BACKGROUND:Carcinoma of the breast infrequently presents initially as axillary adenopathy. In such cases, after biopsy proves the presence of metastatic carcinoma, the primary tumor generally is assumed to be in the ipsilateral breast, despite negative mammographic findings and the lack of a clinically palpable breast mass.METHODS:The authors recently studied a case of a 50-year-old woman in whom recurrent neuroendocrine carcinoma of the breast presented as a contralateral axillary lymph node metastasis. After mastectomy ipsilateral to the metastasis proved negative for tumor, a histologic comparison of the previous contralateral tumor with that in the lymph node was performed, followed by biopsy of the clinically and mammographically negative original lumpectomy site.RESULTS:Histologic and immunohistochemical studies proved that the original, metastatic, and locally recurrent tumors were identical, sharing unusual neuroendocrine features. The patient is currently disease free after chemotherapy.CONCLUSION:Contralateral mammary carcinoma should be considered in the workup of a patient who presents with evidence of an axillary lymph node metastasis. Locally recurrent breast carcinoma may be clinically and mammographically occult. Histologic review of prior biopsy material and comparison with current tissue is essential in proper patient management.

Gold, J. E.; Itzkowitz, S. H.; Stevens, A.; Reddish, M.; Longenecker, B. M. Author Information

Article Tools Article Tools OPTIONS & TOOLS Export Citation Track Citation Add To Favorites Rights & Permissions COMPANION ARTICLES No companion articles ARTICLE CITATION DOI: 10.1200/JCO.1993.11.9.1836 Journal of Clinical Oncology - published online before print September 21, 2016 PMID: 8355052 Adoptively transferred anti-CD3-activated T cells for human tumor immunotherapy. J E GoldxJ E GoldSearch for articles by this author https://doi.org/10.1200/JCO.1993.11.9.1836 PDF "Adoptively transferred anti-CD3-activated T cells for human tumor immunotherapy.." Journal of Clinical Oncology, 11(9), pp. 1836–1837© 1993 by American Society of Clinical Oncology

Background. Lymphocytes that display a phenotype of mature B-cells, T-cells, natural killer (NK) cells, or a combination of T-cells and NK cells can be found in patients with lymphoproliferations that manifest as expansions of peripheral blood lymphocytes (PBL). If these PBL expansions exhibit clonality, they can be classified as chronic lymphocytic leukemia (CLL).Methods/Results. A patient who had two simultaneous, clonal lymphoproliferative disorders manifested as an unusual T-cell CLL in conjunction with systemic light chain amyloidosis is described. Gene rearrangement studies of the PBL of the patient showed clonal rearrangements of both the T-cell receptor beta (T(beta)) chain and the immunoglobulin genes. Additional immunologic and microscopic studies of the T-cells of the patient showed that they were large, agranular, CD4+ T-cells that also expressed the NK cell marker CD57. Cytogenetics disclosed an unusual karyotype in the PBL.Conclusions. The pathogenesis of this T-cell CLL and whether it truly represents a malignant disorder, as well as its relation to amyloidosis, is discussed.

Intermediate‐ and high‐grade B‐cell non‐Hodgkin lymphoma (NHL) occurring in a human immunodeficiency virus (HIV)‐infected patient is considered diagnostic of the acquired immunodeficiency syndrome (AIDS). Other neoplasms (both hematopoietic and nonhematopoietic) have also been reported in patients with HIV infection, although none except Kaposi sarcoma carries the same diagnosis of AIDS as B‐cell NHL in an HIV‐infected host. There have been previous reports in the literature of Hodgkin disease (HD) in HIV‐infected patients. We describe our clinical and pathological experience with HD from 1984–1989, in 18 patients with documented HIV infection and also review the literature on HD in HIV‐infected patients. Almost all patients described herein presented with advanced disease and mixed cellularity histology and did very poorly despite some good initial responses to therapy. By statistical analysis, we found that the patients with HIV‐associated HD had a strong tendency to be outside the age range seen in non‐HIV‐associated HD (P <0.005). We also discuss the possible relationship between HIV and HD and consider whether HIV‐associated HD, like B‐cell NHL, is a manifestation of AIDS.

Hodgkin's disease (HD) was diagnosed in 24 patients who were either seropositive for human immunodeficiency virus (HIV) (21) or members of a high-risk group (three), but had not developed acquired immune deficiency syndrome (AIDS). Clinical presentation of the disease was characterized by constitutional symptoms in all, especially fever (23/24) and disseminated disease (22/24) at diagnosis. Mediastinal adenopathy was rare. Bone marrow involvement was particularly frequent (12/24), and a positive bone marrow biopsy preceded lymph node biopsy in 5 of the 12. Histopathologic features of these tumors included an increased number of nonlymphoid stromal cells, i.e., histiocytic and/or fibroblastoid. In some tumors these fibrohistiocytoid stromal cells were arranged in bundles, but distinct nodule with birefringent collagen band formation was not observed. Twenty-two patients were treated, most with combination chemotherapy; one was untreated; one, unknown. Sixteen, including the one untreated, died with disease at 3 to 25 months; one died of an unrelated cause; four were alive at 3 to 24 months; three were lost to follow-up. Frequent bone marrow involvement at presentation suggests the usefulness of the bone marrow biopsy for diagnosis in subjects at risk, especially when they present with spiking fever of unknown origin. Contrary to most previous series, virtually all of our cases were of mixed cellularity type, characterized by increased fibrohistiocytoid stromal cells in place of depleting lymphocytes. The classic nodular sclerosing feature with birefringent collagen band formation was not observed. In conclusion, HIV-associated HD was characterized by advanced stage with fever at presentation, preponderance of mixed cellularity histologic type with increased fibrohistiocytoid stromal cells, and poor outcome. Hodgkin's disease in AIDS patients presents an intriguing biological model to study the role of stromal histiocytes in immunodeficient patients.

The development of malignant neoplasms in patients with the acquired immune deficiency syndrome (AIDS) or with a positive human immunodeficiency virus (HIV) antibody test is a well known phenomenon. According to the guidelines from the Centers for Disease Control (Atlanta, GA), the presence of intermediate-grade or high-grade B-cell non-Hodgkin's lymphoma in HIV antibody-positive patients is considered a diagnostic criterion for AIDS. The authors describe two cases of malignant plasma cell tumors in two young HIV-infected patients. In light of this and other reports of plasma cell tumors in patients at risk for AIDS or with a positive HIV antibody test, the finding of another manifestation of B-cell neoplasia in these patients may enlarge the spectrum of AIDS-related tumors.

Although the great majority of acute leukemias have been designated as being of lymphocytic or myelocytic origin, recent reports have described elements of both in some patients. We describe here the first case of hybrid acute leukemia in an HIV-antibody-positive patient as well as the first hybrid involving B-cell (Burkitt) acute lymphocytic leukemia and acute myelomonocytic leukemia proven by cytochemical, immunologic, and cytogenetic methods. This case illustrates the increasingly complex difficulties in the diagnosis and treatment of AIDS-related malignancies.

Marrow cytogenetic and granulocyte-macrophage colony formation (CFU-GM) studies were performed on 34 previously untreated patients with documented myelodysplastic syndromes seen between January 1978 and June 1982. All patients were managed without chemotherapy until progression to acute leukemia was observed. All 10 patients with exclusively abnormal marrow metaphases developed acute leukemia (100%) while only one (7%) of 14 patients with solely normal marrow metaphases subsequently developed leukemia (p less than 0.001). Three (42%) of the seven patients with both normal and abnormal marrow metaphases developed acute leukemia. Fifteen (86%) of the 19 patients with either large cluster or no growth patterns developed acute leukemia while only two (13%) of 15 patients with either small cluster or colony forming growth patterns developed acute leukemia (p less than 0.001). Abnormal marrow cytogenetic status correlated with abnormal marrow CFU-GM growth pattern (p less than 0.05). Analysis of CFU-GM sensitivity to inhibition by prostaglandin E was performed in 12 patients. Nine patients showed CFU-GM refractoriness to inhibition by prostaglandin E. Seven of these patients eventually developed leukemia. Three patients had CFU-GMs which were initially sensitive to prostaglandin E inhibition. In these three patients, a loss of CFU-GM sensitivity to prostaglandin E was observed prior to their progression to morphologically identifiable acute leukemia.