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Biomedical subjects

G B Pierce

Publications and source records attributed to G B Pierce.

At least 37 records · Page 2Linked to original sources
PubMed1984

Trophectoderm in control of murine embryonal carcinoma.

It has been shown previously that the intact blastocyst of the mouse can regulate tumor formation and colony formation of murine embryonal carcinoma. This effect is consistent with the close histogenetic correspondence between embryonal carcinoma and the inner cell mass of the blastocyst. The ability of inner cell mass, blastocele fluid, and inner and outer surfaces of trophectoderm to abrogate colony formation of a variety of malignant tumors has now been tested. Direct contact of the embryonal carcinoma cells with the blastocele surface of trophectoderm proved to be necessary for abrogation of colony formation of embryonal carcinoma. This effect was not seen with any of the other tumors tested. Some tumors, which lack a normal cellular counterpart in the blastocyst, grew poorly in the blastocele unless a fistula was made in the wall of the blastocyst. Colony formation of the embryonal carcinoma was regulated in blastocysts with fistulas, but the other tumors were not regulated under these conditions. It is concluded that colony formation of embryonal carcinoma cells is regulated by direct contact with the trophectoderm of its corresponding embryonic field in an unknown but specific manner.

Animals↗
PubMed1982

The endodermal origin of the endocrine cells of an adenocarcinoma of the colon of the rat.

A transplantable adenocarcinoma of the colon of the rat, which contained mucous, columnar, endocrine, and undifferentiated carcinoma cells, were cloned to see if each of the differentiated cell lineages had a common cell or origin. Four clonal lines were produced by the transplantation of single cells using micropipettes. Each tumor contained all four cell lineages but in markedly differing proportions. A confirmatory experiment was performed using a lung colony cloning assay. Seven tumors were obtained; each had mucous, columnar, endocrine, and undifferentiated cells. It is concluded that the endocrine cells of the colon are derived by differentiation from endoderm. They are not of neural crest origin.

Adenocarcinoma↗
PubMed1982

Biosynthesis of basement membrane by parietal yolk sac cells.

The biosynthesis of basement membrane (Reichert's membrane) by parietal yolk sac cells of the mouse embryo was studied using immunohistochemistry and autoradiography with the electron microscope. Fab' fragments of characterized antisera to either a mixture of type IV collagen and laminin, or to type IV collagen alone, were conjugated to horseradish peroxidase for the immunohistochemical study; radiolabeled proline, leucine, and glucosamine were utilized either in vivo or in isolated yolk sac membranes in vitro for autoradiography. Whereas neither of the two antisera employed localized in either the Golgi apparatus or in the cytosol, both localized in the rough endoplasmic reticulum (RER) and in the extracellular basement membrane. Furthermore, no evidence of passage of isotopically labeled precursors of basement membrane from the RER to the Golgi apparatus was observed. Consequently, it is concluded that the basement membrane precursors are synthesized in the RER of parietal yolk sac cells and neither traverse the Golgi apparatus nor diffuse across the cytosol of the cell in the process of secretion. By elimination, secretion must be via direct communications between RER and plasma membrane or via small vesicles observed in the cytosol between RER and plasma membrane. These data are not in accord with the concept of the universality of the Golgi apparatus in the biosynthesis of glycoprotein. Parietal yolk sac cells do not use the Golgi apparatus in the biosynthesis of basement membrane, but do use the Golgi apparatus for the biosynthesis of other proteins.

Animals↗
PubMed1982

Specificity of the control of tumor formation by the blastocyst.

An assay to determine the mechanism of regulation of embryonal carcinoma cells by the blastocyst, which is based on a comparison of tumors produced when the cancer cells are cloned alone or after incorporation into blastocysts, was refined by labeling embryonal carcinoma cells with fluorescent microspheres and by following their fate after injection into the blastocysts. Through the use of the new techniques, it was observed that cells of one line of nullipotent embryonal carcinoma were controlled at the 50% level, those from another were not controlled, and those from a multipotent but undifferentiated line were controlled in almost absolute fashion. Single Sarcoma 180 of L1210 leukemia cells were not controlled when injected into the blastocele, but C1300 neuroblastoma cells were partially controlled. None of these tumors have a normal cellular counterpart in the blastocyst, as does embryonal carcinoma, but neurulation follows blastulation by only a few days, so that the neuroblastoma cells may be regulated at that time. Parietal yolk sac carcinoma cells, which have a counterpart in the late blastocyst, were not controlled. On the basis of these data, it is postulated that, if one embryonic field can regulate its closely related cancer, then there may be an embryonic field capable of regulating each carcinoma.

Animals↗
PubMed1979

Tumorigenicity of embryonal carcinoma as an assay to study control of malignancy by the murine blastocyst.

A bioassay, based on tumorigenicity, has been developed to determine the mechanism whereby the blastocyst of the mouse controls malignant expression of embryonal carcinoma. The assay is based upon the incidence of tumors obtained when known numbers of cells of the 402AX strain of embryonal carcinoma are injected into strain 129 mice, compared to the incidence obtained when the same number of embryonal carcinoma cells are incorporated into Swiss-Webster blastocysts that are then injected in strain 129 animals. The results indicate that the blastocyst can regulate one embryonal carcinoma cell consistently; it may have a slight effect on three, but it cannot regulate four or five of them. The position of the embryonal carcinoma cell in the blastocyst is important. Regulation occurs if the embryonal carcinoma cell is placed in the blastocoele cavity, but enhancement of tumorigenicity is obtained if it is placed between the zona pellucida and the trophectoderm. By contrast, the blastocyst is unable to regulate a single B-16 melanoma cell placed in the blastocoele cavity, indicating a degree of specificity for the regulatory process.

Animals↗
PubMed1977

Yolk sac carcinoma (endodermal sinus tumor): ultrastructure and histogenesis of gonadal and extragonadal tumors in comparison with normal human yolk sac.

Human yolk sac carcinomas have been studied only twice with the electron microscope, and have never been compared at this level with normal human yolk sac. In the present study, the ultrastructural features of three primary ovarian yolk sac carcinomas, omental metastases from one of these, and a primary retroperitoneal yolk sac carcinoma in a male are reported, as are the ultrastructural findings in human yolk sac from normal 7- and 12-week gestations. The most prominent feature of the tumors is the presence of voluminous basement membrane material (the nature of which is confirmed by indirect enzyme-labeled antibody technique in one case) in both intra-and extracellular location, corresponding to the PAS-positive hyaline globules seen in these tumors by light microscopy. The tumor cells are also demonstrated to produce this material in tussue culture. Although basement membrane has not been described previously in normal human yolk sac at 8 and 10 weeks' gestation, it was present in the 7-week specimen which we studied, suggesting that its production may be a feature of only very young sac. Other ultrastructural findings are also similar in human yolk sac carcinoma, normal human yolk sac, and rodent yolk sac and yolk sac carcinomas. Thus, these studies confirm the suggested germ cell-derived yolk sac origin of the human tumor.

Adult↗
PubMed1977

Relationship between differentiation and carcinogenesis.

Carcinomas are caricatures of the normal process of tissue renerwal. Malignant stem cells proliferate, and some of their progeny differentiati and form benign functional cells. In teratocarcinoma, it has been demonstrated that the stem cells are the target in carcinogenesis and become malignant stem cells. The normal and malignant stem cells are equally differentiated. Normal stem cells of breast and colon are no more differentiated than their counterparts. If they are the target in carcinogenesis, then the concept of dedifferentiation is bypassed as an explanation for the undifferentiated appearance of tumors. While the focus of this meeting has been on mutation as an explanation for carcinogenesis, in this paper emphasis is placed on electrophilic carcinogens acting on cytoplasmic molecules that control gene expression. A type of gene control in addition to the operon is postulated.

Animals↗
PubMed1977

Ultrastructural comparison of differentiation of stem cells of murine adenocarcinomas of colon and breast with their normal counterparts.

Two rats with chemically induced transplantable adenocarcinomas of the colon were given pulses of [3H]thymidine, and autoradiography with electron microscopes was used to compare the degrees of differentiation of the stem cells of the tumor and colon. The best differentiated portions of the tumor had acini composed of vacuolated, mucous, and argentaffin cells in various stages of differentiation. Vacuolated and mucous cells incorporated [3H]thymidine and corresponded in degree of differentiation to that of their labeled normal counterparts in the normal colon. An exceedingly undifferentiated labeled cell, hitherto undescribed, was identified in the tumor and crypts of the colon; this may be an undifferentiated colon stem cell that differentiates into vacuolated and mucous stem cells and/or into argentaffin cells. Normal stem cells of the breast and malignant stem cells of spontaneous adenocarcinomas of the breast of C3H mice had comparable degrees of differentiation. Since normal stem cells in these tissues were as undifferentiated as the least differentiated stem cells of the tumors, there is now no need to postulate dedifferentiation as a mechanism to explain the undifferentiated appearance of tumors.

Adenocarcinoma↗
PubMed1976

Latent carcinoma and carcinoma in situ.

Lesions exist in the cervix that are diagnosed as carcinoma in situ; some may progress to invasive carcinoma and some may regress. Many are probably overdiagnosed, may represent effects of promoting agents rather than intiating agents, and may entail risk for the patient in that the lesion may be an unusualy good target in carcinogenesis. Latent carcinomas are small foci of initated cells unable to express their malignant phenotype because of environmental controls. Latent cells are produced in experimental carcinogenesis and occur in spontaneous tumors as G-O stem cells.

Adenocarcinoma↗
PubMed1976

Removal of basement membrane in the involuting breast.

Morphologic and immunohistochemical studies by light and electron microscopy indicated that basement membrane was removed during the process of involution of the murine breast. Removal of the basement membrane started 2 days postweaning, was maximal at 4 days, and correlated with degeneration of epithelial cells. There was no evidence of phagocytosis of basement membrane, so the removal of this antigen was attributed to enzymatic hydrolysis. To determine the activity of breast homogenate on the specific basement membrane antigen, insoluble basement membrane embedded in agarose gels was incubated with breast liver and kidney homogenates. When basement membrane antigen was demonstrated by the specific antibody, it was found that breast homogenate solubilized basement membrane but liver and kidney failed to solubilize basement membrane. To quantify the reaction and determine some of the characteristics of the responsible enzyme(s), insoluble basement membrane was labeled with 125I and the release of radioactivity into the supernatant following incubation with extracts of involuting breast indicated hydrolysis of basement membrane. Extracts of breast homogenate extensively hydrolyzed labeled basement membrane if naturally occurring inhibitors were removed by previous washing, whereas liver or kidney extracts prepared in a similar manner were devoid of activity. The hydrolysis of basement membrane was time and concentration dependent and had a pH optimum. The reaction was blocked by prior heating of the extract at 100 degrees C. for 30 minutes, removal of divalent cations, and presence of diisopropylfluorophosphate (a specific serine esterase inhibitor); prolonged dialysis failed to remove the hydrolytic activity. It is concluded that an enzyme system present in the involuting breast is capable of basement membrane hydrolysis

Animals↗
PubMed1974

Intracellular localization of basement membrane antigen in parietal yolk sac cells.

Basement membrane antigen was localized in murine parietal yolk sac cells using the peroxidase-labeled antibody technic. In these cells the antigen can be localized in the rough endoplasmic reticulum and perinuclear space. In spite of the proven ability of the antibody to permeate all cell compartments, the antigen was never localized within elements of the Golgi complex. These findings suggest that the rough endoplasmic reticulum of the parietal yolk sac cells is responsible for the synthesis of the antigenic portion of the basement membrane molecule. At the present time there is no evidence implicating the Golgi complex in the synthesis or intracellular transport of the antigenic portion of basement membrane.

Animals↗
PubMed1974

Neoplasms, differentiations and mutations.

Evidence has been presented to support the concept that malignant tumors are postembryonic differentiations superimposed upon the process of tissue maintenance and renewal. Malignant stem cells are derived from normal stem cells. They have a capacity for proliferation and differentiation that operates at a different level of control than the normal. Even so, malignant stem cells are responsive to enviornmental control, suggesting that it may be possible to direct their differentiation or at least to control their ability to replicate. A tumor is a caricature of normal tissue and appears undifferentiated because of the preponderance of undifferentiated proliferating stem cells in relationship to the number of cells that have differentiated and become benign.

Animals↗