PubMed Health⌕ Search

Biomedical subjects

C W Ross

Publications and source records attributed to C W Ross.

At least 37 records · Page 2Linked to original sources
PubMed1998

Evaluation of CD23 expression in paraffin-embedded gastric lymphomas of mucosa-associated lymphoid tissue.

The CD23 antigen is expressed in a normal subset of B lymphocytes and in some non-Hodgkin's lymphomas. Reactivity for anti-CD23 (BU38) is present in paraffin-embedded tissue in the large majority of nodal small lymphocytic lymphomas, as well as in follicular center cell lymphomas. Most studies of gastric lymphomas of mucosa-associated lymphoid tissue (MALT) reported a lack of CD23, but these studies were performed on frozen tissue. We evaluated CD23 staining in paraffin-embedded tissue in a large series of gastric MALT lymphomas, as well as in cases of chronic gastritis. We assayed 49 well-characterized gastric lymphomas (9 high-grade non-MALT and 40 MALT [20 low grade, 13 mixed low and high grade, and 7 high grade]). High-grade MALT lymphomas without a low-grade component were distinguished from high-grade non-MALT lymphomas by the presence of lymphoepithelial lesions composed of large cells. In addition, we studies nine cases of chronic gastritis containing B-cell aggregates. We used anti-CD23 (BU38) in formalin-fixed, paraffin-embedded tissue. All of our low-grade gastric MALT lymphomas lacked CD23 immunoreactivity. One of the 13 mixed low-grade and high-grade lesions showed CD23 expression in the high-grade component. All of the high-grade MALT and high-grade non-MALT lesions lacked CD23. All of the nine cases of chronic gastritis lacked CD23. CD23 highlighted residual follicular dendritic cells and gastric epithelium. We concluded that gastric MALT lymphomas lacked CD23 (BU38) in paraffin-embedded tissue, with rare exceptions. This lack of CD23 expression might represent a useful feature in small or partially crushed biopsy specimens, particularly in the differential diagnosis with follicular small cleaved cell lymphoma presenting in the gastrointestinal tract.

Chronic Disease↗
PubMed1997

Successful treatment of autoimmune neutropenia with recombinant human granulocyte-colony stimulating factor (R-metHuG-CSF).

Autoimmune neutropenia (AIN) is characterized by antibody mediated peripheral destruction of neutrophils. Since there is no effective treatment, antibiotics have to be used frequently for recurrent infections. Five selected patients with serologically proven AIN were treated with r-metHuG-CSF at 5-8 micrograms/kg body weight (300-480 micrograms) daily; the dose and frequency of r-metHuG-CSF was reduced after neutrophil counts above 1.0 x 10(9)/l were obtained. R-metHuG-CSF is effective in AIN and causes a sustained rise in ANC which can be maintained on a low dose administered twice or thrice weekly.

Adult↗
PubMed1997

The t(2;5)-associated p80 NPM/ALK fusion protein in nodal and cutaneous CD30+ lymphoproliferative disorders.

A high percentage of extracutaneous CD30+ anaplastic large cell lymphomas (nodal ALCL) carry a specific chromosomal translocation, t(2;5) (p23;q35), that results in abnormal expression of p80 NPM/ALK chimeric protein (p80). The protein p80 may be detected by immunohistochemistry using polyclonal (anti-p80) or monoclonal (ALK1) antibody directed against the ALK epitope. Although nodal ALCL, primary cutaneous ALCL, and lymphomatoid papulosis type A (lyp A) have similar histologic and immunohistochemical features, the expression of p80 in these cutaneous lesions has not been extensively studied. We immunostained tissues from 10 nodal ALCL, 8 primary cutaneous ALCL, 24 lyp A, and positive and negative controls using polyclonal rabbit anti-p80 and the avidin-biotin-peroxidase labeling method. Reactivity was determined by comparing staining intensity to positive controls [4 nodal ALCL with t(2;5)] and negative controls (21 non-ALCL lymphomas). Only cutaneous lesions staining positively with anti-p80 were further studied with the monoclonal antibody ALK1 and reverse transcription polymerase chain reaction (RT-PCR) for p80 messenger RNA. All positive controls (4/4), but none of the negative controls (0/21) nor lyp A (0/24), were immunoreactive for anti-p80. Sixty percent (6/10) of nodal ALCL and a single case (12%) of primary cutaneous ALCL were immunoreactive for anti-p80. In this exceptional cutaneous lesion, although we did not find NPM/ALK by RT-PCR, we detected strong expression of ALK using ALK1. We conclude that t(2;5) is rarely involved in the pathogenesis of cutaneous CD30+ lymphoproliferative disorders.

Anaplastic Lymphoma Kinase↗
PubMed1997

Ruptured spleens with expanded marginal zones do not reveal occult B-cell clones.

An indolent variant of splenic marginal zone lymphoma (SMZL) lacking massive splenomegaly has been described as an incidental finding in spleens removed for rupture or hypersplenism. We studied traumatically ruptured spleens with expanded marginal zones (MZs) to assess the incidence of occult monoclonal B-cell populations in this setting. Ninety-one ruptured or lacerated spleens removed from 1984 to 1995 were classified as to whether they had expanded MZs (> 12 cell layers thick). When available, paraffin-embedded, formalin-fixed tissue from cases with expanded MZs was examined for immunoglobulin heavy chain gene rearrangement by polymerase chain reaction (PCR) and stained for CD20, CD43, and kappa and lambda light chains. Splenectomies were performed for blunt (70 patients) and penetrating (7 patients) trauma, surgical misadventure (13 patients), or spontaneous rupture (1 patient). There were 58 men and 33 women in our study, ranging in age from 17 to 87 years (mean, 40 yr). Average spleen weight was 183 g (range, 44-505 g). Twenty-seven (30%) of 91 patients had expanded MZs. There were no significant differences in age, sex, spleen weight, or reason for excision between those cases with and without MZ expansion. Germinal centers varied from absent to inactive to floridly reactive. Paraffin blocks were available in 24 cases; the 20 with amplifiable DNA were polyclonal by PCR. Follow-up was available for 25 of the 27 patients with expanded MZs (range, 1-85 mo; median, 6 mo); lymphoma did not develop in anyone, although one patient's spleen was morphologically suspicious for lymphoma, showing involvement of red pulp by MZ-type B-cells; PCR revealed a polyclonal pattern. This patient's 3-year follow-up revealed no evidence of lymphoma. Traumatically ruptured spleens with expanded MZs do not seem to harbor occult B-cell clones, as detected by PCR. Although a few cases of incidentally removed spleens have been reported to contain low-stage SMZL, this seems to be an infrequent event.

Adolescent↗
PubMed1996

Detection of immunoglobulin heavy chain gene rearrangement by polymerase chain reaction in chronic active gastritis associated with Helicobacter pylori.

Chronic active gastritis associated with Helicobacter pylori (CAG-Hp) has been linked to the pathogenesis of gastric B-cell lymphomas of mucosa-associated lymphoid tissue (MALT). To determine whether monoclonal lymphoid populations are present in CAG-Hp and histological predictors of monoclonality exist, the authors examined 46 endoscopic biopsies from 41 patients with CAG-Hp. The authors scored gastric biopsies for the presence of lymphoepithelial lesions (LELs), intensity of lymphoid infiltrate, presence of lymphoid aggregates and germinal centers, coexpression of CD43 (Leu 22) on B cells, and cytoplasmic immunoglobulin light chain restriction in formalin-fixed, paraffin embedded tissues. DNA extracts from these routinely processed tissues were analyzed for immunoglobulin heavy chain (IgH) gene rearrangement by polymerase chain reaction (PCR). Histological features, immunophenotype, gene rearrangement status, and clinical information were correlated. Six of the 46 biopsies (13%) from six of 41 patients (15%) showed a monoclonal PCR pattern. Monoclonal PCR patterns correlated with the presence of LELs (P<.015) but not with intensity of lymphoid infiltrate, presence of germinal centers, or presence of lymphoid aggregates. LELs correlated with germinal centers (P<.003) and intensity of infiltrate (P<.0001). None of the cases showed cytoplasmic light chain restriction nor coexpression of CD43 on B cells by immunohistochemistry. Clinical follow-up was available in all six patients whose gastric biopsies had a monoclonal PCR pattern (median, 58 months; range, 1 to 66 months) and 33 of the 35 patients with biopsies showing a polyclonal PCR pattern (median, 41 months; range 0.1 to 63 months). No patient developed gastric lymphoma. Monoclonality of lymphoid cells was detected by IgH PCR in 13% of patients with CAG-Hp. Although the authors cannot exclude the possibility that some patients with monoclonal gastric lymphoid infiltrates may eventually develop overt lymphoma, no histological, immunophenotypic, nor clinical evidence of lymphoma was noted at presentation or on clinical follow-up. Given the high incidence of CAG-Hp in the general population and the relatively low incidence of gastric MALT lymphoma, clinicopathologic correlation is needed when interpreting tests for clonality in this setting. The presence of clonal IgH gene rearrangement in CAG-Hp supports the hypothesis that H pylori is involved in the pathogenesis of low grade gastric B-cell MALT lymphomas.

Adult↗
PubMed1996

Follicular lymphoma with involvement of the splenic marginal zone: a pitfall in the differential diagnosis of splenic marginal zone cell lymphoma.

Follicular lymphomas (FL) involving the spleen arise in and expand the germinal centers of the white pulp, whereas mantle cell lymphomas arise in the mantle zone and surround the benign germinal center. The recently described marginal zone cell lymphoma (MZCL) is a B-cell neoplasm characterized by concentric expansion of cells around the follicle, with or without infiltration of the mantle zone or germinal center. In addition, the immunoglobulin heavy chain gene is rearranged although none of the MZCL reported have been shown to be positive for the bcl-2 gene translocation by molecular studies. We report a patient with FL showing preferential involvement of the marginal zone of spleen morphologically mimicking a primary splenic MZCL. The patient reported here had a well-documented previous lymph node diagnosis of FL. The immunoglobulin heavy chain gene and bcl-2 gene rearrangement analysis confirmed the clonal origin of both the original FL, as well as the lymphoma, with a marginal zone pattern in the spleen.

Base Sequence↗
PubMed1996

Ki-1 anaplastic large cell lymphoma with a prominent leukemic phase.

Patients with Ki-1 (CD30)-positive anaplastic large cell lymphoma (ALCL) occasionally have rare circulating lymphoma cells. We report a case of ALCL with a prominent leukemic phase. A 36-year-old man presented with widespread ALCL involving lymph nodes, spleen, pleural fluid, cerebrospinal fluid, and bone marrow. His white blood cell count was 106,000/mm3 with 20% lymphoma cells. The circulating neoplastic cells were large, and had irregular nuclei with multiple small nucleoli, ample cytoplasm, and multiple clear cytoplasmic vacuoles. This case illustrates that ALCL may have a marked leukemic phase composed of large anaplastic cells.

Adult↗
PubMed1996

Analysis of immunoglobulin heavy chain gene rearrangement in myoepithelial sialadenitis by polymerase chain reaction.

Myoepithelial sialadenitis (MESA) can often be difficult to distinguish from low grade B-cell lymphoma of mucosa-associated lymphoid tissue (MALT). The authors have previously studied a series of 25 patients with MESA and identified histologic and immunologic features predictive of extrasalivary lymphoma (ESL). The authors have now analyzed formalin-fixed, paraffin-embedded salivary gland tissue from 21 of these patients (and 1 new patient) for immunoglobulin heavy chain (IgH) gene rearrangement by a semi-nested polymerase chain reaction (PCR) technique to compare monoclonality by IgH PCR with clinical outcome (median follow-up 6.7 years, range 3 months-19.4 years) and the paraffin section immunophenotype. The PCR technique employed consensus primers from variable (FR3A) and joining regions (LJH, VLJH) of the IgH gene. A monoclonal PCR product was detected in 16 of 28 specimens from 13 of 22 patients. By Fisher's exact test, a monoclonal PCR pattern did not correlate (P > .05) with development of ESL, broad strands of monocytoid B-cells, plasma cell light chain restriction by immunoperoxidase, or CD43 coexpression on monocytoid B cells by immunoperoxidase. This study suggests that the majority of MESA lesions harbor monoclonal B-cell populations and that clonality does not predict progression to clinically overt lymphoma. Acquired salivary gland MALT, in the form of MESA, may progress to a process that is clonal but not necessarily malignant. Extranodal lymphoma develops in a minority of patients with this lesion.

Adult↗
PubMed1996

Iodine-131-anti-B1 radioimmunotherapy for B-cell lymphoma.

PURPOSE: The CD20 B-lymphocyte surface antigen expressed by B-cell lymphomas is an attractive target for radioimmunotherapy, treatment using radiolabeled antibodies. We conducted a phase I dose-escalation trial to assess the toxicity, tumor targeting, and efficacy of nonmyeloablative doses of an anti-CD20 monoclonal antibody (anti-B1) labeled with iodine-131 (131I) in 34 patients with B-cell lymphoma who had failed chemotherapy. PATIENTS AND METHODS: Patients were first given tracelabeled doses of 131I-labeled anti-B1 (15 to 20 mg, 5 mCi) to assess radiolabeled antibody biodistribution, and then a radioimmunotherapeutic dose (15 to 20 mg) labeled with a quantity of 131I that would deliver a specified centigray dose of whole-body radiation predicted by the tracer dose. Whole-body radiation doses were escalated from 25 to 85 cGy in sequential groups of patients in 10-cGy increments. To evaluate if radiolabeled antibody biodistribution could be optimized, initial patients were given one or two additional tracer doses on successive weeks, each dose preceded by an infusion of 135 mg of unlabeled anti-B1 one week and 685 mg the next. The unlabeled antibody dose resulting in the most optimal tracer biodistribution was also given before the radioimmunotherapeutic dose. Later patients were given a single tracer dose and radioimmunotherapeutic dose preceded by infusion of 685 mg of unlabeled anti-B1. RESULTS: Treatment was well tolerated. Hematologic toxicity was dose-limiting, and 75 cGy was established as the maximally tolerated whole-body radiation dose. Twenty-eight patients received radioimmunotherapeutic doses of 34 to 161 mCi, resulting in complete remission in 14 patients and a partial response in eight. All 13 patients with low-grade lymphoma responded, and 10 achieved a complete remission. Six of eight patients with transformed lymphoma responded. Thirteen of 19 patients whose disease was resistant to their last course of chemotherapy and all patients with chemotherapy-sensitive disease responded. The median duration of complete remission exceeds 16.5 months. Six patients remain in complete remission 16 to 31 months after treatment. CONCLUSION: Nonmyeloablative radioimmunotherapy with 131I-anti-B1 is associated with a high rate of durable remissions in patients with B-cell lymphoma refractory to chemotherapy.

Adult↗
PubMed1995

True T-cell chronic lymphocytic leukemia: a morphologic and immunophenotypic study of 25 cases.

We studied 25 T-cell chronic lymphocytic leukemia (T-CLL) cases collected over a 15-year period. Immunophenotypic analysis was performed in each case; 12 cases were evaluated by cytogenetics, and gene rearrangement studies were performed in 14 cases. The median age was 57 years with a male predominance (M:F, 15:10). The median presenting lymphocyte count was 36.3 x 10(9)/L (range, 3.9 to 438 x 10(9)/L). Fourteen patients (56%) had shotty adenopathy and ten (40%) had mild-to-moderate splenomegaly at presentation; four (16%) had erythematous skin lesions. The lymphocytes were predominantly small; some cases had a minor component of medium-sized cells (< 10%). The nuclear: cytoplasmic ratios were uniformly high with round to oval nuclei; however, a wide spectrum of nuclear outlines could be found, ranging from minimally to markedly convoluted. Nucleoli were either absent or small and inconspicuous. These lymphocytes did not have the morphology of prolymphocytes and did not contain cytoplasmic granules. Bone marrow infiltration was generally in an interstitial pattern; the degree of involvement ranged from 15% to 90%. Immunophenotyping showed that the lymphocytes were mature T-cells with a predominant CD4+ immunophenotype. Three cases displayed a CD8+ immunophenotype. The patients were treated with a variety of chemotherapeutic regimens with only a minimal response observed in two of 20 patients. We conclude that T-CLL is an uncommon chronic lymphoproliferative disorder (CLPD) that can be morphologically similar to B-CLL, is distinct from T-prolymphocytic leukemia, and has an aggressive clinical course that is refractory to therapy. It may also be difficult to distinguish T-CLL from other T-CLPD, especially the leukemic phase of peripheral T-cell lymphoma and some cases of Sézary syndrome.

Adult↗
PubMed1995

A clinical and histologic mycosis fungoides simulant occurring as a T-cell infiltrate coexisting with B-cell leukemia cutis.

One year after the onset of chronic lymphocytic leukemia, an elderly man had scaly cutaneous plaques on the thighs that clinically and histologically resembled the mycosis fungoides type of cutaneous T-cell lymphoma. Two years later the patient had indurated, red dermal nodules on the face that clinically and histologically were characteristic of cutaneous chronic lymphocytic leukemia. Immunophenotyping results from a facial nodule confirmed the presence of a B-cell infiltrate (CD20+). Immunophenotyping of a lesion on the right thigh showed that half the cells were composed of a CD2+, CD45RO+ (UCHL-1+) upper dermal and focally epidermotropic population of T cells consistent with mycosis fungoides; however, these T cells coexisted with an equal number of CD20+ B cells arranged in distinct clusters. DNA from the thigh lesion exhibited a B-cell immunoglobulin gene rearrangement, but the T-cell receptor gene rearrangements were germline. In this case, the evidence favors a mycosis fungoides simulant occurring as a reactive T-cell infiltrate to an underlying B-cell chronic lymphocytic leukemia.

Aged↗
PubMed1995

Cyclin D1 protein expression in mantle cell lymphoma.

BACKGROUND: The t(11;14)(q13;q32) is a chromosomal abnormality usually associated with mantle cell (centrocytic) lymphomas, although it has occasionally been reported in other chronic lymphoproliferative disorders such as chronic lymphocytic leukemia, prolymphocytic leukemia, splenic lymphoma with villous lymphocytes, and multiple myeloma. This abnormality results in the translocation of the bcl-1 oncogene from chromosome 11 to the immunoglobulin heavy chain locus on chromosome 14. The bcl-1 oncogene is a member of the cyclin gene family, and high levels of cyclin D1 mRNA are consistently found in malignant B cell proliferations with t(11;14). PATIENTS AND METHODS: We examined cyclin D1 protein expression in 33 patients with low grade lymphoproliferative disorders and 2 patients with reactive hyperplasias by Western blot analysis using a polyclonal antibody. RESULTS: 8/11 mantle cell lymphomas, 0/11 chronic lymphocytic leukemias, 0/4 hairy cell leukemias, 0/2 Sezary syndrome, 0/2 monocytoid B-cell lymphomas, 0/3 follicular lymphomas, and 0/2 reactive hyperplasias had overexpression of cyclin D1. Cytogenetic analysis was performed in four cases of mantle cell lymphoma; three of these cases had the t(11;14), one of which was hypotetraploid with two copies of t(11;14). Immunophenotypically, all cases of mantle cell lymphoma and chronic lymphocytic leukemia had coexpression of CD5 and CD20. CONCLUSION: Mantle cell lymphoma may be difficult to discriminate from chronic lymphocytic leukemia, a more indolent disease, on morphologic and immunophenotypic grounds. Our findings suggest that analysis of cyclin D1 protein expression may be helpful in differentiating mantle cell lymphomas from other low grade lymphoproliferative disorders.

Antigens, Neoplasm↗
PubMed1995

Epstein-Barr virus and bcl-2 protein overexpression are not detected in the neoplastic cells of nodular lymphocyte predominance Hodgkin's disease.

Recent studies have indicated that nodular lymphocyte predominance Hodgkin's disease (nLP-HD) is a B-cell lymphoma. Although molecular events in the neoplastic transformation of B-cells are not well understood, Epstein-Barr virus infection and bcl-2 protein overexpression have been postulated to have etiologic roles in some lymphomas. Epstein-Barr virus has been demonstrated in the Reed-Sternberg cells of Hodgkin's disease cases (other than nLP-HD) as well as in some B-cell lymphomas; bcl-2 overexpression is found in the majority of follicular lymphomas. The biologic role for bcl-2 in HD is controversial. Some reports have indicated the presence of bcl-2 gene rearrangements, associated with the t(14;18) (q32;q21), detected by the polymerase chain reaction in HD; recent studies have failed to confirm this finding. Reports in the literature describe only a few such analyses in the nLP-HD subtype. To address these conflicting issues, we examined 12 cases of nLP-HD to determine whether bcl-2 protein expression (by immunohistochemistry) and Epstein-Barr virus (by in situ hybridization) could be detected in the Reed-Sternberg variants. None of the cases showed expression of bcl-2 protein or Epstein-Barr virus RNA in the neoplastic cells. Epstein-Barr virus does not appear to play an important role in the pathogenesis of nLP-HD. Similarly, we cannot substantiate a role for bcl-2 in the development of this type of Hodgkin's disease.

Base Sequence↗
PubMed1995

Peripheral T-cell non-Hodgkin's lymphoma following treatment of nodular lymphocyte predominance Hodgkin's disease.

Previous reports have suggested that nodular lymphocyte predominance Hodgkin's disease (NLPHD) is a germinal center-derived B-cell lymphoma that is distinct from other types of Hodgkin's Disease. A relationship between NLPHD and simultaneous or subsequent development of large-cell (LC) non-Hodgkin's lymphoma (NHL) has been established. Both Reed-Sternberg cell variants in NLPHD and NHL cells in these cases express B-cell-associated antigens, and in some cases the B-cell lineage of the NHL has been confirmed by immunoglobulin gene rearrangement studies. The B-cell phenotype and the indolent course of both lymphomas suggest histologic progression of NLPHD to B-cell NHL, rather than a de novo LCNHL unrelated to Hodgkin's Disease. We report a unique case of T-large-cell lymphoma (TLCL) following successful chemotherapy of NLPHD. A 54-year-old male was treated with seven cycles of mechlorethamine, vincristine, procarbazine, prednisone chemotherapy for NLPHD and 4 years later developed recurrent adenopathy. Lymph node biopsy showed a diffuse LCNHL. Frozen section immunotyping and gene rearrangement studies confirmed the diagnosis of TLCL. To our knowledge, this case represents only the second report of TLCL associated with NLPHD and is of significance in that: (1) it demonstrates that T-cell neoplasia can occur in the setting of NLPHD; (2) this case does not appear to represent histologic progression of NLPHD and most likely represents de novo disease that may be secondary to chemotherapy; and (3) the clinical course may differ from the favorable prognosis seen in NLPHD associated with B-cell NHL.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed1994

Neural cell-adhesion molecule (CD 56)-positive, t(8;21) acute myeloid leukemia (AML, M-2) and granulocytic sarcoma.

A 49-year-old man with t(8; 21) acute myeloid leukemia relapsed 8 months after successful induction chemotherapy with a paraspinal granulocytic sarcoma. There was no evidence of leukemia in the bone marrow at relapse. At initial presentation, the blasts co-expressed CD 15, CD 33, CD 34, CD 45, CD 19, and CD 56 (a neural cell-adhesion molecule). Expression of certain cell-adhesion molecules on leukemic blasts may determine a tendency to develop extramedullary relapse. The co-expression of CD 56 may have a role in the predisposition of t(8; 21) AML to develop GS.

Antigens, CD↗
PubMed1994

Modeling gas exchange in a closed plant growth chamber.

Fluid transport models for fluxes of water vapor and CO2 have been developed for one crop of wheat and three crops of soybean grown in a closed plant growth chamber. Correspondence among these fluxes is discussed. Maximum fluxes of gases are provided for engineering design requirements of fluid recycling equipment in growth chambers. Furthermore, to investigate the feasibility of generalized crop models, dimensionless representations of water vapor fluxes are presented. The feasibility of such generalized models and the need for additional data are discussed.

Carbon Dioxide↗
PubMed1994

Gamma/delta T-cell posttransplantation lymphoproliferative disorder primarily in the spleen.

A 31-year-old renal transplant recipient developed an unusual T-cell lymphoproliferative disorder 3 years after transplantation. The neoplasm involved the spleen, without concomitant hepatomegaly, lymphadenopathy, or obvious bone marrow involvement. Peripheral blood involvement developed after splenectomy. Immunophenotypically, the neoplastic cells expressed CD2, CD3, CD7, CD16, CD45, CD56, and the gamma/delta T-cell receptor on the surface membrane. The neoplastic cells were negative for surface membrane CD4, CD5, and CD8. Serologic and/or DNA analyses for viruses, including Epstein-Barr virus, human T-cell lymphotropic virus-1, human immunodeficiency virus, and human herpesvirus-6, were negative. Cytogenetic findings included a translocation breakpoint at chromosome 7p15, consistent with involvement of the T-cell receptor gamma-chain locus. Although gamma/delta T-cell lymphomas have been reported to have a predilection for hepatosplenic localization, this is the first well-documented case to be described in the setting of posttransplantation immunosuppression.

Adult↗