Neoplasms of mature T-cells or NK-cells

Adult T-cell leukemia/

lymphoma

Helper T-cell expressing CD25

(IL-2 receptor)

HTLV-1 provirus present in tumor cells Adults with cutaneous lesions, marrow involvement, and

hypercalcemia; Japan, West Africa, and the Caribbean;

aggressive

Anaplastic large cell

lymphoma

Cytotoxic T-cell Rearrangements of ALK Children and young adults, usually with lymph node and soft

tissue disease; aggressive

Extranodal NK/T cell

lymphoma

Natural killer cell (common) or

cytotoxic T-cell (rare)

No specific chromosomal abnormality; uniformly EBV

associated

Adults with destructive extranodal masses, most commonly

sinonasal; often accompanied by hemophagocytic syndrome;

aggressive

Mycosis fungoides/Sézary

syndrome

Helper T-cell No specific chromosomal abnormality Adult patients with cutaneous patches, plaques, nodules, or

generalized erythema; indolent

T-cell granular

lymphocytic leukemia

Two types: (1) CD8+ T-cell, (2)

NK-cell

No specific chromosomal abnormality Adult patients with splenomegaly, neutropenia, and anemia,

sometimes, accompanied by autoimmune disease

Hodgkin lymphoma

Hodgkin lymphoma,

lymphocyte-depletion

subtype

Germinal center or postgerminal

center B-cell

No specific chromosomal abnormality; >70% EBV

associated

More common in the elderly and in HIV+ individuals;

moderately aggressive

Hodgkin lymphoma,

lymphocyte-predominance

subtype

Germinal center B-cell No specific chromosomal abnormality; not associated

with EBV

Young to middle-aged males with cervical or axillary

lymphadenophathy; indolent

Hodgkin lymphoma,

lymphocyte-rich subtype

Germinal center or postgerminal

center B-cell

No specific chromosomal abnormality; 40% EBV

associated

More common in males, usually presents with

lymphadenopathy; moderately aggressive

Hodgkin lymphoma,

mixed cellularity subtype

Postgerminal center memory Bcell

No specific chromosomal abnormality; 70% EBV

associated

More common in males, usually presents with

lymphadenopathy; moderately aggressive

Hodgkin lymphoma,

nodular sclerosing subtype

Germinal center or postgerminal

center B-cell

No specific chromosomal abnormality; rarely EBV

associated

Commonly presents as a mediastinal mass in young females;

moderately aggressive

Figure 14-5 A, Acute lymphoblastic leukemia/lymphoma. Lymphoblasts with condensed nuclear chromatin, small nucleoli, and scant agranular cytoplasm. B and C represent the

phenotype of the ALL shown in A, analyzed by flow cytometry. B, Note that the lymphoblasts represented by the red dots express TdT and the B-cell marker CD22. C, The same cells are

positive for two other markers, CD10 and CD19, commonly expressed on pre-B lymphoblasts. Thus, this is a pre-B cell ALL. (A, courtesy of Dr. Robert W. McKenna; B and C, courtesy of

Dr. Louis Picker, Oregon Health Science Center, Portland, OR.)

Figure 14-6Small lymphocytic lymphoma/chronic lymphocytic leukemia (lymph node). A, Low-power view shows diffuse effacement of nodal architecture. B, At high power, the

majority of the tumor cells are small round lymphocytes. A "pro-lymphocyte," a larger cell with a centrally placed nucleolus, is also present in this field (arrow). (A, courtesy of Dr. José

Hernandez, Department of Pathology, University of Texas Southwestern Medical School, Dallas, TX.)

Figure 14-7Chronic lymphocytic leukemia. This peripheral blood smear is flooded with small lymphocytes with condensed chromatin and scant cytoplasm. A characteristic finding is the

presence of disrupted tumor cells (smudge cells). A coexistent autoimmune hemolytic anemia (see Chapter 13 ) explains the presence of spherocytes (hyperchromatic, round erythrocytes).

A nucleated erythroid cell is present in the lower left-hand corner of the field. In this setting, circulating nucleated red cells could stem from premature release of progenitors in the face of

severe anemia, marrow infiltration by tumor (leukoerythroblastosis), or both. (Courtesy of Dr. Jacqueline Mitus, Brigham and Women's Hospital, Boston, MA.)

Figure 14-8Small lymphocytic lymphoma/chronic lymphocytic leukemia (liver). Low-power view of a typical periportal lymphocytic infiltrate. (Courtesy of Dr. Mark Fleming,

Department of Pathology, Brigham and Women's Hospital, Boston, MA.)

Figure 14-9Follicular lymphoma (lymph node). A, Nodular aggregates of lymphoma cells are present throughout lymph node. B, At high magnification, small lymphoid cells with

condensed chromatin and irregular or cleaved nuclear outlines (centrocytes) are mixed with a population of larger cells with nucleoli (centroblasts). (A, courtesy of Dr. Robert W.

McKenna, Department of Pathology, University of Texas Southwestern Medical School, Dallas, TX.)

Figure 14-10Follicular lymphoma (spleen). Prominent nodules represent white pulp follicles expanded by follicular lymphoma cells. Other indolent B-cell lymphomas (small lymphocytic

lymphoma, mantle cell lymphoma, marginal zone lymphoma) can produce an identical pattern of involvement. (Courtesy of Dr. Jeffrey Jorgenson, Department of Pathology, Brigham and

Women's Hospital, Boston, MA.)

Figure 14-11BCL2 expression in reactive and neoplastic follicles. BCL2 protein was detected by using an immunohistochemical technique that produces a brown stain. In reactive

follicles (A), BCL2 is present in mantle zone cells but not follicular center B cells, whereas follicular lymphoma cells (B) exhibit strong BCL2 staining (Courtesy of Dr. Jeffrey Jorgenson,

Department of Pathology, Brigham and Women's Hospital, Boston, MA.)

Figure 14-12Diffuse large B-cell lymphoma. Tumor cells have large nuclei, open chromatin, and prominent nucleoli. (Courtesy of Dr. Robert W. McKenna, Department of Pathology,

University of Texas Southwestern Medical School, Dallas, TX.)

Figure 14-13Diffuse large B-cell lymphoma (spleen). The presence of an isolated large mass is typical. In contrast, indolent B-cell lymphomas usually produce multifocal expansion of

white pulp (see Fig. 14-10 ). (Courtesy of Dr. Mark Fleming, Department of Pathology, Brigham and Women's Hospital, Boston, MA.)

Figure 14-14Burkitt lymphoma. A, At low power, numerous pale tingible body macrophages are evident, producing a "starry sky" appearance. B, At high power, tumor cells have multiple

small nucleoli and high mitotic index. The lack of significant variation in nuclear shape and size lends a monotonous appearance. (B, courtesy of Dr. José Hernandez, Department of

Pathology, University of Texas Southwestern Medical School, Dallas, TX.)

Figure 14-15Multiple myeloma of the skull (radiograph, lateral view). The sharply punched-out bone lesions are most obvious in the calvarium.

Figure 14-16Multiple myeloma (bone marrow aspirate). Normal marrow cells are largely replaced by plasma cells, including forms with multiple nuclei, prominent nucleoli, and

cytoplasmic droplets containing immunoglobulin.

Figure 14-17 M protein detection, multiple myeloma. Serum protein electrophoresis (SP) is used to screen for a monoclonal immunoglobulin (M protein). Polyclonal IgG in normal serum

(denoted by the arrow) appears as a broad band; in contrast, serum from a patient with multiple myeloma contains a single sharp protein band in this region of the electropherogram. The

suspected monoclonal immunoglobulin is confirmed and characterized by immunofixation. In this procedure, proteins separated by electrophoresis within a gel are reacted with specific

antisera. After extensive washing of the gel, only proteins that are cross-linked by antisera are retained. These are detected with a protein stain. Note the sharp band in the immunoglobulin

region of the patient SP that is recognized by antisera against IgG heavy chain (G) and kappa light chain (k), indicating the presence of a IgGk M protein. Levels of polyclonal IgG, IgA

(A), and lambda light chain (l) are also decreased in the patient serum relative to normal, a common finding in multiple myeloma. (Courtesy of Dr. David Sacks, Department of Pathology,

Brigham and Women's Hospital, Boston, MA.)

Figure 14-18Lymphoplasmacytic lymphoma. Bone marrow biopsy shows a characteristic mixture of small lymphoid cells exhibiting various degrees of plasma cell differentiation. In

addition, a mast cell with purplish-red cytoplasmic granules is present at the left-hand side of the field.

Figure 14-19Mantle cell lymphoma. A, At low power, neoplastic lymphoid cells surround a small, atrophic germinal center, exhibiting a mantle zone pattern of growth. B, High-power

view shows a homogeneous population of small lymphoid cells with somewhat irregular nuclear outlines, condensed chromatin, and scant cytoplasm. Large cells resembling

prolymphocytes (seen in chronic lymphocytic leukemia) and centroblasts (seen in follicular lymphoma) are absent.

Figure 14-20Hairy cell leukemia (peripheral blood smear). A, Phase-contrast microscopy shows tumor cells with fine hairlike cytoplasmic projections. B, In stained smears, these cells

have round or folded nuclei and modest amounts of pale-blue, agranular cytoplasm. (Courtesy of Dr. David Weinberg, Department of Pathology, Brigham and Women's Hospital, Boston,

MA.)

Figure 14-21Peripheral T-cell lymphoma, unspecified (lymph node). A spectrum of small, intermediate, and large lymphoid cells, many with irregular nuclear contours, is seen.

Figure 14-22Anaplastic large cell lymphoma. A, Several "hallmark" cells with horseshoe-like or "embryo-like" nuclei and abundant cytoplasm lie near the center of the field. B,

Immunohistochemical stain demonstrating expression of ALK protein. (Courtesy of Dr. Jeffrey Kutok, Department of Pathology, Brigham and Women's Hospital, Boston, MA.)

Figure 14-23Reed-Sternberg cells and variants. A, Diagnostic Reed-Sternberg cell, with two nuclear lobes, large inclusion-like nucleoli, and abundant cytoplasm, surrounded by

lymphocytes, macrophages, and an eosinophil. B, Reed-Sternberg cell, mononuclear variant. C, Reed-Sternberg cell, lacunar variant. This variant is characteristic of the nodular sclerosis

subtype. It has a folded or multilobated nucleus lying within a clear space created by disruption of its cytoplasm during processing and cutting of the tissue. D, Reed-Sternberg cell,

lymphohistiocytic (L&H) variant. Several such variants are present with complex nuclear irregularities, small nucleoli, fine chromatin, and abundant pale cytoplasm. (A, courtesy of Dr.

Robert W. McKenna, Department of Pathology, University of Texas Southwestern Medical School, Dallas, TX.)

TABLE 14-5-- Clinical Staging of Hodgkin and Non-Hodgkin Lymphomas (Ann Arbor Classification)

Date: 2016-04-22; view: 731