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Axillary lymph node status is an important factor for staging and treatment planning in breast cancer. Our study was performed in vitro on a node-by-node basis to evaluate the ability of B-mode ultrasonographic images to distinguish metastatic from nonmetastatic nodes. Immediately prior to histologic examination, individual dissected axillary nodes were scanned in a water bath using a 10 MHz B-mode ultrasonographic transducer. Four B-mode features (size, circularity, border demarcation, and internal echo) were evaluated for their ability to distinguish metastatic from nonmetastatic lymph nodes. Lymph node metastasis was indicated by (1) a large size (i.e., a length of the longest axis of 10 mm or greater); (2) a circular shape (i.e., the ratio of the shortest axis to the longest axis between 0.5 and 1.0); (3) a sharply demarcated border compared with surrounding fatty tissue; and (4) a hypoechoic internal echo, with obliteration of the fatty hilum. The sensitivity and specificity were compared for all combinations of features. We examined 84 histologically characterized axillary nodes from 27 breast cancer patients, including 64 nonmetastatic and 20 metastatic nodes. Of the criteria cited, circular shape was the best single feature for distinguishing metastatic from nonmetastatic nodes (sensitivity, 65%; specificity, 73%). The best combination of sensitivity (85%) and specificity (73%) was obtained using the criterion that a lymph node contained cancer when at least three positive features were present. The present in vitro study demonstrated that the sensitivity and specificity of B-mode ultrasonography for diagnosing lymph node metastasis were lower than 90%. Therefore, B-mode ultrasonography may not be an optimal noninvasive screening method for diagnosing axillary lymph node metastasis in breast cancer patients, particularly under in vivo clinical conditions.

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Axillary lymph node status is of particular importance for staging and managing breast cancer. Currently, axillary lymph node dissection is performed routinely in cases of invasive breast cancer because of the lack of accurate noninvasive methods for diagnosing lymph node metastasis. We investigated the diagnostic ability of ultrasonic tissue characterization based on spectrum analysis of backscattered echo signals to detect axillary lymph node metastasis in breast cancer in vitro compared with in vitro B-mode imaging. Immediately after surgery, individual lymph nodes were isolated from axillary tissue. Each lymph node was scanned in a water bath using a 10-MHz instrument, and radio frequency data and B-mode images were acquired. Spectral parameter values were calculated, and discriminant analysis was performed to classify metastatic and nonmetastatic lymph nodes. Forty histologically characterized axillary lymph nodes were enrolled in this study, including 25 nonmetastatic and 15 metastatic lymph nodes. A significant difference existed in the spectral parameter values (slope and intercept) for metastatic and nonmetastatic lymph nodes. Spectral parameter-based discriminant function classification of metastatic vs. nonmetastatic lymph nodes provided a sensitivity of 93.3%, specificity of 92.0%, and overall accuracy of 92.5%. In comparison, B-mode ultrasound images of in vitro lymph nodes provided a sensitivity of 73.3%, specificity of 84.0%, and overall accuracy of 80.0%. Receiver operating characteristic (ROC) analysis comparing the efficacy of both methods gave an ROC curve area of 0.9888 for spectral methods, which was greater than the area of 0.8980 for B-mode ultrasound. Hence, this in vitro study suggests that the diagnostic ability of spectrum analysis may prove to be markedly superior to that of B-mode ultrasound in detecting axillary lymph node metastasis in breast cancer. Because of these encouraging results, we intend to conduct an investigation of the ability of spectral methods to classify metastatic axillary lymph nodes in vivo.

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Lymph node involvement is one of the major factors affecting the prognosis of colorectal cancer. Various imaging methods, including ultrasound and computed tomography, are not sufficiently sensitive or specific for reliably determining lymph node involvement. We investigated the feasibility of using ultrasonic tissue characterization (UTC) based on spectrum analysis of backscattered echo signals for diagnosing lymph node metastasis of colorectal cancer in vitro. Forty lymph nodes, including 17 metastatic and 23 nonmetastatic nodes, from 11 colorectal cancer operations were investigated. Lymph nodes were scanned using a clinical instrument; B-mode imaging was performed for each lymph node, and radiofrequency (RF) data were acquired. The UTC parameters, slope and intercept, were calculated from the normalized power spectrum of the backscattered echo signals from each lymph node. The mean values of UTC parameters of metastatic and nonmetastatic lymph nodes were compared. The accuracy of UTC in distinguishing metastatic from nonmetastatic lymph nodes was calculated using discriminant analysis. Receiver operating characteristic (ROC) analysis was performed to compare the classification efficacy of UTC and B-mode ultrasound. UTC parameters demonstrated a significant difference in parameter values between metastatic and nonmetastatic lymph nodes. The overall accuracy in diagnosing the lymph node metastasis was 87.5% for UTC and 77.5% for B-mode ultrasound. ROC analysis produced an ROC curve area of 0.92 or 0.89 for UTC (depending on the performance-assessment algorithm) and 0.84 for B-mode ultrasound, which indicated that UTC performed markedly better than B-mode ultrasound in diagnosing metastatic lymph nodes. The advantages of UTC over conventional B-mode ultrasound in discriminating metastatic lymph nodes from nonmetastatic lymph nodes are extremely encouraging, and warrant an in vivo UTC study.

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In a study of 7498 American men of Japanese ancestry in Hawaii, 26 incident cases of leukemia or non-Hodgkin's lymphoma were identified after a follow-up period of 19 years. Two of the cases, who were brothers, were diagnosed with adult T-cell leukemia/lymphoma (ATL). Both of these brothers had human T-cell lymphotropic virus type I (HTLV-I) antibodies in their stored serum which were obtained 4 and 18 years before diagnosis. None of the 24 patients with other hematologic malignancies or the 26 matched controls were HTLV-I antibody positive. This finding lends further support for a role of HTLV-I in the etiology of adult T-cell leukemia/lymphoma.

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Concomitant strongyloidiasis and human T-cell lymphotropic virus type I (HTLV-I) infection has been reported from areas in Japan where both organisms are endemic. We present four cases of concomitant infection with these organisms from an area that is not endemic for Strongyloides stercoralis. Three of the four patients had adult T-cell leukemia, an aggressive neoplasm resulting from HTLV-I infection, while the other was an asymptomatic carrier of HTLV-I. Three of the patients had spent their childhoods in an endemic location for both organisms, suggesting an initial infection at that time. Three patients were symptomatic from their parasitism. We conclude that strongyloidiasis may be found in nonendemic locations in patients with either adult T-cell leukemia or an asymptomatic HTLV-I carrier state. Whether infestation with this parasite contributes to the leukemogenesis of HTLV-I, as postulated by others, cannot at this time be determined.

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A retrospective morphologic survey (1973-1983) of 146 cases of malignant lymphoma among the Hawaii-Japanese (migrant Japanese and their offspring) was conducted to determine whether differences in the incidence and cytologic types of malignant lymphoma exist when compared to those of native Japanese (lifetime residents of Japan). The age-adjusted incidence rates for malignant lymphoma among the Hawaii-Japanese were similar to rates for U.S. whites. However, higher rates for follicular centre cell (FCC) lymphoma with a follicular pattern were observed in the Hawaii-Japanese population when compared with rates for native Japanese. On the basis of the cytologic types of the Lukes-Collins classification, non-Hodgkin's lymphomas among the Hawaii-Japanese resembled those of Western countries, rather than those of Japan. B-cell lymphomas predominated (72 per cent), while T-cell types comprised 23 per cent of cases. Follicular centre cell types were encountered most often (59 per cent), and the small cleaved FCC subtype was the most common (30 per cent). The high degree of follicularity (29 per cent) was at variance with the consistently low rates reported in Japan. This may be explained, in part, by higher rates of nodal lymphomas among the Hawaii-Japanese. Of the T-cell lymphomas, diffuse large cell types (T-cell immunoblastic sarcoma, T-IBS), often with cytologic pleomorphism, were relatively frequently encountered (16 per cent), and comprised 15 per cent of non-Hodgkin's lymphomas; this observation necessitates special clinical and epidemiologic consideration in view of the large Japanese migration to Hawaii from HTLV-I endemic regions of southern Japan. No registered cases of non-Hodgkin's lymphoma or of Hodgkin's disease were documented in Hawaii-Japanese subjects under the age of 15 years. The age-adjusted incidence rates for Hodgkin's disease among the Hawaii-Japanese were similar with those of native Japanese. Nodular sclerosis was the most frequent histologic subtype. The difficulty in distinguishing between Hodgkin's disease and non-Hodgkin's lymphoma, particularly when immunologic cell surface markers are not available, is addressed. Low rates for chronic lymphocytic leukemia among the Hawaii-Japanese were confirmed. Not one well-documented case was identified in the 11-year period surveyed.

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Adult T-cell leukemia-lymphoma (ATLL) is a distinct clinicopathologic entity etiologically linked to HTLV-I infection. We have identified five cases of retrovirus-associated ATLL among Hawaii-born first generation offspring (nisei) of migrant Japanese. Four patients were offspring of migrant Japanese (issei) who emigrated to Hawaii from Okinawa, an HTLV-I endemic area. The fifth patient was born of parents who emigrated to Hawaii from Fukushima and Miyagi prefectures, HTLV-I nonendemic areas. Epidemiologic implications and family studies with regard to HTLV-I antibody testing of the index cases are discussed. The high rate of HTLV-I antibody seropositivity among family members and relatives indicates that the risk of acquiring HTLV-I infection and of developing ATLL persists long after migration. Documentation of ATLL among offspring of Japanese immigrants to Hawaii is an important observation because it confirms the potential for long latency between putative exposure to virus and the development of overt disease. Changing marriage patterns among the Hawaii-Japanese may weaken the risk of vertical virus transmission to the descendents of migrants from southern Japan, while increasing the risk to children born of mixed marriages. In addition, blood products derived from high-risk donors will constitute a continuing hazard if they are not subject to screening.

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Adult T-cell leukemia (ATL) is a disease found endemic in Southern Japan and the Caribbean basin. The human T-cell leukemia virus I (HTLV-I) has been implicated epidemiologically as the causative agent in this disease. This paper describes the identification of this disease in Hawaii in a second generation immigrant from Southern Japan. The disease was initially indolent, then clinically explosive, characterized by cutaneous lesions, leukemic lymphocytes with convoluted nuclei of T-cell phenotype, hypercalcemia, and a terminal infection.

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The histological features of a distinctive follicular hyperplasia observed in twenty-nine male patients with AIDS or the AIDS related complex are described. The group includes four patients with Kaposi's sarcoma, five with lymphoma, 16 with persistent generalized lymphadenopathy, and four with hemophilia. Histopathology is correlated with lymphocyte phenotyping and clinical findings and a model for the pathogenesis of this unique syndrome is presented.

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Multiparameter studies of an unusual patient exhibiting cutaneous manifestations of both mycosis fungoides and Sezary's syndrome are presented. The neoplastic cells of dermal and nodal infiltrates and peripheral blood expressed both helper and suppressor immunologic phenotypes. Cytofluorographic analysis of cells isolated from lymph node and peripheral blood showed a population of neoplastic cells that were stained with the monoclonal antibodies OKT 3, 4, 8, and 11. Immunoperoxidase staining of frozen sections with monoclonal antibodies Leu 1, 2, and 3 provided a topographical identification of an identically marking population of cells in dermis and lymph node. In light of current models depicting normal T-cell lineage, the authors suggest that the neoplastic population in this patient, expressing both helper and suppressor phenotypes, reflected a phenotypic stage of immunologic maturation (OKT 6-, OKT 10-, OKT 3+, OKT 11+, OKT 4+, OKT 8+) in which the neoplastic cells had not yet segregated into distinctive T-cell subsets. While excess helper activity was suggested by serum hypergammaglobulinemia, in vitro helper and suppressor function was not determined. The range of studies employed illustrates the wide variety of technics required to adequately characterize complex clinico-immunopathologic disorders, as represented by this case, and the wealth of information that can be gleaned.

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Lymph nodes from 13 cases of reactive hyperplasia were examined with four different monoclonal antibodies to B cells. B-1 recognizes an antigen of 30,000 daltons on B cells. CB-2 was prepared with normal spleen and binds to a glycolipid. BA-1 labels surface immunoglobulin-positive cells, but not T lymphocytes or monocytes. B-532 recognizes an antigenic determinant of 45,000 daltons. Using the immunoperoxidase method on frozen sections of reactive lymph nodes, the staining patterns of these four unique antibodies showed dramatic differences. B-1 labeled 80%-90% of the germinal center cells and 10%-50% of the mantle region. Few interfollicular cells were positive. CB-2 stained predominantly in the mantle area (50%-90% positive cells), with moderate staining in the germinal center as well and less than 1% positive cells in the diffuse cortex. BA-1 exhibited predominant labeling in the mantle (50%-90%), with little staining in the germinal center. A large number of cells in the interfollicular, subcapsular, and medullary regions expressed the BA-1 antigen. The B-5 antibody demonstrated intense staining in the follicle (50%-95%). This staining often appeared to be polarized within the germinal center. The mantle zone demonstrated staining of 30%-50% of the cells. The different staining patterns of the B-cell antibodies, as demonstrated by the in situ distribution of positive cells within the lymph node, may reflect stages of development or activation of the B-cell population.

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This is a report of the finding of a T-cell subpopulation bearing T-helper cells and Ia antigens in specimens of skin from patients with mycosis fungoides and the Sézary syndrome. Frozen sections of skin tissue from eight patients examined with monoclonal antibodies against mature T-cells, helper T-cells, suppressor T-cells, and Ia antigens exhibited similar staining patterns by a modified immunoperoxidase method. Antibodies against mature T-cells and helper T-cells stained 70-80% of the lymphocytes in the dermis. The antibody defining the phenotype of suppressor T-cells labelled 5-10% of the lymphocytes scattered throughout the lesions. Eighty to 90% of the lymphocytes took the stain for Ia antigen. Anti-thymocyte antibody (OKT6) stained cells in both the epidermis and dermis of the specimens. Of nonmalignant conditions examined, lesions from five cases of lichen planus exhibited a quantitatively different staining pattern than that of mycosis fungoides in that the number of T-helper cells was about equal to the number of T-suppressor cells. The findings reported are evidence for a homogeneous population of T-helper, Ia-positive lymphocytes in the cutaneous lesions of mycosis fungoides and the Sézary syndrome.

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Leukemic cells of bone marrow and peripheral blood showing clusters of distinctive, large, uniform, rounded intracytoplasmic inclusions were found in a patient who had acute lymphoblastic leukemia. These membrane-bound inclusions ranged from 0.8 to 1.4 microgram in diameter and were clearly demonstrated on routinely stained preparations. Electron microscopy disclosed transitions between well-developed mitochondria and the electron-dense structures. The functional significance of these presumably altered mitochondria is uncertain. Whorled lamellar internal structures, in occasional fingerprintlike arrangements, may represent duplication of mitochondrial cristae and, functionally, may reflect increased metabolic rate or otherwise abnormal metabolism. Cytochemical studies demonstrated the presence of both periodic acid-Schiff positivity and nonspecific esterase activity in these inclusions, but no peroxidase or acid phosphatase was found. These findings support the lymphoid nature of the disorder. Immunologic surface membrane markers are consistent with this case being, as with the majority of acute lymphoblastic leukemias, of non-B, non-T cell type. Cytogenetic studies on cultured leukemic cells from bone marrow and peripheral blood showed a consistently abnormal karyotype associated with the presence of an XXY chromosomal constitution. Since no other tissues (e.g., dermal fibroblasts) were examined, the diagnosis of Klinefelter's syndrome cannot be confirmed. A causal relationship between the coexistence of the abnormal karyotype and the acute leukemia was not proven but was suspected.

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