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The ultrastructural findings of two cases of "blue nevus" in ovarian benign cystic teratomas are described. The bipolar or dendritic pigmented cells showed features of Schwann cells with melanin synthesis, but not of ordinary melanocytes. This study supports the neural origin of blue nevus.
Using in vitro cell-marking experiments and transplantation in tail regenerates, we have recently shown (Benraiss et al., 1996) that clonal cells derived from adult newt spinal cord (SC) cultures could find suitable cues in blastemal mesenchyme to enable them to differentiate into melanocytes or Schwann cells. This led to the question of whether neural crest-like cell derivatives might emerge from the ependymal tube as tail regeneration proceeded. To address this question we used the biolistic method for in situ transfection of caudal SC cells. These cells were transfected with an alkaline phosphatase marker gene. The potentialities of transfected cell derivatives in tail regenerates were analyzed using histochemistry or immunohistochemistry. As early as eight days after transfection, labeled cells were detected in the regenerating SC and around its "terminal vesicle" (TV). Two to four weeks following transfection, most of the labeled cell derivatives could be identified either by dark granules as melanocytes or by galactocerebroside staining as Schwann cells. Electron microscopic investigations revealed the incompletely organized cytoarchitecture of the TV, suggesting that an exit of cells was possible at this level, at least from its "open" dorsal part. Furthermore, the localization of ciliated cells in the blastemal mesenchyme, especially around the TV, supported this view by suggesting that they might be ependymal cells detached from it. Our findings therefore led us to believe that in the newt, during tail regeneration, neural crest-like cells emerging from the TV could participate in the formation of the peripheral nervous system, especially by providing Schwann cells and melanocytes.
Most lymphoblastic lymphomas (LBLs) are regarded as neoplasms of immature T cells because they express cytoplasmic CD3 and frequently carry T-cell receptor (TCR) gene rearrangements. Immature natural killer (NK) and T cells, however, have a common bipotent T/NK-cell precursor in the thymus, and NK cells also express cytoplasmic CD3. Thus, some LBLs could arise from immature NK cells. Mature NK cells express 2 CD94 transcripts: 1A, induced by interleukin 15 (IL-15), and 1B constitutively. Because immature NK cells require IL-15 for development, CD94 1A transcripts could be a marker of NK-LBL. To test this hypothesis, we used laser capture microdissection to isolate IL-15 receptor alpha(+) lymphoid cells from the thymus and showed that these cells contained CD94 1A transcripts. We then assessed for CD94 transcripts in 21 cases of LBL that were cytoplasmic CD3(+), nuclear terminal deoxynucleotidyl transferase positive (TdT(+)), and CD56(-), consistent with either the T-cell or NK-cell lineage. We found that 7 LBLs expressed CD94 1A transcripts without TCR gene rearrangements, suggesting NK-cell lineage. Patients with NK-LBL were younger than patients with T-LBL (15 years versus 33 years; P = .11) and had a better 2-year survival (100% versus 27%; P < .01). These results improve the current classification of LBL and contribute to our understanding of NK-cell differentiation.
The specificities of six monoclonal antibodies produced against plasminogen activator of the human Bowes melanoma cell line are described. They have been used to detect membrane-bound plasminogen activator on cultured human lymphoid cell lines and in neoplastic human lymphocytic and myeloid cells of leukemic patients. These studies indicate that only certain phenotypic subsets of the T-cell lineage derived from patients with chronic lymphocytic leukemia or with Szezary syndrome express plasminogen activator on their surface membrane.
A calf with a lymphoproliferative disease resembling human mycosis fungoides, had multiple, ulcerated skin nodules with enlarged regional lymph nodes. Tumor cells were 10-15 micron in diameter and had round to oval nuclei without indentations. Mitoses were regularly present. Pautrier's microabscesses were in the epidermis, and T-cell areas of regional lymph nodes were infiltrated by neoplastic cells. Demonstration of the T-helper/inducer origin of neoplastic lymphocytes suggested classification in analogy with human mycosis fungoides.
Human B-cell lines derived from normal donors (LCL) or from Burkitt lymphomas (BL) were compared for their sensitivity to natural (NK) and interferon (IFN)-activated (IAK) cytotoxicity, mediated by effector cells from normal human blood. In four cases, a BL and an LCL line were derived from the same donor and had been kept in culture for the same period of time. The BL series included both Epstein-Barr virus (EBV)-carrying and EBV-negative lymphoma lines. The latter were compared with their own EBV-converted, Epstein-Barr nuclear antigen (EBNA)- and EBV-DNA-positive sublines, established by in vitro infection with two different viral substrains. LCL and BL lines from the same donor were lysed with equal efficiency by both NK and IAK effectors. There was no relationship between the NK sensitivity and the nude mouse tumorigenicity of different EBV-converted Ramos sublines, or the expression of differentiation markers such as insulin receptor, surface IgD, and the B2 surface antigen. Moreover, EBV-converted sublines of BJAB differed in their NK sensitivity, in spite of closely similar expression of these markers. NK-sensitive Ramos and BJAB sublines induced a stronger proliferative response upon confrontation with allogeneic lymphocytes than their NK-resistant counterparts. This suggests that the target cell may play an active role in triggering the lytic interaction. There was no correlation between this property and any of the other parameters studied.
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Processed pseudogenes emerge by reverse transcription of spliced mRNAs followed by incorporation of the resultant cDNA into the genome. Their genesis requires that retrotransposition occurs within the germ line, a provision that significantly limits random distribution of source genes. We previously identified embryonic stem cell-specific genes as an enriched source of retropseudogene origin. Nanog, Oct4, and Dppa3 (Stella/PGC7) presented as source genes for >30 processed pseudogenes within the human genome. In the current study, we extended our previous analysis and focused on the pluripotent cell-specific Dppa gene family. Of the five Dppa genes characterized, four were associated with putative retropseudogenes as determined by nucleotide BLAST (basic local alignment sequence tool) searches of the respective mRNA transcripts against the human genome. A subset of the 11 Dppa3-derived hits were then screened against a human adult tissue cDNA panel for evidence of transcriptional activity. One of the putative Dppa3-derived retropseudogenes, Dppa3(d), located on human chromosome 16p13, tested positive for mRNA transcript in bone marrow, peripheral blood, pancreas, adrenal gland, and thyroid gland. Specificity against the source Dppa3 gene expression was sequence verified, and independent human tissue samples were obtained to confirm Dppa3(d) expression. These data substantiate the existence of human adult tissue-specific transcripts that originate via retrotransposition of the pluripotent cell-specific gene, Dppa3. Further studies may reveal an evolutionary role for this example of genetic diversity, but in the short term our observations serve a cautionary purpose regarding the use of Dppa3 transcripts in adult tissue-derived cells as a potential marker of pluripotency.
We have studied the cellular pharmacology of doxorubicin in a line of mouse sarcoma cells isolated from a dimethylbenzanthracene-induced autochthonous tumor. We have studied the cytotoxicity of the drugs as a function of the exposure dose and of the exposure time to the drug. Cytotoxicity was evaluated as the inhibition of the incorporation of [3H-methyl]-thymidine in the cellular nucleic acids. Intracellular drug concentrations were measured by spectrofluorometry. We have shown that the intracellular drug concentration was a linear function of the extracellular drug concentration up to 5 micrograms/ml; the cytotoxicity was an exponential function of the exposure dose up to 1 micrograms/ml, but it was not an exponential function of the exposure time: the cytotoxicity may therefore be very different for similar total drug exposures. Incubation with a low dose for a long time did not provide a cytotoxicity as high as that obtained with a high dose for a short period of time. These results emphasize the role of the peak concentration of doxorubicin for its maximal action in the target cell.
Canine distemper virus (CDV) growth and the morphological characterization were examined in a cell line established from a canine malignant histiocytosis (CCT cell line). The susceptibility of the CCT cells to 3 CDV strains, FXNO, YSA-TC and MD-77 was shown by detection of the antigen in the indirect fluorescent assay. After passaging 4 and 9 times through the CCT cells, only FXNO strain could produce the syncytia where demonstrated the antigens. Titers of 9 passaged viruses through the CCT cells showed slightly higher in the CCT cells than those in Vero cells. Morphological characterization of karyorrhexis and specific DNA ladder by extracted DNA electrophoresis indicated apoptosis in the CDV infected CCT cells.
A case of bilateral testicular germ cell tumors in a 23-year-old male is reported. He was admitted to the Department of Urology, Yamagata Prefecture Kahoku Hospital with the chief complaint of painless swelling in the left intrascrotal contents. Left high inguinal orchiectomy was carried out. At the same time, right hydrocele operation and right testicular biopsy were performed. Subsequent histological examination revealed anaplastic seminoma in the left testis and typical seminoma in the right. On July 21, 1988, he was referred to our clinic and right high inguinal orchiectomy was carried out. Postoperative chemotherapy was performed with CDDP, VP-16 and peplomycin, and postoperative course was uneventful with no distant metastasis or local recurrence. A total of 136 cases of bilateral testicular germ cell tumors in the Japanese literature are reviewed.
We examined the arrangement of the mu heavy-chain immunoglobulin (Ig) genes in the leukemic blast cell DNA of 93 children with acute lymphoblastic leukemia (ALL). All cases met morphologic and cytochemical criteria for ALL, lacked detectable T cell surface antigens, and expressed HLA-DR (Ia) antigens. Eighty-three of the 93 patients (89%) were positive for the common acute lymphoblastic leukemia antigen (CALLA), and 20 of 91 (22%) tested had detectable cytoplasmic immunoglobulin. As expected, the heavy-chain lg gene was rearranged in all cases, and the pattern of rearrangements was variable; 23 had one allele rearranged and one in the germ line configuration; 15 had one rearranged and one deleted; and 37 had two rearranged. Unexpectedly, in 18 patients the presence of more than two mu gene-hybridizing bands was detected. Combinations of enzymes and heavy-chain gene probes were used to confirm that the extra bands were not the result of underdigestion of the DNA or DNA restriction site polymorphism. In eight of the 18 patients, we identified an extra chromosome 14 as a possible cause of the extra bands' hybridizing to the mu heavy-chain constant-region probe. In the remaining ten patients, the presence of three or four bands hybridizing with the mu probe suggests the presence of two populations of leukemic cells that may have arisen either by separate leukemic transformation events or by clonal evolution of one clone into two related lines. Although preliminary (2-year follow-up), our data suggest that childhood ALL of B lineage with more than two mu heavy-chain genes, but without extra copies of chromosome 14, may be more resistant to therapy.
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