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Biomedical subjects

M E Kadin

Publications and source records attributed to M E Kadin.

At least 19 recordsLinked to original sources
PubMed1992

Epidemiology of lymphomatoid papulosis.

BACKGROUND: Lymphomatoid papulosis is a rare skin disease with malignant potential. Its epidemiology is largely unknown. METHODS: A case-control study of lymphomatoid papulosis was done to characterize the patient population and investigate the risk factors for its development. Fifty-seven patients with biopsy-proven lymphomatoid papulosis and 67 individually matched control subjects who were recruited among relatives and acquaintances of the patients answered a standard questionnaire over the telephone. RESULTS: Among patients with lymphomatoid papulosis, 3 had a history of Hodgkin disease, 3 had non-Hodgkin lymphoma, and 10 had mycosis fungoides; none of the control subjects reported such histories. No significant differences were observed between patients and control subjects in regard to residence or travel history or exposures to various physical, chemical, and biologic agents. A higher, although not statistically significant, percentage of patients than control subjects reported a history of radiation therapy and nonlymphoid malignant lesions. No differences were found between patients and control subjects in regard to other medical conditions or family medical history. CONCLUSIONS: Patients with lymphomatoid papulosis have a significantly increased frequency of prior or coexisting lymphoproliferative disorders, an increased frequency of nonlymphoid malignant lesions, and exposure to radiation therapy.

Adolescent↗
PubMed1992

Hodgkin's disease, lymphomatoid papulosis, and cutaneous T-cell lymphoma derived from a common T-cell clone.

BACKGROUND: Lymphomatoid papulosis is a benign cutaneous eruption that in 10 to 20 percent of patients is associated with the development of lymphoma. The atypical cells of lymphomatoid papulosis histologically resemble the malignant cells of cutaneous T-cell lymphoma or the Reed-Sternberg cells of Hodgkin's disease. We studied a patient in whom lymphomatoid papulosis developed in 1971, Hodgkin's disease in 1975, and cutaneous T-cell lymphoma in 1985, to determine whether these diseases are clonally related. METHODS: The T-cell-receptor alpha-chain gene was cloned and sequenced from a cell line derived from the advanced-stage cutaneous T-cell lymphoma, and the polymerase chain reaction was used to search for this rearrangement of the alpha-chain gene in tissues obtained earlier that were affected by Hodgkin's disease or lymphomatoid papulosis. RESULTS: The tumor-specific rearrangement of the alpha-chain gene was detected in the patient's earlier tissues affected by lymphomatoid papulosis and Hodgkin's disease, but not in control tissue, including uninvolved tissues from the staging laparotomy for Hodgkin's disease. Cytogenetic studies revealed a translocation, t(8;9)(p22;p24), in cutaneous T-cell lymphoma lines and in a dermatopathic lymph node removed two years before the clinical onset of the cutaneous T-cell lymphoma. Immunohistochemical findings were consistent with an activated T-cell phenotype for the atypical cells of lymphomatoid papulosis, the Reed-Sternberg cells of Hodgkin's disease, and the malignant cells of the T-cell lymphoma. CONCLUSIONS: Lymphomatoid papulosis, Hodgkin's disease, and cutaneous T-cell lymphoma can be derived from a single T-cell clone. A t(8;9) genetic translocation may be involved in the pathogenesis of lymphomatoid papulosis or its progression to malignant disease.

Adult↗
PubMed1992

Cutaneous T-cell lymphoma. Evaluation of pretreatment skin biopsy specimens by a panel of pathologists.

BACKGROUND AND DESIGN: Cutaneous T-cell lymphoma (CTCL) frequently presents a difficult diagnostic challenge for the clinician and pathologist. To assess the diagnostic validity of conventional histopathologic findings in CTCL, pretreatment skin biopsy specimens were scored prospectively and independently by a panel of five to seven dermatopathologists and pathologists. Scores were compared with disease outcome. Repeatability of these scores was examined among observers and for the same observer. The study population consisted of 165 subjects, initially referred for suspected mycosis fungoides or Sézary syndrome. Ninety-two patients determined to have CTCL have been followed up for 6.3 +/- 3.5 years (mean +/- SD) and are categorized according to disease outcome: 22 are in complete remission, 35 are in partial remission, three have progressive lymphoma, 15 died of disease, 13 died of other causes, and four were unavailable for follow-up. Seventy-three patients determined not to have CTCL have been followed up for 5.3 +/- 3.2 years without subsequent clinicopathologic evidence of CTCL. These longitudinal data allowed comparisons of the clinical course with the original histologic interpretations. RESULTS: Data showed that the histologic scores rendered by the pathology panel did not correlate with stage of disease and were not an accurate predictor of clinical outcome, because the histologic ratings did not discriminate between patients who eventually had complete remission and those with either progressive lymphoma or who have died of disease. The results also substantiate the low inherent reliability of histopathologic findings in CTCL. Large differences existed among pathologists in scoring the study populations and repeated reading of selected cases by the same panel member resulted in a change of diagnosis 15% of the time. Among the histologic features evaluated, only the presence of mitoses in the infiltrating cells showed a trend toward an unfavorable outcome. CONCLUSION: Pathologic diagnosis in the CTCL disease spectrum should be interpreted with caution and then only in conjunction with the clinical evaluation. As expected, the use of an average value from a panel of readers added a component of stability to the histologic interpretation.

Biopsy↗
PubMed1992

Cutaneous T-cell lymphoma with porokeratosis-like lesions.

We describe two black patients who had widespread, sharply demarcated, round, hyperpigmented or hypopigmented macules that clinically resembled disseminated superficial actinic porokeratosis (DSAP). One patient was known to have cutaneous T-cell lymphoma (CTCL), and the other patient had only the DSAP-like lesions. Histopathologic and immunohistochemical studies of the DSAP-like lesions revealed characteristic features of patch-phase CTCL. This unusual variant of patch-phase CTCL should be differentiated from DSAP and the hypopigmented variant of CTCL.

Adult↗
PubMed1992

Neutralizing antibodies against transforming growth factor beta potentiate the proliferation of Ki-1 positive lymphoma cells. Further evidence for negative autocrine regulation by transforming growth factor beta.

Activated lymphocytes and malignant lymphoma cells derived from them (Ki-1 positive lymphoma cells) share similar mechanisms of proliferation. To further examine the inhibitory role of endogenous transforming growth factor beta (TGF beta) in Ki-1 positive lymphoma cells, the authors studied anti-TGF beta antibodies and measured their effect on proliferation. A monoclonal antibody (T1A5) prepared against a unique antigenic epitope of high molecular weight Hodgkin's TGF beta and a polyclonal rabbit antibody prepared against highly purified 25,000 D porcine platelet TGF beta 1 were used. Both antibodies are shown here to inhibit the biological activity of Hodgkin's TGF beta and to crossreact with their respective antigens in immunoblotting. DNA synthesis by Ki-1 lymphoma cells was increased 138-fold by anti-TGF beta 1 antibody and 262-fold by anti-Hodgkin's TGF beta. Exogenous TGF beta 1 suppression was completely reversed by anti-TGF beta 1 antibody and IL-2-induced proliferation was markedly potentiated (41 fold). L-428 Reed-Sternberg cells secrete physiologically active TGF beta but have fewer than 500 TGF beta receptor sites per cell; no significant proliferative response was measured for either anti-TGF beta 1 or anti-Hodgkin's TGF beta. These results show the suppressive effect of exogenous TGF beta 1 on indolent Ki-1 lymphoma cells and suggest that the endogenous secretion of high molecular weight physiologically active TGF beta is important in maintaining the indolent nature of this low-grade Ki-1 positive lymphoma.

Antibodies↗
PubMed1992

Perivascular Ki-1 + lesions.

We describe three male patients diagnosed by histologic and immunophenotypic criteria to have a Ki-1 + lymphoproliferative disorder. All three cases shared a unique morphologic finding, not previously described: prominent perivascular cuffing of anaplastic/pleomorphic tumor cells around small and medium sized vessels. One case was a Ki-1 + anaplastic large cell lymphoma (ALCL) which developed in the setting of a low grade follicular B-cell lymphoma. A pseudoglandular pattern caused referral for consultation as a possible adenocarcinoma. One case was a cutaneous Ki-1 + lymphoproliferative disorder consistent with lymphomatoid papulosis (LyP). The third case was a cutaneous Ki-1 + ALCL. This study provides evidence that although perivascular cuffing of tumor cells is not frequently seen in Ki-1 + lymphoproliferative disorders (3 of 116 cases in our consultation file), it may be a prominent architectural feature causing confusion with epithelial or mesenchymal tumors. For this reason we recommend inclusion of this feature in the list of architectural features already described for Ki-1 + lymphoproliferative disorders.

Adult↗
PubMed1991

Aggressive peripheral T-cell lymphomas containing Epstein-Barr viral DNA: a clinicopathologic and molecular analysis.

The Epstein-Barr virus (EBV) has been shown to be associated with posttransplant lymphoma, Hodgkin's disease, and T-cell lymphoma, in addition to African Burkitt's lymphoma. In a retrospective study of 56 consecutive cases of T-cell lymphoma, EBV DNA was found by Southern blot and in situ DNA hybridization in 10 (20%) of 50 peripheral T-cell lymphomas, but in none of six cases of T-lymphoblastic lymphoma. Peripheral T-cell lymphomas containing EBV DNA could be subclassified into three categories according to histology and immunophenotypic studies: (1) T-cell lymphoma of the helper phenotype, five cases. Two cases had histologic features resembling angioimmunoblastic lymphadenopathy (AILD). (2) T-cell lymphoma of the cytotoxic/suppressor phenotype, four cases. AILD-like features could also be recognized in two cases. Reed-Sternberg-like giant cells were identified in three cases designated Hodgkin-like T-cell lymphoma. (3) Angiocentric T-cell lymphoma or lymphomatoid granulomatosis in one case, initially affecting the skin and nose; no T-cell subset could be defined. Six of the eight EBV DNA-positive patients tested for serum EBV antibodies had elevated titers of IgG antiviral capsid antigen (greater than 640) and/or early antigen (greater than 10). From combined studies of Southern blot hybridization by using EBV termini fragment probe and in situ DNA hybridization, the EBV genomes appeared to be clonotypically proliferated in the neoplastic T cells. The patients in all three groups usually had prolonged fever preceding the diagnosis, hepatosplenomegaly, an aggressive clinical course, and poor response to chemotherapy; nine died with a median survival of only 8 months. We propose that these EBV-associated aggressive T-cell lymphomas, like human T-cell leukemia/lymphoma virus-positive T-cell lymphoma, have characteristic clinicopathologic features and should be treated as a separate disease entity.

Adolescent↗
PubMed1991

Cutaneous multilobated T-cell lymphoma with aggressive course.

Cutaneous multilobated T-cell lymphoma is an uncommon variant of skin-based peripheral T-cell lymphoma typically characterized by cutaneous nodules in elderly patients and a chronic clinical course. We report a case of the disease that led to the patient's death within 2 years after onset. This disease may be associated with a more aggressive clinical course than generally recognized.

Aged↗
PubMed1991

Lymphomatoid papulosis, Ki-1+ lymphoma, and primary cutaneous Hodgkin's disease.

Lymphomatoid papulosis (LyP), Ki-1 lymphoma, and primary cutaneous, Hodgkin's disease (HD) appear to be histogenetically related disorders derived from activated T cells that express HD-associated antigens. Despite their morphologic and immunologic similarities, each disorder has a different clinical presentation and prognosis. LyP is associated with a long benign course of regressing papular lesions. The risk of developing a malignant lymphoma is approximately 10% to 20%. Ki-1 lymphoma, formerly known as regressing atypical histiocytosis (RAH), usually presents as one to several large lesions that can metastasize to regional lymph nodes. Single lesions can be treated by excision and local radiotherapy. Chemotherapy is necessary to control extracutaneous disease. Primary cutaneous HD probably does exist as a rare, often deep seated, nodular disorder that usually has a good prognosis. It should be distinguished from stage IV HD, which carries a grave prognosis. Evidence of associated nodal HD should be investigated in patients who present with skin lesions morphologically and immunologically indistinguishable from HD.

Antigens, CD↗
PubMed1990

Cutaneous T cell lymphoma with suppressor/cytotoxic (CD8) phenotype: identification of rapidly progressive and chronic subtypes.

We identified nine patients with cutaneous T cell lymphoma in whom the neoplastic cells expressed the CD8 (T8) suppressor T cell phenotype instead of the more common CD4 (T4) helper T cell phenotype. Five had rapidly progressive disease characterized by distinctive papulonodular skin lesions (four patients), involvement of palms or soles (four patients) or oral cavity (two patients), and poor response to standard topical therapy (four patients). Histologic examination showed extensive epidermotropism often associated with pagetoid features. Immunoperoxidase studies revealed a novel aberrant T cell phenotype characterized by lack of expression of CD4 and CD2 (T11) but positive staining for CD3 (T3) and CD7 (3A1). In contrast, the neoplastic cells from four patients with clinically more chronic CD8+ cutaneous T cell lymphoma, although also commonly epidermotropic, had a different aberrant T cell phenotype similar to that often seen in CD4+ mycosis fungoides; that is, there was lack of expression of CD7 but a positive reaction to staining for CD2. In two cases the tumor cells acquired the CD7 antigen or lost the CD2 antigen with progression of the disease. Two cases were analyzed with Southern blotting and both showed rearranged DNA bands that confirmed the presence of clonal populations of T cells. Our findings suggest the following: (1) CD8+ cutaneous T cell lymphoma can be rapidly progressive or chronic. (2) These two types cannot be reliably distinguished by histologic features. (3) Rapid progression was associated with a CD2-, CD7+ phenotype whereas chronicity was associated with a CD2+, CD7- phenotype.

Aged↗
PubMed1990

Cutaneous manifestations of postthymic T cell malignancies: description of five clinicopathologic subtypes.

This study was undertaken to identify the cutaneous manifestations among different prognostic subgroups of postthymic T cell malignancies. Cutaneous involvement was demonstrated in 43 of 88 cases. We recognized five clinicopathologic subtypes: type I, classical cutaneous T cell lymphoma (CTCL) or mycosis fungoides, six cases; type II, primary large cell type CTCL, Ki-1 antigen (Ki-1+ or Ki-1-), seven cases; type III, primary angioinvasive T cell lymphoma, three cases; type IV, human T-lymphotropic virus type I (HTLV-I+) adult T cell leukemia/lymphoma (ATL), eight cases; type V, secondary cutaneous involvement by peripheral T cell lymphoma (PTL), 19 cases. Primary CTCL and ATL tend to involve papillary dermis with or without epidermotropism, whereas PTL and angioinvasive T cell lymphoma predominantly affect skin adnexae, vessels, and subcutis. Cutaneous lesions in type V PTL are heterogeneous and may be confused with panniculitis, vasculitis, or an eczematous eruption. Classic CTCL, Ki-1+ lymphoma, and angioinvasive T cell lymphoma have a chronic course, whereas ATL, Ki-1- large cell lymphoma, and PTL are clinically aggressive.

Female↗
PubMed1990

Immunohistochemical distinction of lymphomatoid papulosis and pityriasis lichenoides et varioliformis acuta.

Lymphomatoid papulosis (LyP) and pityriasis lichenoides et varioliformis acuta (PLEVA) are benign self-healing cutaneous eruptions that may be clinically and histologically similar. However LyP has a 5% to 20% risk of associated lymphoid malignancy, whereas PLEVA does not. To determine whether the immunophenotype of lymphoid cells is useful in the distinction of these two disorders, the pattern of expression of lymphoid cell lineage and activation antigens in nine cases of LyP and seven cases of PLEVA were compared. In all cases of LyP most larger cells expressed the activation antigen Ki-1 (CD30) and lacked expression of the T-cell antigen CD7 and at least one other T-cell antigen (CD2, CD3, CD5). In contrast, CD30-antigen expression was rare or absent in PLEVA, CD3- and CD7-antigen expression was found in all cases, and diminished expression of T-cell antigens (CD2 and CD5) was seen in only one case. Diffuse expression of HLA-DR antigen by epidermal keratinocytes was found in a greater proportion of PLEVA cases (6 of 7) than LyP cases (3 of 6). In addition, CD8+ cells predominated at the dermal/epidermal junction in 3 of 6 cases of PLEVA but in only 1 of 7 cases of LyP. We conclude that LyP and PLEVA can be distinguished immunohistochemically in most, if not all, cases. Furthermore these results suggest that LyP and PLEVA are separate disorders, thus accounting for their variable prognoses.

Adult↗
PubMed1990

Immunohistochemical evidence of a role for transforming growth factor beta in the pathogenesis of nodular sclerosing Hodgkin's disease.

Transforming growth factor beta (TFG-beta) is a multifunctional growth factor that promotes the growth of fibroblasts, collagen synthesis and angiogenesis, and stimulates monocyte migration and activation, but suppresses the growth and differentiation of immune lymphocytes and killer cells. Previously we demonstrated biologic activity for TGF-beta in supernatants of fresh Hodgkin's disease (HD) cell cultures and the cell line L428 derived from nodular sclerosing HD. This study was undertaken to find evidence of TGF-beta activity directly in tissues affected by HD. Formalin-fixed tissue from 14 patients with HD, including 8 nodular sclerosis, 4 mixed cellularity, 1 lymphocyte predominance, and 1 lymphocyte depletion type were studied by immunoperoxidase technique with antibody CC (1-30) raised against a synthetic polypeptide with the same N-terminal amino acid sequence as TGF-beta 1. Transforming growth factor beta activity was demonstrated in six cases of nodular sclerosis but not in other histologic types of HD. Staining for TGF-beta was found in the cytoplasm of Reed-Sternberg (RS) cells in one case and on the surface of RS cells and their lacunar variants in five cases. Transforming growth factor beta activity associated with the extracellular matrix was localized mainly around blood vessels, zones of necrosis, at the margins of bands of collagen sclerosis, and in areas containing syncytia of RS cells. In two cases TGF-beta was associated with collections of epithelioid histiocytes or granulomas. Small lymphocytes, granulocytes, and germinal center cells were unreactive. These results suggest that TGF-beta is a growth factor of biologic importance in HD and may be responsible for many of the histologic features, such as nodular sclerosis and granulomas, that may have prognostic significance.

Adolescent↗