93 Burkitt lymphoma with characteristic starry sky appearance Figure 37.94 Presence of EBV genome in Burkitt lymphoma, as dem- onstrated with in situ hybridization for EBER Figure 37.95 High-Grade B-Cell Lymphoma With MYC and BCL2 Rearrangements. The morphologic features are intermediate between diffuse large B-cell lymphoma and Burkitt lymphoma. The presence of a so-called double hit of the two translocations confirms this diagnosis Figure 37.96 Polymorphic lymphoproliferative process associated with necrosis in lymph node of a renal transplant patient. There was evidence of active EBV infection Figure 37.97 Monomorphic posttransplant lymphoproliferative disorder (diffuse large B-cell lymphoma) in a recipient of a renal transplant Figure 37.98 Lymph Node Involvement by Angioimmunoblastic T-Cell Lymphoma. A, Low-power view showing a moderate effacement of the architecture by a polymorphic infiltrate composed of lymphocytes, plasma cells, and histiocytes. There is also marked vascular proliferation. B and C, The PAS stain highlights the prominence of the postcapillary venules. D, Atypical lymphoid cells are present in this polymorphic infiltrate, often with clusters of cells with clear cytoplasm. There are also scattered eosinophils Figure 37.99 Angioimmunoblastic T-cell lymphoma with a uniform proliferation of large neoplastic lymphoid cells Figure 37.100 Anaplastic Large Cell Lymphoma. A, Packing of the peripheral sinus. B, Vascular involvement Figure 37.101 So-called lymphohistiocytic variant of anaplastic large cell lymphoma with only scattered, large neoplastic cells Figure 37.102 Strong membranous and Golgi-type immunoreactivity for CD30 in anaplastic large cell lymphoma Figure 37.103 ALK immunoreactivity in anaplastic large cell lymphoma Figure 37.104 Gross appearance of follicular dendritic cell tumor Figure 37.105 Follicular Dendritic Cell Tumor of Lymph Node. A, The admixture of neoplastic cells with predominantly oval vesicular nuclei and non-neoplastic small lymphocytes results in an appearance reminiscent of thymoma. B, Prominent whorling in a case of follicular dendritic cell tumor, engrafted upon Castleman disease Figure 37.106 Electron Microscopic Appearance of Follicular Dendritic Cell Tumor. A characteristic feature is the presence of well-developed cytoplasmic prolongations joined by desmosomes Figure 37.107 Immunoreactivity of the cells of Langerhans cell histiocytosis for langerin Figure 37.108 Lymph Node Involvement by Langerhans Cell Histiocytosis. A, The infiltrate has a predominantly sinus distribution. B, High-power view showing mononuclear and multinucleated Langerhans cells. There are also numerous eosinophils Figure 37.109 Low-power (A) and medium-power (B) views of nodal hemangioma Figure 37.110 Lymph Node Involvement by Bacillary Angiomatosis. An intense vascular proliferation featuring epithelioid endothelial cells is seen in the interfollicular region, accompanied by neutrophils and other inflammatory cells Figure 37.111 A and B, Vascular transformation of lymph nodes. The process involves the sinuses, and it has a reactive appearance Figure 37.112 Solid Form of Vascular Transformation of Lymph Nodes. This process has also been designated as nodal angiomatosis. A, Predominantly sinus distribution of the lesions. B, Example in a retroperitoneal lymph node in a patient with renal cell carcinoma Figure 37.113 A and B, Lymph node involvement by Kaposi sarcoma. The infiltrate is predominantly in sinuses and is characterized by a proliferation of spindle cells forming slits containing red blood cells Figure 37.114 Angiosarcoma of Skin of Scalp Metastatic to a Posterior Cervical Lymph Node. The nodal lesion was the first manifesta- tion of the disease Figure 37.115 Medium-power (A) and high-power (B) views of lymph node involvement in systemic mastocytosis. Note the perfectly round shape of the centrally located nuclei, the finely granular cytoplasm, and the well-defined cell membranes Figure 37.116 Lymph Node Involved by Acute Myeloid Leukemia (Myeloid Sarcoma). A, The infiltrate is medium in size with irregular nuclear contours but fine nuclear chromatin. B, The cells express the myeloid-associated antigen CD33 Figure 37.117 Scattered Megakaryocytes in Lymph Node Involved by Extramedullary Hematopoiesis. These elements should not be confused with Reed-Sternberg cells or carcinoma cells Figure 37.118 Hemorrhagic Spindle Cell Tumor With Amianthoid Fibers. A, Prominent deposition of "amianthoid" collagen throughout the tumor. B, The admixture of neoplastic spindle cells and extravasated red blood cells results in a Kaposi sarcoma-like appearance Figure 37.119 Inflammatory Pseudotumor of Lymph Node. A, Low- power appearance showing partial effacement of architecture and expansion of the sinusal and perinodal regions by a reactive proliferation. B, High-power view showing a polymorphic infiltrate composed of lymphocytes, plasma cells, and myofibroblasts Figure 37.120 Inflammatory Pseudotumor of Lymph Node Due to Mycobacterium avium-Intracellulare Infection in an HIV-Infected Patient. A, Low-power view, showing spindle cell admixed with lym- phocytes. B, High-power view. C, Acid-fast stain Figure 37.121 Anthracosilicotic Nodules in Mediastinal Lymph Node. When florid, these changes may acquire pseudoneoplastic features Figure 37.122 Salivary Gland Inclusion Composed of Ductal Struc- tures in a High Cervical Lymph Node. This is a very common occurrence Figure 37.123 Pelvic Lymph Node Involved by Endosalpingiosis. Glands lined by cuboidal cells with a müllerian appearance and lacking atypical figures are present in the capsule of the node Figure 37.124 Nevus Cells in the Capsule of an Axillary Lymph Node. These inconsequential formations should not be mistaken for metastatic melanoma or metastatic carcinoma Figure 37.125 A and B, Blue nevus involving lymph node capsule Figure 37.126 A-C, Large B-cell lymphoma that has undergone massive infarct-type necrosis. A, The outlines of the tumor cells can still be discerned. B, A totally necrotic area, indistinguishable from that of a "benign" infarct. C, There is a remarkable degree of retained immuno- reactivity for CD20 in the necrotic area Figure 37.127 Hyaline Deposits in Pelvic Lymph Node. This change is of no clinical significance Figure 37.128 Low-power (A) and medium-power (B) appearances of silicone lymphadenitis. The sinuses are massively expanded by a histiocytic infiltrate, which simulates the appearance of Rosai-Dorfman disease Figure 37.129 A and B, Lymph node changes in a patient who had a prosthesis implanted in the joint drained by this node. A fine particulate black material can be appreciated in the high-power view. It is easy to dismiss this material as "dirt." Figure 37.130 A and B, Lymph node involved by metastatic mesothe- lioma. The tumor massively expands the sinuses and is composed of cuboidal cells with a central nucleus and acidophilic cytoplasm. The primary tumor was located in the peritoneal cavity Figure 37.131 Hyperplastic Mesothelial Cells in Lymph Node. A, Sinusal distribution. B, Bland cytologic appearance. C, Strong immunoreactivity for keratin. Ker, Keratin Figure 37.132 Alveolar Rhabdomyosarcoma Metastatic to a Lymph Node. This is a relatively common occurrence in this tumor type, and it may be the first clinical manifestation of the disease Figure 37.133 Lymph Node Involved by Metastatic Lymphoepi- thelioma From the Nasopharynx. The relatively diffuse pattern of the proliferation may result in a mistaken diagnosis of malignant lymphoma Figure 37.134 Breast Carcinoma of Lobular Type Metastatic to the Sinuses of a Lymph Node. The cytologic appearance may be confused with that of a malignant lymphoma or a benign histiocytic proliferation Figure 37.135 Poorly Differentiated Adenocarcinoma With Signet Ring Features Initially Misinterpreted as a Malignant Lymphoma. The mistake may have been partially induced by the fact that the tumor developed in a renal transplant recipient. A, Hematoxylin-eosin. B, Mucicarmine stain, showing a few droplets of intracytoplasmic mucin Figure 37.136 Balloon cell melanoma metastatic to a lymph node and simulating a histiocytic disorder Figure 37.137 Squamous Cell Carcinoma Metastatic to Lymph Node.The tumor has undergone partial cystic transformation Figure 37.138 Squamous Cell Carcinoma Metastatic to Cervical Lymph Node. A, Medium-power view, showing marked cystic change that may result in a mistaken diagnosis of branchial cleft cyst. B, High-power view showing malignant cytologic features involving the entire thickness of the epithelial strip
