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PubMed1992

Lineage alteration in precursor B cell acute lymphoblastic leukemia following T cell lymphoblastic lymphoma.

A 10-year-old girl was diagnosed with lymphoblastic lymphoma; staging evaluation revealed a large mediastinal mass and normal peripheral blood and bone marrow morphology. Tumor cell immunologic marker analysis and Southern blot gene rearrangement studies demonstrated a T-cell lineage. She achieved a complete remission following multi-agent chemotherapy; however, 19 months following initial diagnosis while on maintenance therapy, she presented with typical acute lymphoblastic leukemia (ALL). The bone marrow was replaced by lymphoblasts, though the mediastinum was normal and there was no peripheral lymphadenopathy. Repeat immunophenotypic and genotypic studies demonstrated a precursor B-cell ALL lineage without expression of the T-cell surface antigens present on the original neoplasm. Repeat genotypic analysis showed immunoglobulin heavy and light chain gene rearrangements without the T-cell receptor gamma and beta gene rearrangements noted in the original lymphoblastic lymphoma. The complete alteration of lineage in these lymphoblastic processes suggests the de novo occurrence of a second neoplasm or, alternatively, an ALL relapse from a lineage-uncommitted neoplastic lymphoid progenitor cell.

Burkitt Lymphoma↗
PubMed1992

Does lineage determine the dopamine phenotype in the tadpole hypothalamus?: A quantitative analysis.

The ancestry of dopaminergic (DA) neurons in the Xenopus laevis hypothalamus was investigated by combining intracellular lineage dye injections of 16- and 32-cell blastomeres with the immunofluorescent detection of tyrosine hydroxylase at tadpole stages. At these stages, DA neurons in the hypothalamus comprise a discrete nucleus that contains from 22 to 45 cells on each side [mean = 32.6 +/- 6.6 (SD)]. The DA nucleus descends from only four of the 16-cell blastomeres. The two dorsal midline blastomeres (D1.1) are the major progenitors, and in all embryos studied they contributed to the DA nucleus. The two dorsal lateral blastomeres (D1.2) contribute to the DA nucleus in only about half of the embryos. Thus, the DA nucleus descends only from a discrete group of progenitors, and the participation of some of the progenitors in the DA lineage is only probabilistic. The number of DA neurons generated by the same blastomere varied greatly in different animals. This variation in cell number correlated with the degree of coherence and the density of the clone in the hypothalamus, rather than with clonal ancestry. Bilateral deletion of the major 32-cell progenitor (D1.1.1) resulted in a nearly complete restitution of the DA nucleus in 74% of the embryos that successfully completed gastrulation and neurulation. In the rest, the hypothalamus was smaller than normal or missing, and the DA nucleus was significantly reduced in size or absent. These results show that the DA nucleus can be restored after its normal lineage is deleted, but complete regulation is not always accomplished. Several blastomere progenitors dramatically altered their contribution to the DA nucleus after D1.1.1 ablation, including two blastomeres that normally do not contribute to the DA lineage. Thus, the fate to produce DA neurons is not determined at cleavage stages.

Animals↗
PubMed2004

Two mitochondrial lineages in Korean freshwater Corbicula (Corbiculidae: bivalvia).

The Korean freshwater Corbicula was surveyed genetically by sequencing 614-bp homologous fragment of mitochondrial cytochrome oxidase I subunit. Among a total of 127 individuals collected from 12 Korean freshwater localities we found only two COI haplotypes and these differed by a total of 9 base substitutions. Although the sequence divergence between the two haplotypes is moderate (p = 1.47%), placing the two mitotypic sequences in the context of Asian mtDNA phylogeny reveals that Korean freshwater Corbicula is comprised of two independent freshwater mitochondrial lineages. These results are in serious disagreement with the long-standing conclusions of earlier conchology-based taxonomic work on Korean Corbicula in which a number of species names (a minimum of 10 nominal species) have been used. This indicates that morphological characteristics alone are poor criteria for species-level identification in this group. In addition, our COI dataset shows that there is an extremely low level of genetic variation in Korean freshwater populations, suggesting that these populations have passed through a severe population bottleneck that greatly reduced their genetic variability. Our data also provide new information on the biogeographic distribution of Korean freshwater Corbicula. When haplotypic frequencies were compared, it was evident that the two Korean freshwater mitochondrial lineages have achieved very different distribution ranges: the predominant lineage (FWKR1) is widely distributed in Korean freshwater systems, whereas the minor lineage (FWKR2) is restricted to a relatively narrow range.

Animals↗
PubMed2005

Comparative analysis of morphological diversity: does disparity accumulate at the same rate in two lineages of centrarchid fishes?

Evolutionary lineages differ with regard to the variety of forms they exhibit. We investigated whether comparisons of morphological diversity can be used to identify differences in ecological diversity in two sister clades of centrarchid fishes. Species in the Lepomis clade (sunfishes) feed on a wider range of prey items than species in the Micropterus clade (black basses). We quantified disparity in morphology of the feeding apparatus as within-clade variance on principal components and found that Lepomis exhibits 4.4 and 7.4 times more variance than Micropterus on the first two principal components. However, lineages are expected to diversify morphologically and ecologically given enough time, and this pattern could have arisen due to differences in the amount of time each clade has had to accumulate variance. Despite being sister groups, the age of the most recent common ancestor of Lepomis is approximately 14.6 million years ago and its lineages have a total length of 86.4 million years while the age of the most recent common ancestor of Micropterus is only about 8.4 million years ago, and it has a total branch length of 42.9 million years. We used the Brownian motion model of character evolution to test the hypothesis that time of independent evolution of each clade's lineages accounts for differences in morphological disparity and determined that the rates of evolution of the first two principal components are 4.4 and 7.7 times greater in Lepomis. Thus, time and phylogeny do not account for the differences in morphological disparity observed in Lepomis and Micropterus, and other diversity-promoting mechanisms should be investigated.

Adaptation, Biological↗
PubMed2006

New laboratory assay for diagnostic testing of avian influenza A/H5 (Asian Lineage).

On February 3, 2006, the Food and Drug Administration (FDA) announced clearance of the Influenza A/H5 (Asian Lineage) Virus Real-Time Reverse Transcription-Polymerase Chain Reaction (RT-PCR) Primer and Probe Set and inactivated virus as a source of positive RNA control for the in vitro qualitative detection of highly pathogenic influenza A/H5 virus (Asian lineage). Two genetic lineages of influenza A/H5 viruses exist: Eurasian (Asian) and North American. The primer and probe set, developed at CDC, is designed to detect highly pathogenic influenza A/H5 viruses from the Asian lineage associated with recent laboratory-confirmed infections of avian influenza in humans in east Asia and, most recently, in Turkey and Iraq.

Clinical Laboratory Techniques↗
PubMed1991

Cell lineage analysis of the gynoecium of maize using the transposable element Ac.

The maize gynoecium develops from a primordium comprising two distinct cell lineages: an epidermal LI and a subepidermal LII lineage. We have analyzed somatic gynoecial sectors marked with red flavonoid pigments by excision of Ac from the P locus. Somatic sector analysis indicates the epidermal lineage starts as a single cell layer at the base of the ovary and thickens into several cell layers, presumably by periclinal divisions, near the silk attachment point. The silk attachment point appears to be mainly an epidermal outgrowth of two of three fused carpels and presumably the silk contains only LI, or mostly LI, with only traces of subepidermal LII cells. The third carpel, covering the germinal face of the kernel, retains a multicellular LII and unicellular LI organization but fails to contribute substantially to stylar outgrowth. Ac transpositions in subepidermal somatic sectors are transmitted to the archesporial cell lineage. Ac transpositions that occur in epidermal sectors are not transmitted to offspring. These results demonstrate that the female megasporocyte is derived from subepidermal (LII) cells.

Clone Cells↗
PubMed1991

Microinjection of fluorescent tracers to study neural cell lineages.

The examination of cell lineages is an important step towards understanding the developmental events that specify the various cell types in the organism. The mechanisms that control which cell types are formed, their locations, and their numbers remain unknown. Analyses of cell lineage in the frog neural retina have revealed that individual precursors are multipotent and are capable of producing almost any combination of cell types. In addition to giving rise to a wide range of phenotypes, the precursors can give rise to a wide range of clone sizes. Cell lineage studies in other systems indicate that some precursors are multipotent, like those in the retina, while others appear to produce a more restricted range of descendants, perhaps even a single phenotype. These differences in the developmental potential of precursor cells suggest that the nervous system uses several strategies for producing its many cell types. Investigation of these strategies, at the cellular and molecular level, requires more than a description of the normal cell lineages. We are now exploiting the frog neural retina to perform the experimental manipulations needed to elucidate these strategies.

Animals↗
PubMed1991

Expression of the c-fgr and hck protein-tyrosine kinases in acute myeloid leukemic blasts is associated with early commitment and differentiation events in the monocytic and granulocytic lineages.

Two members of the src proto-oncogene family of intracellular tyrosine kinases, c-fgr and hck, are selectively expressed in differentiated myeloid cells. To study the expression of these genes in acute myeloid leukemia (AML) and to determine the specific myeloid lineages and stages of myeloid differentiation at which the expression of these genes is acquired, we used a series of 79 cases of de novo AML as a differentiation model. The levels of c-fgr, hck, and c-fms (encoding the colony-stimulating factor-1 receptor) mRNA transcripts were correlated with the presence of specific cell surface antigens and the morphologic and cytochemical features in these AML blasts. Relatively undifferentiated leukemic myeloblasts with an HLA-DR, CD34, CD33, CD13+/- cell surface immunophenotype (French-American-British [FAB] M1 or M2) were characterized by a lack of c-fms and c-fgr expression, while low levels of c-fms and c-fgr could be detected in undifferentiated myeloblasts (FAB M1 or M2), which also expressed CD14 at low antigen density. The hck transcripts were either undetectable in these cells or were expressed at low levels. In contrast, only hck mRNA transcripts could be identified in blasts with progranulocytic morphology (FAB M3), while c-fms, c-fgr, and hck were all expressed at high levels in blasts with differentiated myelomonocytic or monocytic features (FAB M4 and M5). No c-fms, c-fgr, or hck transcripts were evident in leukemic cells of the erythroid lineage (FAB M6). When undifferentiated leukemic myeloblasts (HLA-DR, CD34, and CD33) were induced to differentiate in vitro to cells with monocytic characteristics, the expression of c-fms, c-fgr, and the CD14 cell surface antigen were induced to high levels, accompanied by the acquisition of hck and CD13 expression. In contrast, when HLA-DR, CD34, and CD33 blasts were induced to differentiate in vitro to cells with granulocytic characteristics, only hck and CD13 expression were induced. Our data suggest that the acquisition of c-fgr and/or hck expression is associated with early commitment and differentiation events in distinct myeloid lineages. Assessment of the expression of these kinases may provide a molecular tool to assign lineage in AML in conjunction with morphology, cytochemistry, and cell surface antigen expression.

Cell Differentiation↗
PubMed1991

[Myelodysplasia predominantly involving in megakaryocytic lineage successfully treated with low-dose Ara-C].

A 17 year old male was admitted because of pancytopenia. Bone marrow aspiration revealed myelodysplasia, no increase of blast cells and excessive expansion of megakaryocytic lineage. Although mild increase of bone marrow reticulin fiber was observed, no hepatosplenomegaly was recognized. Therefore he was diagnosed as refractory anemia (RA) or MDS with myelofibrosis and treated with low dose Ara-C regimen. Remission was achieved in June 1987, but the relapse occurred in Oct. 1987. His bone marrow at the relapse showed more remarkable dysplastic change than before. Sequential bone marrow examinations thereafter, revealed an increase of megakaryocytic lineage, especially immature dysplastic megakaryocytes, leading to the appearance of the abnormal megakaryoblasts (detected with anti GP IIb/IIIa antibody) as well as uncharacterized blast cells in his terminal stage. Transformation from MDS to megakaryocytic leukemia was strongly suggested. He died of severe pneumonia in March 1989. The invasion of abnormal immature megakaryocytic cells including megakaryoblasts was observed in liver, spleen and lymph nodes at autopsy. There are several reports on cases having a common hematological features such as 1) pancytopenia in peripheral blood, 2) myelodysplasia, 3) excessive growth of megakaryocytic lineage, 4) myelofibrosis without hepatosplenomegaly, although other clinical features were different. We propose all these cases should be reviewed at the point of MDS mainly involved in megakaryocytic lineage.

Adolescent↗
PubMed1990

Autologous bone marrow transplantation in high-risk remission T-lineage acute lymphoblastic leukemia using immunotoxins plus 4-hydroperoxycyclophosphamide for marrow purging.

Fourteen patients with high-risk T-lineage acute lymphoblastic leukemia (ALL) in complete remission underwent autologous bone marrow transplantation (BMT) in an attempt to eradicate their residual disease burden. A combined immunochemotherapy protocol using a cocktail of two immunotoxins directed against CD5/Tp67 and CD7/Tp41 T-lineage differentiation antigens in combination with the in vitro active cyclophosphamide congener 4-hydroperoxy-cyclophosphamide (4-HC) was used to purge autografts. Despite high dose pretransplant radiochemotherapy and effective purging of autografts, 9 of 14 patients relapsed at a median of 2.5 months (range, 1.2 to 16.8 months) post BMT. Two patients remain alive and disease free at 26 and 28 months post BMT. We used a novel quantitative minimal residual disease (MRD) detection assay, which combines fluorescence activated multiparameter flow cytometry and cell sorting with leukemic progenitor cell (LPC) assays, to analyze remission bone marrow (BM) samples from T-lineage ALL patients for the presence of residual LPCs. Notably, high numbers of residual LPC detected in remission BM before BMT constituted a poor prognostic indicator, providing the first evidence for the biologic significance and clinical value of in vitro T-lineage ALL LPC assays. The median value for the residual leukemia burden before BMT, was approximately 8.6 x 10(3) LPC/10(8) mononuclear cells (MNC) (approximately 0.0086% LPC). Patients with a residual leukemia burden less than this median value appeared to have a better outlook for remaining free of relapse after autologous BMT than patients with a greater leukemia burden (53 +/- 25% v 14 +/- 13%, P = .006, Mantel-Cox). By comparison, the log kill efficacy of purging, the remaining numbers of LPC in purged autografts, or the estimated numbers of reinfused LPC, did not correlate with the probability of disease-free survival (DFS). These results indicate that the primary reason for the recurrence of leukemia was inefficient pretransplant radiochemotherapy rather than inefficient purging of autografts.

Adolescent↗
PubMed1990

14q32 translocations are associated with mixed-lineage expression in childhood acute leukemia.

The frequency and characteristics of childhood acute leukemia with a 14q32 translocation [other than the t(8;14)(q24;q32)] were determined in 335 cases of newly diagnosed acute lymphoblastic leukemia (ALL) and 105 cases of acute nonlymphoblastic leukemia (ANLL). Ten children, representing 2.3% of the entire cohort, had this abnormality (1.5% of ALL patients and 4.8% of ANLL patients). By French-American-British (FAB) criteria, 4 cases were classified as L1, 1 as L2, 2 as M1, 1 as M2, and 2 as M5. Remarkably, mixed-lineage expression was found in 6 of these 10 cases, but in only 21 of the other 430 cases without a 14q32 translocation (P less than .001). Leukemic cells from 5 of these 6 cases (4 ANLL, and 1 ALL) coexpressed CD13, a myeloid-associated antigen, and CD2, a T-cell-associated antigen; blasts from the sixth case (ALL) coexpressed CD13 and CD19, a B-lineage-associated antigen. Thus, in addition to the well-described 11q23 translocations and t(9;22), 14q32 translocations also appear to be associated with mixed lineage antigen expression. Break-points of the reciprocal chromosomes from chromosome 14 were identified in five of these cases: 1q23, 6q23-q25, 7p15, 8q11, and 12q13. Of the four mixed-lineage cases that were tested, none showed rearrangement of the immunoglobulin heavy chain (IgH) gene. This suggests that the 14q32 breakpoint does not involve the IgH gene and that an unidentified important gene may reside on 14q32.

Adolescent↗
PubMed1988

Use of a monoclonal antibody (GA3) to demonstrate lineage restricted O-glycosylation on leukosialin during terminal erythroid differentiation.

A murine monoclonal antibody (GA3) obtained by immunizing mice with cells of the human erythroleukemic cell line K562 is shown to define a 105 kilodalton (kd) membrane antigen on K562 cells that is restricted within the hematopoietic system to the erythroid lineage and to a minor population of CD3, CD4 positive T lymphocytes. Cocapping studies and immunoprecipitation experiments performed with GA3 and L10, an anti-sialophorin monoclonal antibody reacting with leukosialin (Gp 105) on K562 cells, demonstrate that the antigen detected by GA3 on K562 cells is identical to leukosialin. Neuraminidase treatment but not tunicamycin treatment of K562 cells abolishes the expression of the GA3-epitope without affecting the L10-epitope thus providing evidence that terminal sialic acid present on O-linked oligosaccharide chains on Gp 105 is essential for the expression of the GA3-epitope. Further analysis by flow cytometry and immune panning experiments performed on bone marrow cells with GA3 or L10 demonstrate that, in contrast to L10, which reacts with all types of hematopoietic progenitors, the epitope recognized by GA3 is restricted to the erythroid lineage, and appears during erythroid differentiation before glycophorin A on the earliest morphologically recognizable erythroid precursor, the proerythroblast. Our results therefore suggest that O-linked oligosaccharides on leukosialin express lineage restricted and even maturation restricted antigenic structures that might serve as cell lineage specific markers.

Animals↗
PubMed1989

Sufficiency of the CD8+ T cell lineage to mount an effective tumoricidal response to syngeneic tumor-bearing novel class I MHC antigens.

The origins of "help" in rejection of syngeneic tumors by the CD8 T cell lineage was examined with a model tumor inappropriately expressing novel class I MHC and subject to cytolytic T cell (CTL)-mediated rejection. The requirement for CD4+ Th cells to induce CD8+ CTL effectors in vivo was investigated by using C3H mice selectively depleted of either CD4+ or CD8+ T cells. Rejection of the tumor was vigorous and indistinguishable from normal mice after depletion of CD4+ T cells in vivo. In contrast, in CD8+ T cell-depleted mice tumors grew progressively, confirming that T cells of the CD8+ lineage are required for a tumoricidal immune response, and cells of this lineage are sufficient for a primary response. Taken together, these results demonstrate that, in the absence of CD4+ T cells in vivo, unprimed cells of the CD8+ lineage are fully competent to mount an effective CTL immune response to syngeneic cells expressing novel class I Ag, consistent with the concept that only T cells with class I recognition specificity may be required to satisfy the need for both help and effector functions in the response.

Animals↗
PubMed1989

Molecular genetic analysis of three AIDS-associated neoplasms of uncertain lineage demonstrates their B-cell derivation and the possible pathogenetic role of the Epstein-Barr virus.

Each of three individuals with acquired immunodeficiency syndrome (AIDS) developed a pleomorphic malignant neoplasm in which a precise histopathologic diagnosis could not be rendered. In each case, the tumor cells expressed leukocyte common antigen and a variable constellation of antigens associated with B- and T-cell activation (HLA-DR, T9, T10, BL2, BL3, Ki-24, BLAST-2). They lacked all B cell, T cell, myeloid, and monocyte lineage-restricted antigens, resulting in their classification as hematopoietic neoplasms of uncertain lineage. However, antigen receptor gene rearrangement analysis demonstrated that each of these three neoplasms exhibited clonal immunoglobulin heavy chain and kappa light chain gene rearrangements and lacked T-cell receptor beta chain gene rearrangements and therefore were B cell-derived non-Hodgkin's lymphomas (NHL) representative of an equivalent, relatively mature stage of B-cell differentiation. In contrast with most AIDS-associated NHLs, each of these three neoplasms lacked c-myc gene rearrangements and contained Epstein-Barr virus (EBV) proteins and/or sequences. These studies demonstrate that these three AIDS-associated neoplasms of uncertain lineage exhibit a strikingly similar constellation of distinctly uncommon morphologic, immunophenotypic, and molecular genetic characteristics that distinguishes them substantially from the vast majority of NHLs that have been reported to occur in association with AIDS. The consistent presence of EBV proteins and/or DNA sequences suggests that the Epstein-Barr virus played a pathogenetic role in the development of these three AIDS-associated neoplasms. Finally, these studies further illustrate the utility of antigen receptor gene rearrangement analysis in the diagnosis and classification of hematopoietic neoplasms of uncertain lineage.

Acquired Immunodeficiency Syndrome↗
PubMed1989

Dual lineage of astrocytomas.

Experimental observations suggest that type 1 and type 2 astrocytes have distinct lineages distinguished, respectively, by the absence or presence of the A2B5 antigen. To investigate the hypothesis that the strikingly different biological behaviors of low-grade and high-grade astrocytomas might be related to cell lineage, 38 astrocytomas (grades I through IV), were examined for the presence of the A2B5 antigen, glial fibrillary acidic protein (GFAP), and galactocerebroside (GC), a marker for oligodendrocytes. Twenty-nine of the tumors (76%) were composed of moderate or high densities of GFAP+ and unlabeled cells, and were devoid of A2B5+ and GC+ neoplastic cells. Only four tumors had high densities (75% to 100%) of A2B5+ cells, three of which were grade I tumors; two tumors, also Grade I, contained moderate densities (20% to 25%) of GC+ cells that had cytologic features of astrocytoma or oligodendroglioma. The findings suggest that most cerebral astrocytomas lack the A2B5 antigen and thus may represent neoplasia along the type 1 astrocyte lineage. In contrast, A2B5+ lineage among astrocytomas, ie, neoplasia with differentiation toward type 2 astrocytes and GC+ oligodendrocytes, is less common and may be correlated with prognostically favorable histopathologic features.

Adult↗
PubMed1989

Human bone marrow cytogenetics: growth factors stimulate metaphases for specific lineages.

Fresh and/or frozen bone marrow cells from five healthy individuals and seven patients with myeloid leukemia were studied using growth factors and a cytogenetic technique which allows simultaneous analysis of karotype and cell lineage. Cell lineages were identified using monoclonal antibodies in an alkaline phosphatase antialkaline phosphatase staining method. In general, cultures stimulated with a colony stimulating factor containing conditioned medium (CSF) and erythropoietin (EPO) had a higher (approximately 2-fold) mitotic index (MI) than cultures without these growth factors (maximum 7.0 vs. 3.8 after 4-day culture). The significantly higher MI in cultures with growth factors was shown to result from an increase in both erythrocytic and granulocytic-monocytic mitoses. Every culture with CSF and EPO had more erythrocytic metaphases than the identical culture without these growth factors (mean erythrocytic MI 3.1 vs. 0.3, p = 0.01 in healthy subjects; 6.9 vs. 0, p = 0.05 in leukemia). In each of the three patients showing an increased MI where lineage-specific MI was studied, the granulocytic-monocytic MI increased (mean 4.0 vs. 2.1, p = 0.05). These data suggest that growth factors increase the number of metaphases available for cytogenetic analysis from fresh or frozen marrow, and may be used to stimulate metaphases from specific lineages.

Adolescent↗
PubMed1989

Lineage-specific gene rearrangement/deletion: a nonconservative model.

For the lymphocytic descendants of the hematopoietic differentiation pathway, characteristic gene rearrangements result in deletions of significant portions of chromosome regions specifying lymphocyte-specific gene products on either or both chromosomes of each involved pair. Molecular mechanisms facilitating the rearrangement/deletion events have been elegantly and fruitfully elaborated in the years since the first documentation of their occurrence by Hozumi and Tonegawa (N. Hozumi and S. Tonegawa, Proc. Natl. Acad. Sci. USA, 73:3628-3632, 1976). Numerous genetic phenomena observed in experiments or the literature suggest to us that specific genome rearrangement/deletion may be characteristic of and necessary for many, perhaps all, differentiating lineages. Thus we propose that on the way to terminal differentiation, cells within a particular lineage must rearrange specific chromosome regions characteristic for that lineage in order to switch off or on, perhaps concomitantly, requisite genes for that differentiation program. Such rearrangements and their ensuing deletions may have been undetected cytogenetically because of small size and/or because normal terminally differentiated cells do not enter mitosis. However, footprints of these rearrangements, most likely in aberrant form, may be preserved in preneoplastic cells and cancer cells of various lineages which exhibit characteristic deletions. An understanding of the cellular recombinational machinery involved in normal physiological genome rearrangements such as we propose may clarify some puzzling aspects of current theories concerning retinoblastoma, Wilms' tumor, and other "deletion syndromes" and the role of parental genome imprinting [B. M. Cattanach and M. Kirk, Nature (Lond.), 315: 496-498, 1985; C. Sapienza et al., Nature (Lond.), 328: 251-254, 1987; D. Solter, Annu. Rev. Genet., 22: 127-146, 1988]. The recombinatorial activity, when inappropriately expressed in dividing cells (i.e., cells which should be terminally differentiated but are still cycling for various reasons) could be responsible for such diverse phenomena as large deletions; chromosomal translocations into commonly deleted regions; amplicons; apparent nonrandom chromosome integration of viral genomes such as hepatitis B, human papilloma virus, papovaviruses, and retroviruses; and the observation of fragile sites. It could explain why these various phenomena often involve the same restricted regions of the genome. Some clues and consequences integral to the proposal are discussed.(ABSTRACT TRUNCATED AT 400 WORDS)

Cell Differentiation↗
PubMed1989

Cell lineage and determination of cell fate in ascidian embryos.

A detailed cell lineage of ascidian embryos has been available since the turn of the century. This cell lineage was deduced from the segregation of pigmented egg cytoplasmic regions into particular blastomeres during embryogenesis. The invariant nature of the cell lineage, the segregation of specific egg cytoplasmic regions into particular blastomeres, and the autonomous development of most embryonic cells suggests that cell fate is determined primarily by cytoplasmic determinants. Modern studies have provided strong evidence for the existence of cytoplasmic determinants, especially in the primary muscle cells, yet the molecular identity, localization, and mode of action of these factors are still a mystery. Recent revisions of the classic cell lineage and demonstrations of the lack of developmental autonomy in certain embryonic cells suggest that induction may also be an important mechanism for the determination of cell fate in ascidians. There is strong evidence for the induction of neural tissue and indirect evidence for inductive interactions in the development of the secondary muscle cells. In contrast to the long-accepted dogma, specification of cell fate in ascidians appears to be established by a combination of cytoplasmic determinants and inductive cell interactions.

Animals↗