A subclone (5C6) of the human mast cell line HMC-1 represents a more differentiated phenotype than the original cell line.
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Antigens, Surface↗
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Stromal-mediated down-regulation of CD13 in bone marrow cells originating from acute myeloid leukemia patients.
The metallopeptidase CD13 is expressed on normal myeloid cells of monocytic and granulocytic origin and on the surface of leukemic blasts in most acute myeloid leukemias (AML). To study the mechanisms regulating lineage restricted CD13 expression in AML we determined normalised CD13 mRNA levels in bone marrow cells and peripheral blood cells of 27 AML patients. Cells of bone marrow origin had lower levels of normalised CD13 mRNA than cells of peripheral blood origin, even though fluorescence intensity and fraction of cells expressing CD13 on the surface was unchanged. In particular, AML patients with very low levels of normalised CD13 mRNA in bone marrow cells showed an increase in CD13 mRNA expression in peripheral blood. To evaluate the effects of bone marrow microenvironment on CD13 mRNA expression, we cultured leukemic myeloid cells with and without murine stromal cells. Bone marrow cells with high and low CD13 surface expression that entered the stromal layers all down-regulated CD13 mRNA expression as compared to cells in suspension above. For peripheral blood cells within stromal layers, CD13 mRNA expression was diminished in only 3 out of 6 cases. The ambiguous effect of stromal cells on peripheral blood cells may illustrate a differentiation-dependent response towards stroma. We determined the polyadenylation status of CD13 mRNA for 9 bone marrow aspirates and 7 peripheral blood samples. Polyadenylation was diminished in bone marrow cells from AML patients with low levels of normalised CD13 mRNA, raising the possibility of involvement of mRNA instability in regulation of CD13 mRNA expression in this subgroup of patients.
Acute Disease↗
Different morphology and proliferative ability of cumulus and granulosa cells originating from cystic follicles aspirated from stimulated in vitro fertilization patients.
OBJECTIVE: To investigate the morphology and proliferative ability of cumulus and granulosa cells (GCs) originating from cystic follicles and normal-sized follicles after ovarian stimulation. DESIGN: Granulosa cells, cumulus cells, and follicular fluid (FF) were aspirated from cystic follicles and normal-sized follicles from the same ovary. Morphology and proliferative ability of cumulus and GCs were assessed by Giemsa stain and thymidine incorporation, respectively. Cell proliferation was assessed in medium or FF originating from cystic follicles or normal-sized follicles. RESULTS: An oocyte was found in 40% of the cystic follicles versus 68% in the normal-sized follicles. Changes in dispersion and adhesion properties were observed in cystic versus normal aspirated corona cumuli complex. Proliferative ability was consistently lower in GCs originating from cystic follicles versus normal-sized follicles. Proliferation of GCs originating from normal-sized follicles or cystic follicles was inhibited or increased when grown in FF from cystic follicles or FF from normal-sized follicles, respectively. Differences in embryo quality were significantly in favor of oocytes originating from normal-sized follicles. Although the fertilization rate of those oocytes appeared to be higher, the difference was not of statistical significance. CONCLUSIONS: Inhibition of GC proliferation in FF from cystic follicles can be reversed by incubating cells in FF from normal-sized follicles. We conclude that factors in the FF may affect cell proliferation.
Cell Division↗
Mouse papillary lung tumors transplacentally induced by N-nitrosoethylurea: evidence for alveolar type II cell origin by comparative light microscopic, ultrastructural, and immunohistochemical studies.
A histogenetic study was designed to evaluate controversial findings on the cell of origin of tubular/papillary lung tumors in mice, i.e., bronchiolar Clara cell versus alveolar type II cell. N-Nitrosoethylurea (0.5 mmol or 0.74 mmol/kg) was given to pregnant C3H (C3H/HeNCr MTV-) and Swiss Webster [Tac:(SW)fBR] mice as a single i.p. injection on Day 14, 15, 16, or 18 of gestation. The offspring were studied at various ages ranging from 7 days to 52 wk. Serial sections of the whole lung (100 to 200 sections per mouse) showed that solid/alveolar and papillary tumors arose from the pulmonary acinus, invading the bronchioles only as the tumors grew. Furthermore, a mixture of solid and papillary patterns within a single module did not represent a merging of two tumors but a progression from the solid to the papillary form. By use of two rabbit antisera against mouse lung surfactant apoproteins found in normal alveolar type II cells, it was shown by the avidin-biotin peroxidase complex procedure, by the peroxidase-antiperoxidase technique, and by indirect immunofluorescence that both solid and papillary tumors contained these proteins that are specific markers for alveolar type II cells. With a rabbit anti-rat Clara cell antiserum, none of the tumors studied was immunoreactive while normal Clara cells were reactive. The nitroblue tetrazolium formazan stain for dehydrogenase enzymes, found particularly in Clara cells, did not reveal these enzymes in any lung tumors from either strain. Ultrastructurally, no typical features of the mature Clara cell were detected in papillary or other pulmonary neoplasms. However, all tumors showed characteristic alveolar type II cell structures such as various stages of lamellar body formation, although these features were less well differentiated in the papillary tumors. Argentaffin dense bodies, representing lysosomes and immature forms of lamellar bodies, were commonly observed in papillary tumors. Some features of the papillary tumors such as cell shape, high glycogen content, and primary cilia were equivalent to those seen in pulmonary epithelial precursor cells during fetal development. With age, the papillary tumors became invasive, accumulated neutral lipids, and developed bizarre cleaved nuclei and lamellated nuclear pseudoinclusions. In conclusion, the papillary lung tumors of the mouse, at least those induced transplacentally by N-nitrosoethylurea, constitute less well-differentiated or poorly differentiated alveolar type II cell adenomas or carcinomas with fetal morphological and biochemical properties.
Age Factors↗
Malignant lymphomas of follicular center cell origin in man. II. Ultrastructural and cytochemical studies.
Tissues from malignant lymphomas with both nodular and diffuse growth patterns, thought by light microscopy to be composed of cells of follicular center cell (FCC) origin, Were examined by electron microscopy; the tumor cells were similar to lymphoid cells found in reactive follicular centers. Tumor cells from neoplasms thought to be composed of cleaved FCC often had more pronounced nuclear folding than did cleaved FCC of reactive follicles, whereas cells in tumors of noncleaved FCC type were indistinguishable from their presumed counterparts in reactive follicles. Large cell noeplasms, previously classified as "histiocytic" lymphomas were composed of cells with ultrastructural characteristics of transformed lymphocytes; they showed neither ultrastructural nor cytochemical features of mononuclear phagocytes. These findings support the concept that a major group of lymphomas arises from lymphocytes of follicular centers.
B-Lymphocytes↗
Free serosal cells originating from the embryo of the wasp Diadromus pulchellus in the pupal body of parasitized leek-moth, Acrolepiosis assectella. Are these cells teratocyte-like?
In braconid species, teratocytes are derived from a serosal cell membrane which envelops the developing parasitoid embryo. On hatching, this membrane dissociates into individual cells, the teratocytes, which then circulate in the haemolymph of the host. We describe herein such a membrane, surrounding the embryo in eggs of the ichneumonid parasitoid wasp, Diadromus pulchellus. This membrane consisted of a single sheet of tightly packed cells with large 12+/-1.4 &mgr;m nuclei. These cells were released after hatching in vitro and cells of the same size were detected in vivo, in the vicinity of the D. pulchellus embryo. The number of nuclei detected suggests that the serosal membrane consists of about 450+/-150 cells. These cells did not grow after hatching of the parasitoid egg in the parasitized host, Acrolepiosis assectella, during the development of the parasitoid wasp larva. Southern blot experiments, using D. pulchellus satellite DNA or the ribosomal genes as probes, showed that free-living floating cells of wasp origin were present in the body of the parasitized host. This is the first time that free-floating teratocyte-like cells have been described in species of the Ichneumonidae.
Journal Article↗
Demonstration of mouse cells on human teeth by fluorescent antibody technique after replacement of the original cells.
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Animals↗
Clues to leukemia and blood cell origins revealed.
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Animals↗
Simultaneous chronic lymphocytic leukemia and chronic myelogenous leukemia. Evidence of a separate stem cell origin.
The authors studied a patient with the simultaneous occurrence of chronic lymphocytic leukemia (CLL) and chronic myelogenous leukemia (CML). The coexistence of these two hematologic malignancies leads to questions about their cell of origin. Through analysis of this patient's DNA, the authors studied the derivation of the two malignancies. They separated the blood into a myeloid-rich fraction and a fraction containing the malignant lymphocytes. JH and bcr probes were used to study these loci in the myeloid and lymphoid fractions and in unfractionated white blood cells. The authors found that the unfractionated leukocytes contained the bcr and JH rearrangements. Conversely, the lymphoid fraction contained only the JH rearrangement, and the myeloid fraction contained only the bcr rearrangement, suggesting that these malignancies arose from separate stem cells. This is the first reported patient with simultaneously occurring CML and CLL definitively shown to arise from distinct progenitors, and this report raises questions about the origin of these two cell lines.
Aged↗
Heterogeneous in situ immunophenotyping of follicular dendritic reticulum cells in malignant lymphomas of B-cell origin.
The phenotype of follicular dendritic reticulum cells (DRC) was analyzed with monoclonal antibodies (DRC-1, OKB7, BA-2, Leu-M3, and antidesmoplakin 1 and 2) in 28 frozen biopsy specimens of both morphologically and phenotypically analyzed B-cell lymphomas and 21 normal or reactive controls. The former included 15 follicular center cell lymphomas (FCCL), four intermediately differentiated lymphocytic lymphomas (ILL), four mantle zone lymphomas (MZL), and five well-differentiated lymphocytic lymphomas (WDLL). In controls, DRC-1+ and OKB7+ DRC were localized in both follicular centers (FC) and mantle zones (MZ), but BA-2+ and Leu-M3+ DRC were confined to FC only. FCCL were usually accompanied by DRC-1+, OKB7+, and BA-2+ DRC, and either lost or maintained positively with Leu-M3 from case to case. By contrast, MZL consistently lacked BA-2+ and Leu-M3+ DRC, and was associated with DRC-1+ and OKB7+ DRC only. Desmoplakin-positive DRC occurred in variable proportions in both FCCL and MZL. As opposed to FCCL and MZL, all WDLL and all but one of the ILL (associated only with DRC-1+, OKB7+, and desmoplakin+ DRC) did not show any DRC as identifiable with the antibody panel used. Remarkably, the difference in the distribution of BA-2+ and Leu-M3+ DRC in the normal FC and MZ appears to be maintained in their neoplastic counterparts (FCCL and MZL) also. Such a difference represents an example of the possible interactions between lymphoma cells of different phenotype and their microenvironment, as portrayed by phenotypically heterogeneous DRC.
Antibodies, Monoclonal↗
Gut mucosal mast cells. Origin, traffic, and differentiation.
Gut mucosal mast cells (MMC), which are nearly absent in normal mice are abundant during nematode infection. In normal mice, study of MMC precursors (MMC-P: cells giving rise to MMC colonies in the presence of IL-3) show that: (a) their frequency, judged by limiting dilution is very high in bone marrow (BM) and gut, and very low in most lymphoid organs and thoracic duct lymph (TDL); (b) gut MMC-P are Thy-1- Lyt-1-2- and are not rapidly replicating; (c) they are the progeny of less differentiated BM MMC-P which are attracted from the blood to the gut mucosa by local factor(s), other than antigen and T cell factors (since normal amounts of gut MMC-P are found in germ-free, nude, and newborn mice). In mice bearing the Wehi 3 tumor (which releases enough IL-3 to produce detectable blood levels) spleen and mesenteric lymph nodes (LN) show increased MMC-P frequency, the greatest increase being in the gut and BM, where numerous differentiated MMC are found. In Nippostrongylus brasiliensis (Nb)-infested mice (known to develop a large, T cell-dependent, gut MMC infiltration), gut MMC-P proliferation is induced by IL-3 released from gut mucosal Thy-1+ Lyt-2- cells, whose in vitro IL-3 release capability is much higher than that of similar cells from normal mice. Both Nb-stimulated T blasts and proliferating MMC-P undergo cyclic traffic, migrating into the TDL and then seeding the whole length of the gut (a process which allows a widespread immune defense after a local antigenic stimulus). Experiments using 2-d interruption of this traffic and fetal gut grafts, suggest that the continuous homing of T blasts back to the gut which leads to permanent Nb-stimulated IL-3 release, is essential for the full maturation of MMC. Transfer experiments in the rat show that TDL circulating MMC-P rapidly mature into MMC when they home back to the Nb-infested gut. It is proposed that gut MMC arise after several stages of progressive differentiation of MMC-P, influenced both by IL-3 and unidentified gut factor(s).
Animals↗
Regenerating goldfish retinal explants: induction and maintenance of neurites by conditioned medium from cells originated in the nervous system.
Fiber outgrowth from goldfish regenerating retinas can be induced by conditioned medium of cloned cells which originated in the nervous system, i.e. glioma and neuroblastoma. Dilution of the released factor(s) was required to achieve optimal effect; high concentrations are detrimental. The fibers can be maintained for at least 2 weeks in vitro, and reach a length of several millimeters. This system may provide a means to purify and characterize neurotrophic factors involved in nerve regeneration.
Animals↗
Amplified env and gag products on AKR cells. Origin from different murine leukemia virus genomes.
Thymocytes of AKR mice express two species of gp70, the envelope glycoprotein of murine leukemia virus (MuLV), encoded by the env gene. One is denoted Ec+ gp70 in reference to the type-antigen Ec and association with ecotropic virus. The other, Ec- gp70, resembles gp70 found also on thymocytes of mouse strains that are not overt producers of MuLV, and has no evident relation to ecotropic virus. Expression of Ec- gp70 type, but not of Ec+ gp70 type, is amplified with age on AKR thymocytes. In contrast, viral core polyproteins, encoded by the gag gene and simultaneously amplified with age, appear to be related to ecotropic virus. These observations imply selective amplification of products of env and gag genes from two sorts of provirus, a phenomenon which may be connected to the dual genetic origin of recombinant mink-cell-focus inducing viruses in AKR mice.
Animals↗
An extracellular body of plasma cell origin in inflammatory infiltrates within the dermis.
During examination of a biopsy specimen of skin by conventional microscopy, numerous round, basophilic, extracellular bodies suggestive of fungal organisms were seen in the dermis. Further evaluation and special staining suggested that their origin was from the plasma cells. Examination of biopsy material from 48 patients with cutaneous plasma cell infiltrates revealed similar bodies in 20 cases (42%). Sizes of bodies varied, the largest being 5.0 microns in diameter. In every case, staining reactions were identical to those of plasma cell cytoplasm. Immunoperoxidase methods showed that, like plasma cells, the bodies contained either kappa or lambda light chains. In one case of plasmacytoma associated with multiple myeloma, both the bodies and the surrounding neoplastic cells stained for kappa chains only. Electron microscopy revealed rounded structures composed of aggregates of rough endoplasmic reticulum, which contained varying amounts of moderately electron-dense material within the cisternae. Fragmented plasma cells were also seen. The evidence suggests that plasma cell bodies are distinct from Russell bodies. They probably form as a result of trauma during processing of tissue, but could also represent a degenerative process in vivo. They should be distinguished from pathogenic micro-organisms and other extracellular bodies.
Adult↗
Malignant fibrous histiocytoma. Evidence of perivascular mesenchymal cell origin immunocytochemical studies with monoclonal anti-MFH antibodies.
Using whole cell antigens prepared from the established lines of human malignant fibrous histiocytoma (MFH), the authors have generated two different monoclonal antibodies (FU3 and FU4) by a mouse hybridoma technique. By indirect immunoperoxidase in frozen tissue sections, FU3 and FU4 revealed strong staining of perivascular mesenchymal cells and fibroblasts. In the spleen FU3 stained perivascular cells of the ellipsoids and the marginal zone of the lymph follicles. Macrophages in granulation tissues as well as monocytes and other blood cells in normal peripheral blood were uniformly negative for the antigen detected by FU3. Among various soft-tissue tumors, MFH and liposarcoma reacted strongly with FU3 and FU4, but synovial sarcoma revealed no reaction with either of the antibodies. Immunoelectron-microscopic studies demonstrated positive reactions with FU3 and FU4 on the surface of MFH cell membrane, which suggests that these antibodies recognized cell surface antigens. In conclusion, MFH shares antigenicity with perivascular mesenchymal cells and fibroblasts as well as liposarcoma. MFH and liposarcoma may have a common origin from the perivascular mesenchymal cells that are supposed to have a potential for multidirectional differentiation.
Animals↗
MMC-E cells--origin and changes in karyotype accompanying malignant transformation.
Karyotype analysis of an established nontumorigenic cell line (MMC-E) indicated that the cells are of rat origin instead of mouse, as interpreted earlier. This cell line, now termed RE (rat epithelial) had a karyotype of 39,X,-5,-15,-?16,+t(3q11q) in the stem line. There was also one subline that had a karyotype of 40,X,-5,-15,-?16,+t(3q11q), +?t(5;?). Chromosome changes and frequency of sister chromatid exchanges (SCEs) were studied from seven malignantly transformed RE cell lines. These included cells transformed by Moloney murine sarcoma virus, the acute transforming retrovirus 3611-MSV, murine leukemia virus, or ethylnitrosourea. Changes in chromosomes #3 and #5 seemed to be associated with malignant transformation of RE cells. In addition to the t(3q11q) and monosomy for chromosome #5 seen in the parent cell line, monosomy for chromosome #3 and the t(5;?) were observed in all malignant cell lines. The latter changes either were absent (monosomy for chromosome #3) or present only occasionally [t(5;?)] in the parental cells. The results of SCEs showed that the malignantly transformed cell lines do not have increased frequency of SCEs as compared with that of the parental cell line.
Animals↗
[The idea of cell origin from noncellular elements in the light of results in microbiology and biological cell research].
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Biological Evolution↗
Possible stem cell origin of human cholangiocarcinoma.
AIM: To investigate the expression of CD34 and c-kit (receptor of stem cell factor) in cholangiocarcinoma. METHODS: Fifteen cases of intrahepatic cholangiocarcinoma and 17 cases of extrahepatic cholangiocarcinoma were studied in this experiment. Using Envision detection system, paraffin-embedded sections of the resected cholangiocarcinoma tissue were stained with antibodies against CD34 and c-kit, respectively. The sections were counterstained with hematoxylin, and the results were examined under light microscope. Normal tonsil and mammary tissues were used as positive controls for CD34 and c-kit, respectively. RESULTS: CD34 was positive in all sections, but only in capillary endothelial cells of tumor tissue. No cholangiocarcinoma cells were positive for CD34. In one case of extrahepatic cholangiocarcinoma, a few tumor cells (about 5%) were immunoreactive with c-kit. CONCLUSION: CD34 or c-kit positive cells in liver tissue may represent liver stem cells, as they can differentiate into mature biliary cells in vitro. The expression of c-kit by some cholangiocarcinoma cells suggests that cholangiocarcinoma might originate from liver stem cells. However, other mechanisms of hepatocarcinogenesis, such as de-differentiation of mature cholangiocytes, may also exist.
Adult↗