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The clinical and pathological features of two patients with chronic myeloid leukaemia who died from lymphosarcoma are described. Both had been treated with busulphan which, at the time of development of lymphosarcoma and at death, appeared to be controlling the leukaemia satisfactorily.
Homogenous populations of malignant cells from the spinal fluids of two patients with metastatic lymphosarcoma were studied immunologically and by scanning electron microscopy (SEM). The malignant cells in both spinal fluids were shown to be of B-cell origin. The surface morphology of these cells was variable with the majority of the cells having numerous microvilli and a minority having few or no microvilli. This appears to be the first report on the surface ultrastructure of B-lymphosarcoma cells suspended in spinal fluid.
Peripheral blood from 125 patients (160 specimens) with various types of lymphoid leukemias was evaluated for B- and T-cell markers (E rosettes, C3 and Fc receptors, and surface immunoglobulin). B-cell leukemias (comprised 82% of the series and included chronic lymphocytic leukemia (69/71 cases), acute lymphocytic leukemia (1/18 cases), lymphosarcoma cell leukemia (15/18 cases), prolymphocytic leukemia (one case), plasma cell leukemia (one case), hairy cell leukemia (12/12 cases), and leukemic phase of "histiocytic" lymphoma and Waldenström's macroglobulinemia (one case each). Within the B-cell group, certain leukemias exhibited distinct patterns of lymphocyte surface markers. Three cases of lymphosarcoma cell leukemia revealed both T and B cell markers (E-rosette formation and monoclonal SIg). T-cell leukemias comprised 12% of the series and included chronic lymphocytic leukemia (2/71 cases), acute lymphocytic leukemia (11/18 cases), and Sézary's syndrome (2/2 cases). In eight cases of acute lymphocytic leukemia, the majority of the cells demonstrated no definable markers (non-B, non-T cell type). Ultrastructural studies, performed in selected cases, were correlated with immunologic findings. Distinctive morphologic features were observed for different variants of B- and T-cell leukemias. Neoplastic cells of T-cell leukemias revealed a greater nuclear irregularity than B-cell proliferations, as assessed by the nuclear contour index (ratio of circumference to the square root of the nuclear area). The cytoplasmic feature most predictive of immunologic cell type was abundant rough endoplasmic reticulum, suggesting plasmacytoid differentiation, observed in some B-cell proliferations.
The mechanism of effectiveness of allogeneic versus syngeneic immunization in mounting a humoral specific immune response against tumor-associated antigens of murine urethan-induced thymic lymphosarcomas was studied. C57BL mice immunized with untreated or blocked C3Hf lymphoma cells yielded sera with complement-dependent cytotoxicity for C57BL lymphosarcomas, whereas they did not respond to repeated injections of blocked syngeneic lymphoma cells, indicating a helper activity of alien alloantigens in the reflex of tumor antigens. Thymectomized, lethally-irradiated and T, but not B-reconstituted mice produced active sera, suggesting a T-dependent response. The anti-tumor activity of the serum ran parallel with the anti-histocompatibility one. The tumor-associated and the alien histocompatibility determinants had to be present on the same cell membrane. In addition, active sera were obtained when immunizing syngeneic lymphoma cell inocula were followed by allogeneic normal immunocompetent cells. It is suggested that either a helper mechanism with B and T cells cooperating in recognizing haptenic tumor-associated and carrier histocompatibility antigens or a graft-versus-host reaction determining an abnormal induction of the immune system is needed in order to detect the weak tumor-associated antigens of urethan-induced lymphomas.
A new chlorambucil ester of prednisolone (LEO 1031) has been evaluated in patients with advanced lymphocytic lymphosarcoma and chronic lymphocytic leukemia. All 11 patients had been previously treated with radiotherapy and/or combination chemotherapy. Three complete remissions and one partial remission were seen in 4/7 lymphocytic lymphosarcoma patients treated with LEO 1031. In the chronic lymphocytic leukemia group, 3/4 have had benefit. This new drug is considered worthy of further trial.
This is a retrospective study of 14 patients with lymphosarcoma with hypersplenism. Eight patients received radiation to the spleen followed by splenectomy for recurrence of hypersplenism. Six patients underwent primary splenectomy for hypersplenism. Radiation decreases the size of the spleen but recurrence of hypersplenism is seen in an average of 8 mo. Splenectomy in these cases improves the hematological picture. Average postsplenectomy survival is 27.6 mo. Splenectomy alone in hypersplenism also improves the hematological picture. Postsplenectomy survival in this group is 13 mo. One case of primary lymphosarcoma of the spleen is reported.
Brain lymphosarcoma may be divided into the circumscribed forms, surrounded by marked oedema with fibrin, and the diffuse or infiltrating forms. Cytology of the former is more uniformly lymphocytic, its clinical course is more rapidly fatal. Anatomically primary diffuse lymphosarcoma of the brain may be secondary to 'cured' systemic lymphoma.
Previously we have described the infiltration of lymphosarcoma cells into hepatocyte cultures. The interaction between tumor cells and hepatocytes was comparable to that occurring during the formation of liver metastases. Presently we report that antigen-activated T lymphocytes, but not unstimulated T cells, infiltrate hepatocyte cultures in a manner comparable to the lymphosarcoma cells. Thus, liver-colonizing lymphoid tumor cells and activated non-transformed T cells apparently have common characteristics, that enable them to infiltrate between liver cells. A comparative study of activated and non-activated T cells may aid in elucidating these characteristics. In the intact liver activated lymphocytes did not infiltrate, probably because they were not arrested.
A case of primary lymphosarcoma of testis was studied by light and electron microscopy. The fine structure of the lymphosarcoma cells was simple and monotonous. The cytoplasm was scanty and contained normal-looking organelles. Free ribosomes were abundant and the Golgi apparatus was well developed. The nuclei were large and irregular in shape with prominent nucleoli. "Nuclear pockets" enclosing material similar to the cytoplasmic ground substance were found infrequently. Remnants of disintegrating cells were also encountered.
A detailed survey is given to the problem of malignant tumours of the spermatic cord. The authors present their own case of lymphosarcoma of the spermatic cord. They found only three cases of lymphosarcoma of the spermatic cord in the accessible literature. In the treatment of these malignant tumours they prefer to make radical operation - hemicastration with total extirpation of the spermatic cord - followed by radiotherapy.
In a patient who had a family history of ulcerative colitis and colonic carcinoma, a jejunal lymphosarcoma developed four years after resection for Crohn's disease of the small intestine. It is suggested that the association of lymphosarcoma with Crohn's disease is more than a chance association.
Examination of the records of 378 children with intussusception at our institution revealed that 29 cases were caused by an identifiable intestinal lesion. A Meckel's diverticulum was the causative agent in 21 children, all of whom were under 2 yr of age. A previously undiagnosed ileal lymphosarcoma produced the intussusception in six other children, all between 6 1/2 and 9 yr of age. Our experience indicates that any child over 6 yr of age with the clinical findings of colicky abdominal pain, bloody stools, and a palpable mass plus the radiographic evidence of intussusception must be considered to have ileal lymphosarcoma until proven otherwise. Hydrostatic reduction of the intussusception must be accompanied by extensive small bowel reflux of barium in order to effectively rule out a small intestinal lesion. If this is not accomplished, surgery should be planned with the suspicion that a malignancy may be present. If this suspicion is confirmed by frozen section, the operation procedure should include wide surgical excision of the lesion along with the regional lymph nodes.
Sheep are highly susceptible to BLV infection and can be infected via several different means (routes). In all inoculated animals, specific anti-BLV antibodies can be demonstrated 1 to 3 months post-inoculation (p.i.). Between 10 and 13 months p.i., a moderate but persistent lymphocytosis (PL) may be detected in about 50% of the infected animals. This hematological disorder may be, but is not necessarily, associated with the development of a lymphosarcoma and can (might) be interpreted as a true lymphoid leukemia. According to findings revealed by immunolabelling and mitogen stimulation of peripheral blood lymphocytes, BLV-induced PL appears to be a B-cell disorder. Induced lymphosarcoma appears in about 40% of infected sheep during the 6 years p.i. It too is of B-lymphocyte lineage. In vitro studies demonstrate that BLV antigen is expressed exclusively in B-lymphocytes. Yet, BLV expression is greatly stimulated in whole lymphocyte culture by the addition of T-cell mitogen. This same phenomenon occurs when the supernatant of stimulated T-lymphocyte cultures is added to isolated BLV-infected B-lymphocytes. This observation supports the hypothesis that, as is the case with other retroviruses such as HIV, BLV is able to use the regular activation machinery of the immune system for its own replication and transmission. It seems, therefore, that the leukemia-lymphoma complex in sheep may serve as an accurate experimental model for the study of the biological properties of retroviruses.
Increased synthesis of prostaglandins (PGs) may be an important promoting factor in the development of lymphosarcoma. Thus, inhibition of PG synthesis may represent a logical way of controlling the growth of lymphosarcomatous cells. In order to verify this hypothesis, two groups of rats with lymphosarcoma have been used: the test-group received acetyl salicylic acid (54 mg/animal/day) and the control-group received the same quantity of physiological saline solution. After 4 days of treatment, the lymph nodes stopped growing in the test-group. Microscopic and electron microscopic examinations of lymph node sections were carried out after 11 days of treatment. These showed for the test-group the disappearance of the characteristics of malignancy.
Binding of the glucocorticoid receptor complex to nucleosomes has been studied using the mouse P1798 lymphosarcoma. Cells were incubated with [3H]triamcinolone acetonide (TA), and nuclei prepared and digested with 3 different concentrations of micrococcal nuclease. After fractionation with EDTA and NaCl, it was observed that [3H]TA bound with similar specific radioactivity to mononucleosomes containing both core and linker DNA, of 183 +/- 5, and 168 +/- 4 base pair lengths, respectively, as well as to core size DNA, of 148 +/- 3 base pair length, suggesting that the glucocorticoid receptor bound to the core portion of the nucleosome. Steroid binding was found to be associated with regions of the nucleosome that were depleted in histone H1 and enriched in high mobility group (HMG) proteins 1 and 2; only negligible binding was noted in nucleosomes enriched in histone H1 and depleted in HMG proteins. In addition to binding to core nucleosomes, the glucocorticoid receptor complex was also shown to bind to a fraction sedimenting at 5-6 S on sucrose gradients characterized by subnucleosome and mononucleosome size DNA, as well as by core histones. While binding of the steroid receptor complex to linker regions of the nucleosome cannot be ruled out, this data would appear to present the first concrete evidence that glucocorticoid binding, at least in the P1798 lymphosarcoma, is to core nucleosomes. Some caution in interpretation of the results is indicated, however, on 2 points: (1) receptor redistribution during nuclease digestion cannot be ruled out; (2) only the binding of a small proportion of the steroid receptor complex may be physiologically relevant.
Glucocorticoid receptors (GCRs) were characterized in sublines of the mouse P1798 lymphosarcoma that are sensitive (S) or resistant (R) to glucocorticoid-mediated apoptosis. Previous work had identified two steroid-binding GCRs in S and R cells: a 97 kDa wild-type GCR in S cells (WT-GCR), and a 45 kDa truncated GCR in R cells (TR-GCR). A third GCR, a 97 kDa nonsteroid-binding GCR (NSB-GCR), was also identified in R cells. Using subcellular fractionation and Western blotting, we now show that in contrast to the WT-GCR which is localized in both the cytoplasm and nucleus of S cells, the NSB-GCR is localized predominantly in R cell nuclei. Moreover, gel filtration chromatography revealed that treatment with 400 mM NaCl and heat did not significantly alter the Stokes radius of the NSB-GCR suggesting that this receptor is not present in a heterooligomeric complex with other proteins. The TR-GCR was localized predominantly in the soluble cytoplasmic fraction but also in the crude membrane fractions of R cell nuclei, suggesting that this receptor is tightly associated with nuclear structures. It was not detected in the soluble nuclear fraction. Unexpectedly, a 45 kDa nonsteroid-binding immunoreactive protein was detected in crude membrane fractions of S cells. These studies describe a complex GCR system in the P1798 lymphosarcoma that necessitates a further consideration of glucocorticoid signaling in S and R cells.
The acetylated isoforms of histone H4 from mouse lymphosarcoma cells treated with HDAC inhibitors trichostatin A (TSA) and depsipeptide (DDP) were separated by acetic acid urea-polyacrylamide gel electrophoresis (AU-PAGE), in-gel digested, and analyzed by matrix assisted laser desorption/ionization time-of-flight mass spectrometry (MALDI-TOF MS) and liquid chromatography tandem mass spectrometry (LC-MS/MS). The acetylation pattern of histone H4 in mouse lymphosarcoma cells induced by TSA was established in which acetylation initially occurred at K16 followed by K12 and then K8 and/or K5. An identical order of acetylation was found for cells treated with DDP.
To characterize the cell-surface antigens expressed in tumour cells derived from bovine leukosis and to determine their cell lineages, the immunophenotypes of the tumour cells from 13 bovine lymphosarcomas were examined with 13 monoclonal antibodies (mAbs). Of 13 cattle with lymphosarcomas, four were identified clinically as having the thymic-type sporadic bovine leukosis (SBL) and one as having the skin-type; two had enzootic bovine leukosis (EBL) and six were untypable. Flow cytometric analysis revealed that the tumour cells from nine cases were of T-cell lineage (BoCD5+, BoCD2+ or BoCD2-) and two were of B-cell lineage (MHC-II+, BoCD5+, IgM+); there were two bovine leukaemia virus-infected cattle (EBL). T-cell tumours appeared to originate from immature (BoCD4-, BoCD8-) T cells, but there was no significant relationship between clinical type (EBL, calf-, skin- and thymic-type) and tumour-cell immunophenotype.