Journal articles: 'Teratocarcinoma'

1

Singhal, M., and D. Jhavar. "Primary mediastinal giant teratocarcinoma." Indian Journal of Cancer 45, no. 2 (2008): 73. http://dx.doi.org/10.4103/0019-509x.41778.

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Falcone, Richard A., Andrew W. Knott, Janice F. Rafferty, and Brad W. Warner. "Sacrococcygeal teratoma and teratocarcinoma." Seminars in Colon and Rectal Surgery 15, no. 1 (March 2004): 19–25. http://dx.doi.org/10.1053/j.scrs.2004.06.004.

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3

Shigeta, Hiroyuki, Michiyoshi Taga, Hideya Sakakibara, and Hiroshi Minaguchi. "Epidermal growth factor stimulates the cell growth of the PA-1 teratocarcinoma cell line in an autocrine/paracrine fashion." European Journal of Endocrinology 132, no. 2 (February 1995): 200–205. http://dx.doi.org/10.1530/eje.0.1320200.

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Shigeta H, Taga M, Sakakibara H, Minaguchi H. Epidermal growth factor stimulates the cell growth of the PA-1 teratocarcinoma cell line in an autocrine/paracrine fashion. Eur J Endocrinol 1995;132: 200–5. ISSN 0804–4643 In order to investigate the biological significance of epidermal growth factor (EGF) in the cell function of teratocarcinoma cells, we examined the production, binding and cell proliferative effect of EGF in PA-1 human ovarian teratocarcinoma cell line. The immunoreactivity of EGF in PA-1 cell-conditioned medium was detected by human EGF radioimmunoassay, and prepro-EGF mRNA was demonstrated in PA-1 cells by Northern blot analysis. An [125I] EGF binding study showed the presence of EGF receptor with very high binding affinity and relatively low numbers of binding sites in PA-1 cells. Furthermore, the growth of PA-1 cells was stimulated by EGF and inhibited by anti-EGF monoclonal antibody. These results suggest strongly that EGF plays an important role in controlling the growth of teratocarcinoma cells as an autocrine/paracrine growth factor. Michiyoshi Taga, Department of Obstetrics and Gynecology, Yokohama City University School of Medicine, 3–9 Fukuura, Kanazawa-ku, Yokohama 236, Japan

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Andrews, P. W., M. M. Matin, A. R. Bahrami, I. Damjanov, P. Gokhale, and J. S. Draper. "Embryonic stem (ES) cells and embryonal carcinoma (EC) cells: opposite sides of the same coin." Biochemical Society Transactions 33, no. 6 (October 26, 2005): 1526–30. http://dx.doi.org/10.1042/bst0331526.

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Embryonal carcinoma (EC) cells are the stem cells of teratocarcinomas, and the malignant counterparts of embryonic stem (ES) cells derived from the inner cell mass of blastocyst-stage embryos, whether human or mouse. On prolonged culture in vitro, human ES cells acquire karyotypic changes that are also seen in human EC cells. They also ‘adapt’, proliferating faster and becoming easier to maintain with time in culture. Furthermore, when cells from such an ‘adapted’ culture were inoculated into a SCID (severe combined immunodeficient) mouse, we obtained a teratocarcinoma containing histologically recognizable stem cells, which grew out when the tumour was explanted into culture and exhibited properties of the starting ES cells. In these features, the ‘adapted’ ES cells resembled malignant EC cells. The results suggest that ES cells may develop in culture in ways that mimic changes occurring in EC cells during tumour progression.

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5

Ferreira, L. R., C. E. E. Velano, E. C. Braga, C. C. Paula, H. Martélli-Junior, and J. J. Sauk. "Expression of Sec61alpha in F9 and P19 teratocarcinoma cells after retinoic acid treatment." Brazilian Journal of Biology 63, no. 2 (May 2003): 245–52. http://dx.doi.org/10.1590/s1519-69842003000200009.

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Nascent procollagen peptides and other secretory proteins are transported across the endoplasmic reticulum (RE) membrane through a protein-conducting channel called the translocon. Sec61alpha, a multispanning membrane translocon protein, has been implicated as essential for translocation of polypeptides chains into the cisterns of the ER. However, it is not known whether Sec61alpha is ubiquitously expressed in collagen producing teratocarcinoma cells. Furthermore, the production, expression, and utilization of Sec61alpha may depend on the cell differentiation stage. Stem cells from many cultured teratocarcinoma cell lines such as F9 and P19 cells are capable of differentiation in response to low retinoic acid concentrations. This differentiation of the tumorigenic stem cells results in tumorigenicity loss. For this study, mouse F9 and P19 teratocarcinoma cells were grown in culture medium treated with or without retinoic acid. Expression of Sec61alpha was determined by reverse trancriptase polimerase chain reaction (RT-PCR). In untreated conditions, F9 cells expressed undetected Sec61alpha amounts. It was also demonstrated that Sec61alpha expression is stimulated in F9 cells after retinoic acid treatment for 72 hours. No changes were found in Sec61alpha expression in P19 cells after retinoic acid treatment. These data indicate that the expression of Sec61alpha is enhanced with retinoic acid induced differentiation of F9 teratocarcinoma cells.

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6

Dyban, Pavel A. "Effect of the anticancer drug methotrexate on the ascites form of a teratocarcinoma and survival of mice." Reviews on Clinical Pharmacology and Drug Therapy 16, no. 3 (December 15, 2018): 32–35. http://dx.doi.org/10.17816/rcf16332-35.

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The dose-dependent effect of a methotrexate is established as on an ascite form of a teratocarcinoma CBA9H6, and mice-recipients, however various doses of the entered methotrexate (6; 4 and 2 mkg/g body weights of an animal), at repeated introduction at an interval of 48 and 24 hours, don't destroy all population of embrioid bodies. So, at 3-fold and even 10-fold daily injections in a dose of 2 mkg/g of body weight in an abdominal cavity of mice 1,6 ± 0,2% and 0,038 ± 0,01% embrioid bodies (ascite form of a teratocarcinoma ) remain, respectively, at survival of mice 93,0 ± 8,5% and 14,0 ± 3,0%. The morphological analysis of a mode of a differentiation of embrioid bodies retransplantated from experimental animals to intact has shown earlier that the methotrexate hasn't had effect on histoblastic potentialities of stem cells of a teratocarcinoma CBA9H6.

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7

Niwa, O. "Suppression of the hypomethylated Moloney leukemia virus genome in undifferentiated teratocarcinoma cells and inefficiency of transformation by a bacterial gene under control of the long terminal repeat." Molecular and Cellular Biology 5, no. 9 (September 1985): 2325–31. http://dx.doi.org/10.1128/mcb.5.9.2325-2331.1985.

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The Moloney leukemia virus (M-MuLV) genome was introduced into undifferentiated teratocarcinoma cells by transfection of a plasmid with the virus genome linked to pSV2neo, which carries a bacterial drug resistance gene, neo, or by cotransfection with pSV2neo. In the resulting cells, the M-MuLV genome remained hypomethylated, but its expression was suppressed in cells in an undifferentiated state. The pattern of DNA methylation of the viral genome remained unchanged when the cells were induced to differentiate into epithelial tissues. However, spontaneous M-MuLV expression was detected with differentiation of the cells. To determine to what extent the viral long terminal repeat (LTR) was responsible for this suppression in undifferentiated cells, I constructed plasmids in which neo was placed under the control of the promoter sequence of the dihydrofolate reductase gene or the M-MuLV LTR, and compared the biological activities of the plasmids in Ltk- cells and in undifferentiated teratocarcinoma cells. In Ltk- cells, these plasmids were highly efficient in making the cells resistant to selection by G418. However, in undifferentiated teratocarcinoma cells, the M-MuLV LTR promoted neo gene expression at only 10% of the expected efficiency, as compared with the expression of the neo gene under the control of the simian virus to or dihydrofolate reductase promoter. Thus, the mechanisms of gene regulation are not the same in undifferentiated and differentiated teratocarcinoma cells.

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8

Niwa, O. "Suppression of the hypomethylated Moloney leukemia virus genome in undifferentiated teratocarcinoma cells and inefficiency of transformation by a bacterial gene under control of the long terminal repeat." Molecular and Cellular Biology 5, no. 9 (September 1985): 2325–31. http://dx.doi.org/10.1128/mcb.5.9.2325.

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The Moloney leukemia virus (M-MuLV) genome was introduced into undifferentiated teratocarcinoma cells by transfection of a plasmid with the virus genome linked to pSV2neo, which carries a bacterial drug resistance gene, neo, or by cotransfection with pSV2neo. In the resulting cells, the M-MuLV genome remained hypomethylated, but its expression was suppressed in cells in an undifferentiated state. The pattern of DNA methylation of the viral genome remained unchanged when the cells were induced to differentiate into epithelial tissues. However, spontaneous M-MuLV expression was detected with differentiation of the cells. To determine to what extent the viral long terminal repeat (LTR) was responsible for this suppression in undifferentiated cells, I constructed plasmids in which neo was placed under the control of the promoter sequence of the dihydrofolate reductase gene or the M-MuLV LTR, and compared the biological activities of the plasmids in Ltk- cells and in undifferentiated teratocarcinoma cells. In Ltk- cells, these plasmids were highly efficient in making the cells resistant to selection by G418. However, in undifferentiated teratocarcinoma cells, the M-MuLV LTR promoted neo gene expression at only 10% of the expected efficiency, as compared with the expression of the neo gene under the control of the simian virus to or dihydrofolate reductase promoter. Thus, the mechanisms of gene regulation are not the same in undifferentiated and differentiated teratocarcinoma cells.

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9

Blackshear, P., J. Mahler, L. M. Bennett, K. A. McAllister, D. Forsythe, and B. J. Davis. "Extragonadal Teratocarcinoma in Chimeric Mice." Veterinary Pathology 36, no. 5 (September 1999): 457–60. http://dx.doi.org/10.1354/vp.36-5-457.

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10

Acharya, Utkarsh, Stephen Strobel, Linda Pepe, and Ranko Miocinovic. "Teratocarcinoma Presenting as Testicular Torsion." Journal of Histotechnology 31, no. 4 (December 2008): 175–77. http://dx.doi.org/10.1179/his.2008.31.4.175.

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11

Lachyankar, Mahesh B., Sujna D. Raval, Jyoti J. Kayal, Rajeswari Seshadri, and Vyasarayani S. Lalitha. "A teratocarcinoma-derived neurotrophic activity." NeuroReport 6, no. 8 (May 1995): 1195???1198. http://dx.doi.org/10.1097/00001756-199505000-00030.

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12

Shaw, D. P., and J. E. Roth. "Testicular Teratocarcinoma in a Horse." Veterinary Pathology 23, no. 3 (May 1986): 327–28. http://dx.doi.org/10.1177/030098588602300315.

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13

Stair, J. Michael, D. Richard Stevenson, Robert F. Schaefer, John P. Fullenwider, and Gilbert S. Campbell. "Primary teratocarcinoma of the lung." Journal of Surgical Oncology 33, no. 4 (December 1986): 262–67. http://dx.doi.org/10.1002/jso.2930330413.

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14

Bieda, Katrin, Andreas Hoffmann, and Klaus Boller. "Phenotypic heterogeneity of human endogenous retrovirus particles produced by teratocarcinoma cell lines." Journal of General Virology 82, no. 3 (March 1, 2001): 591–96. http://dx.doi.org/10.1099/0022-1317-82-3-591.

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Human endogenous retrovirus (HERV) sequences represent about 0·5% of the human genome. The only HERV known to express virus particles is human teratocarcinoma-derived virus (HTDV), which is now termed HTDV/HERV-K. Between 25 and 50 different copies of HERV-K are present in the human genome, three of which contain full-length genes for viral structural proteins. To determine whether genes of different HERV-K proviruses can be expressed, the morphologies and protein expression patterns of HTDV/HERV-K produced by various human teratocarcinoma cell lines were compared. Three different types of retrovirus-like particles were observed, showing differences in the presence of viral surface proteins and the existence of free mature virions. These distinct morphological features between virion types were in accordance with the results of immunoblotting analyses that revealed differences in the cleavage of a viral Gag protein precursor and the presence of a putative Env protein. These data suggest that different HERV-K proviruses are transcribed in human teratocarcinoma cell lines.

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15

Zhu, Jiajun, Zhixun Dou, Morgan A. Sammons, Arnold J. Levine, and Shelley L. Berger. "Lysine methylation represses p53 activity in teratocarcinoma cancer cells." Proceedings of the National Academy of Sciences 113, no. 35 (August 17, 2016): 9822–27. http://dx.doi.org/10.1073/pnas.1610387113.

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TP53 (which encodes the p53 protein) is the most frequently mutated gene among all human cancers, whereas tumors that retain the wild-type TP53 gene often use alternative mechanisms to repress the p53 tumor-suppressive function. Testicular teratocarcinoma cells rarely contain mutations in TP53, yet the transcriptional activity of wild-type p53 is compromised, despite its high expression level. Here we report that in the teratocarcinoma cell line NTera2, p53 is subject to lysine methylation at its carboxyl terminus, which has been shown to repress p53’s transcriptional activity. We show that reduction of the cognate methyltransferases reactivates p53 and promotes differentiation of the NTera2 cells. Furthermore, reconstitution of methylation-deficient p53 mutants into p53-depleted NTera2 cells results in elevated expression of p53 downstream targets and precocious loss of pluripotent gene expression compared with re-expression of wild-type p53. Our results provide evidence that lysine methylation of endogenous wild-type p53 represses its activity in cancer cells and suggest new therapeutic possibilities of targeting testicular teratocarcinoma.

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16

Langa, F., C. Kress, E. Colucci-Guyon, H. Khun, S. Vandormael-Pournin, M. Huerre, and C. Babinet. "Teratocarcinomas induced by embryonic stem (ES) cells lacking vimentin: an approach to study the role of vimentin in tumorigenesis." Journal of Cell Science 113, no. 19 (October 1, 2000): 3463–72. http://dx.doi.org/10.1242/jcs.113.19.3463.

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Vimentin is a class III intermediate filament protein widely expressed in the developing embryo and in cells of mesenchymal origin in the adult. Vimentin knock-out mice develop and reproduce without any obvious defect. This is an unexpected finding in view of the high degree of conservation of the vimentin gene among vertebrates. However, it does not exclude the possibility of a role for vimentin in pathological conditions, like tumorigenesis. To address this question directly, we have used a teratocarcinoma model involving the injection of ES cells into syngeneic mice. ES cells lacking vimentin were generated from 129/Sv Vim-/- mice with high efficiency. The absence of vimentin did not affect ES cell morphology, viability or growth rate in vitro. Tumours were induced by subcutaneous injection of either Vim-/- or Vim+/+ ES cells into Vim+/+ and Vim-/- mice, in order to analyse the effect of the absence of vimentin in either the tumorigenic cells or the host mice. No significant differences were found in either tumour incidence, size or vascularization of teratocarcinomas obtained with all possible combinations. Vim-/- ES-derived tumours showed the same cellular composition typical of teratocarcinomas induced by wild-type ES cells together with a very similar apoptotic pattern. Taken together, these results demonstrate that in this model vimentin is not essential for efficient tumour growth and differentiation in vivo.

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17

Mojsin, Marija, Jelena Marjanovic Vicentic, Marija Schwirtlich, Vladanka Topalovic, and Milena Stevanovic. "Quercetin reduces pluripotency, migration and adhesion of human teratocarcinoma cell line NT2/D1 by inhibiting Wnt/β-catenin signaling." Food Funct. 5, no. 10 (2014): 2564–73. http://dx.doi.org/10.1039/c4fo00484a.

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18

Sassone-Corsi, P., D. Duboule, and P. Chambon. "Viral Enhancer Activity in Teratocarcinoma Cells." Cold Spring Harbor Symposia on Quantitative Biology 50 (January 1, 1985): 747–52. http://dx.doi.org/10.1101/sqb.1985.050.01.092.

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19

Charles, Leslie N. "Metastatic Ovarian Teratocarcinoma in a Horse." Journal of Comparative Pathology 181 (November 2020): 68–72. http://dx.doi.org/10.1016/j.jcpa.2020.10.002.

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20

Elmali, Muzaffer, Cinar Koprulu, Meltem Ceyhan, and Levent Yildiz. "Testicular teratocarcinoma associated with testicular microlithiasis." Abdominal Imaging 33, no. 2 (April 27, 2007): 244–46. http://dx.doi.org/10.1007/s00261-007-9238-9.

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21

ISHIKAWA, TOMOICHI. "Tissue Differentiation in Mouse Teratocarcinomas in Lung Colonies from Ascitic Embryoid Bodies. (mouse teratocarcinoma/tissue differentiation/lung colony)." Development, Growth and Differentiation 27, no. 1 (February 1985): 35–40. http://dx.doi.org/10.1111/j.1440-169x.1985.00035.x.

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22

HANAOKA, KAZUNORI, YOSHIHIRO KATO, and TAKEHIKO NOGUCHI. "Comparative Study on the Ability of Various Teratocarcinomas to Form Chimeric Mouse Embryos. (mouse embryo/teratocarcinoma/chimera/aggregation)." Development, Growth and Differentiation 28, no. 3 (May 1986): 223–31. http://dx.doi.org/10.1111/j.1440-169x.1986.00223.x.

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23

TESCH, H., R. FÜRBAβ, J. CASPER, J. LYONS, C. R. BARTRAM, H. J. SCHMOLL, and D. L. BRONSON. "Cellular oncogenes in human teratocarcinoma cell lines." International Journal of Andrology 13, no. 5 (October 1990): 377–88. http://dx.doi.org/10.1111/j.1365-2605.1990.tb01046.x.

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24

MUTO, Norio, Atsuyoshi DOTA, Tetsuya TANAKA, Norio ITOH, Masaru OKABE, Akira INADA, Tsutomu NAKANISHI, and Keiichi TANAKA. "Hinokitiol Induces Differentiation of Teratocarcinoma F9 Cells." Biological & Pharmaceutical Bulletin 18, no. 11 (1995): 1576–79. http://dx.doi.org/10.1248/bpb.18.1576.

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25

Langley, R. E., S. T. Palayoor, C. N. Coleman, and E. A. Bump. "Radiation-induced Apoptosis in F9 Teratocarcinoma Cells." International Journal of Radiation Biology 65, no. 5 (January 1994): 605–10. http://dx.doi.org/10.1080/09553009414550691.

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26

Habacon, George Paul, and Teresita DeGuia. "Infestus Morbus: A Case of Mediastinal Teratocarcinoma." Chest 148, no. 4 (October 2015): 597A. http://dx.doi.org/10.1378/chest.2277014.

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27

Raaijmakers, C., G. Wilms, P. Demaerel, and A. L. Baert. "Pineal teratocarcinoma with drop metastases: MR features." Neuroradiology 34, no. 3 (1992): 227–29. http://dx.doi.org/10.1007/bf00596343.

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28

Kuzel, Timothy M., Al B. Benson, A. Marion Gurley, and Leonard Cerullo. "Aggressive intracranial teratocarcinoma with ventriculoperitoneal shunt metastases." American Journal of Medicine 86, no. 6 (June 1989): 736–38. http://dx.doi.org/10.1016/0002-9343(89)90466-x.

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29

Aizawa, Shinichi, Mochihiko Ohashi, Lawrence A. Loeb, and George M. Martin. "Multipotent mutator strain of mouse teratocarcinoma cells." Somatic Cell and Molecular Genetics 11, no. 3 (May 1985): 211–16. http://dx.doi.org/10.1007/bf01534677.

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30

Lizoňová, A., R. Kurth, and J. Löwer. "Analysis of human teratocarcinoma-derived virus particles." European Journal of Cancer and Clinical Oncology 21, no. 11 (November 1985): 1398. http://dx.doi.org/10.1016/0277-5379(85)90419-5.

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31

Aizawa, Shinichi, Lawrence A. Loeb, and George M. Martin. "Aphidicolin-resistant mutator strains of mouse teratocarcinoma." Molecular and General Genetics MGG 208, no. 1-2 (June 1987): 342–48. http://dx.doi.org/10.1007/bf00330463.

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32

Al-Khalifa, Muneera, Sara Alsaad, Habib Al-Tareef, Zaid Arekat, and Abdulla Darwish. "A Giant Primary Mediastinal Teratocarcinoma in a Male Adult." Case Reports in Surgery 2019 (June 10, 2019): 1–4. http://dx.doi.org/10.1155/2019/7123241.

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Germ cell tumors (GCTs) arise along the midline, in which 50-70% of extragonadal GCTs occur in the mediastinum. Malignant GCTs are more common in males, while benign GCTs occur equally in both males and females. This report presents a case of a giant primary mediastinal nonseminomatous GCT resected from a 35-year-old male who presented with dyspnoea and tightness in the chest. Thorough investigations including a chest MRI were done. It showed a 21×19×15 cm tumor. Thus, surgical resection of the tumor through a midline sternotomy was done. Histopathological analysis diagnosed the tumor as a primary mediastinal teratocarcinoma with a sarcomatous component. Eighteen-month follow-up showed no tumor recurrence. Mediastinal teratocarcinoma is a rare and life-threatening germ cell tumor. Studies recommend the use of chemotherapy prior to resection as an important step in its management. Close and regular follow-up postsurgical resection is advised.

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33

Knössl, Michael, Roswitha Löwer, and Johannes Löwer. "Expression of the Human Endogenous Retrovirus HTDV/HERV-K Is Enhanced by Cellular Transcription Factor YY1." Journal of Virology 73, no. 2 (February 1, 1999): 1254–61. http://dx.doi.org/10.1128/jvi.73.2.1254-1261.1999.

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ABSTRACT The human endogenous retrovirus HTDV/HERV-K, which resides in moderate copy numbers in the human genome, is expressed in a cell-type-specific manner, predominantly in teratocarcinoma cells. We have analyzed the regulatory potential of the 5′ enhancer of the HERV-K long terminal repeat. Protein extracts of HERV-K-expressing teratocarcinoma cell lines (GH and Tera2) and nonexpressing HeLa and HepG2 cells form different protein complexes on the enhancer sequence as detected by electrophoretic mobility shift assays (EMSA). Using competition EMSAs, DNase I footprinting, and supershift experiments, we localized the binding site of these complexes to a 20-bp sequence within the enhancer and showed that the transcription factor YY1 is one component of the HERV-K enhancer complex. Replacement of the YY1 binding site with unrelated sequences reduced expression of the luciferase gene as a reporter in transient-transfection assays.

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34

Seppo, Antti, Leena Penttilä, Anne Makkonen, Anne Leppänen, Ritva Niemelä, Jussi Jäntti, Jari Helin, and Ossi Renkonen. "Wheat germ agglutinin chromatography of GlcNacβ1-3(GlcNAcβl-6)Gal and GlcNAcβ1-3(GlcNAcβ1-6)Galβ1-4GlcNAc, obtained by in vitro synthesis and by partial cleavage of teratocarcinoma poly-N-acetyllactosaminoglycans." Biochemistry and Cell Biology 68, no. 1 (January 1, 1990): 44–53. http://dx.doi.org/10.1139/o90-006.

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GlcNAcβ1-3(GlcNAcβ1-6)[14C(U)]Gal and GlcNAcβ1-3(GlcNAcβ1-6)[14C(U)]Galβ1-4GlcNAc were prepared by in vitro synthesis. They were characterized by enzymatic sequencing, by partial acid hydrolysis, and by periodate oxidation experiments. The two saccharides were isolated also from partial acid hydrolysates of metabolically labeled poly-N- acetyllactosaminoglycans of murine embryonal carcinoma cells (line PC 13). The tetrasaccharide was retarded in a column of agarose-linked wheat germ agglutinin; the trisaccharide was strongly bound. Chromatography in this column separated the trisaccharide into two distinct peaks, which represented interconvertible molecules. Together with our previous data on linear teratocarcinoma saccharides, these findings show that affinity chromatography with immobilized wheat germ agglutinin can be advantageously used in fractionating radiolabeled oligo-N-acetyllactosaminoglycans and saccharides related to them.Key words: GlcNAcβ1-3(GlcNAcβ1-6)Gal, GlcNAcβ1-3(GlcNAcβ1-6)Galβ1-4GlcNAc, wheat germ agglutinin – agarose chromatography, in vitro biosynthesis, teratocarcinoma cell.

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35

Miwa, Y., T. Atsumi, N. Imai, and Y. Ikawa. "Primitive erythropoiesis of mouse teratocarcinoma stem cells PCC3/A/1 in serum-free medium." Development 111, no. 2 (February 1, 1991): 543–49. http://dx.doi.org/10.1242/dev.111.2.543.

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Mouse teratocarcinoma stem cells PCC3/A/1 differentiated into various types of cells, such as red cells, when they were grown in serum-free medium containing transferrin and bovine serum albumin on a KCF cell feeder layer. These red cells were stained well with 2,7-diaminofluorene (DAF), and therefore were erythroid cells. They were nucleated and contained embryonic globin chains, immunologically identified with antiembryonic hemoglobin antisera after acid urea Triton X-100 polyacrylamide gel electrophoresis (UT-PAGE). The addition of erythropoietin to the culture medium enhanced the production of both embryonic and adult globin chains. The addition of interleukin-3 also enhanced the production of embryonic globin chains, but not the production of adult globin chains. These results indicated that primitive erythropoiesis of PCC3/A/1 teratocarcinoma cells did not require exogenous addition of any hematopoietic factor such as erythropoietin or interleukin-3. This culture system will be a new model system for investigating the factors regulating the primitive erythropoiesis in yolk sac blood islands.

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36

Bhat, Gull Mohd, and Atul Sharma. "Pseudocystic Liver Metastasis in Malignant Teratocarcinoma of Testes." Indian Journal of Medical and Paediatric Oncology 28, no. 01 (January 2007): 45. http://dx.doi.org/10.1055/s-0041-1733208.

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37

Weima, S. M., M. A. van Rooijen, L. Rijks, A. Feijen, E. J. J. van Zoelen, C. L. Mummery, and S. W. de Laat. "Growth factors and their receptors in human teratocarcinoma." Cell Differentiation and Development 27 (August 1989): 120. http://dx.doi.org/10.1016/0922-3371(89)90374-2.

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38

Illmensee, K., D. Gerh�user, B. Lioi, and J. A. Modlinski. "Developmental potential of nuclei from mouse teratocarcinoma cells." Naturwissenschaften 76, no. 12 (December 1989): 582–84. http://dx.doi.org/10.1007/bf00462872.

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39

Gonczol, E., P. W. Andrews, and S. A. Plotkin. "Cytomegalovirus Infection of Human Teratocarcinoma Cells in Culture." Journal of General Virology 66, no. 3 (March 1, 1985): 509–15. http://dx.doi.org/10.1099/0022-1317-66-3-509.

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40

Fiddes, Kelsey R., Jerry Murray, and Bruce H. Williams. "Testicular Teratocarcinoma in a Ferret (Mustela putorius furo)." Journal of Comparative Pathology 181 (November 2020): 63–67. http://dx.doi.org/10.1016/j.jcpa.2020.09.017.

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41

Warren, Leonard. "Sialic acid lyase in differentiating murine teratocarcinoma cells." Experimental Cell Research 161, no. 2 (December 1985): 307–16. http://dx.doi.org/10.1016/0014-4827(85)90088-6.

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42

Chambers, Ian, and Austin Smith. "Self-renewal of teratocarcinoma and embryonic stem cells." Oncogene 23, no. 43 (September 2004): 7150–60. http://dx.doi.org/10.1038/sj.onc.1207930.

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43

Moon, Timothy D., Lawrence S. Fox, and Datla G. K. Varma. "Testicular teratocarcinoma with intracaval metastases to the heart." Urology 40, no. 4 (October 1992): 368–70. http://dx.doi.org/10.1016/0090-4295(92)90392-a.

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44

Nelson, J. A., and M. Groudine. "Transcriptional regulation of the human cytomegalovirus major immediate-early gene is associated with induction of DNase I-hypersensitive sites." Molecular and Cellular Biology 6, no. 2 (February 1986): 452–61. http://dx.doi.org/10.1128/mcb.6.2.452-461.1986.

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Human teratocarcinoma cells were used to examine structural features associated with expression of the major immediate-early (IE) gene of human cytomegalovirus. By immunofluorescence, comparison of RNA levels, and in vitro transcription of nuclei, we showed that the major IE gene is inactive in undifferentiated but active in differentiated cells. Therefore, the block in human cytomegalovirus replication in teratocarcinoma cells appears to be at the transcriptional level, in one of the initial genes transcribed. In addition, the in vitro transcription experiments demonstrated that in permissive infections the gene was transcriptionally inactive late in infection. A comparison of the structural features of the promoter region with the active and inactive IE genes showed the presence of constitutive and inducible DNase I-hypersensitive sites. The majority of the constitutive sites existed at -175, -275, -375, -425, and -525 relative to the cap site in an area which has been shown to be capable of simian virus 40 enhancer function. In contrast, the inducible DNase I sites were located outside this region at -650, -775, -875, and -975.

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45

Nelson, J. A., and M. Groudine. "Transcriptional regulation of the human cytomegalovirus major immediate-early gene is associated with induction of DNase I-hypersensitive sites." Molecular and Cellular Biology 6, no. 2 (February 1986): 452–61. http://dx.doi.org/10.1128/mcb.6.2.452.

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Abstract:

Human teratocarcinoma cells were used to examine structural features associated with expression of the major immediate-early (IE) gene of human cytomegalovirus. By immunofluorescence, comparison of RNA levels, and in vitro transcription of nuclei, we showed that the major IE gene is inactive in undifferentiated but active in differentiated cells. Therefore, the block in human cytomegalovirus replication in teratocarcinoma cells appears to be at the transcriptional level, in one of the initial genes transcribed. In addition, the in vitro transcription experiments demonstrated that in permissive infections the gene was transcriptionally inactive late in infection. A comparison of the structural features of the promoter region with the active and inactive IE genes showed the presence of constitutive and inducible DNase I-hypersensitive sites. The majority of the constitutive sites existed at -175, -275, -375, -425, and -525 relative to the cap site in an area which has been shown to be capable of simian virus 40 enhancer function. In contrast, the inducible DNase I sites were located outside this region at -650, -775, -875, and -975.

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46

Boy-Lefèvre, M. L., J. R. Nefussi, D. Paulin, D. J. Hartmann, S. Ricard-Blum, D. Herbage, and N. Forest. "Collagen expression during teratocarcinoma cell line-induced endochondral bone tumor." Journal of Histochemistry & Cytochemistry 34, no. 7 (July 1986): 835–39. http://dx.doi.org/10.1177/34.7.3519748.

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Collagen immunotyping by indirect immunofluorescence was performed in order to investigate the sequential development of bone formation. Osseous tumors were obtained after subcutaneous injection of 3/A/1D-1 teratocarcinoma cell line into 129/Sv mice (Nicolas et al., 1980). Frozen sections of developing tumors were incubated with specific antibodies directed against Types I, II, III, IV, and IX collagens. On Day 9, the expression of Type I and Type III collagens was correlated with the proliferation of mesenchymal cells. From Day 10, chondrogenesis was characterized by the occurrence of cartilaginous collagens, Types II and IX, in the cartilage matrix. Type IV collagen was also detected in focal areas and revealed vascular invasion of the tumor. On Day 13, osteogenesis was demonstrated by the presence of Type I collagen in the bone matrix coating the surfaces. Immunolocalization of Type III collagen on the hemopoietic elements corresponded with the bone remodeling. The sequential transitions of collagen types confirm the development of an endochondral bone tumor. These results suggest that 3/A/1D-1 teratocarcinoma cell line constitutes a valuable system for in vitro study of endochondral bone formation and cell differentiation.

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47

Skowronski, J., T. G. Fanning, and M. F. Singer. "Unit-length line-1 transcripts in human teratocarcinoma cells." Molecular and Cellular Biology 8, no. 4 (April 1988): 1385–97. http://dx.doi.org/10.1128/mcb.8.4.1385-1397.1988.

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We have characterized the approximately 6.5-kilobase cytoplasmic poly(A)+ Line-1 (L1) RNA present in a human teratocarcinoma cell line, NTera2D1, by primer extension and by analysis of cloned cDNAs. The bulk of the RNA begins (5' end) at the residue previously identified as the 5' terminus of the longest known primate genomic L1 elements, presumed to represent "unit" length. Several of the cDNA clones are close to 6 kilobase pairs, that is, close to full length. The partial sequences of 18 cDNA clones and full sequence of one (5,975 base pairs) indicate that many different genomic L1 elements contribute transcripts to the 6.5-kilobase cytoplasmic poly(A)+ RNA in NTera2D1 cells because no 2 of the 19 cDNAs analyzed had identical sequences. The transcribed elements appear to represent a subset of the total genomic L1s, a subset that has a characteristic consensus sequence in the 3' noncoding region and a high degree of sequence conservation throughout. Two open reading frames (ORFs) of 1,122 (ORF1) and 3,852 (ORF2) bases, flanked by about 800 and 200 bases of sequence at the 5' and 3' ends, respectively, can be identified in the cDNAs. Both ORFs are in the same frame, and they are separated by 33 bases bracketed by two conserved in-frame stop codons. ORF 2 is interrupted by at least one randomly positioned stop codon in the majority of the cDNAs. The data support proposals suggesting that the human L1 family includes one or more functional genes as well as an extraordinarily large number of pseudogenes whose ORFs are broken by stop codons. The cDNA structures suggest that both genes and pseudogenes are transcribed. At least one of the cDNAs (cD11), which was sequenced in its entirety, could, in principle, represent an mRNA for production of the ORF1 polypeptide. The similarity of mammalian L1s to several recently described invertebrate movable elements defines a new widely distributed class of elements which we term class II retrotransposons.

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Gorman, C. M., D. P. Lane, C. J. Watson, and P. W. J. Rigby. "The Regulation of Gene Expression in Murine Teratocarcinoma Cells." Cold Spring Harbor Symposia on Quantitative Biology 50 (January 1, 1985): 701–6. http://dx.doi.org/10.1101/sqb.1985.050.01.086.

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Damjanov, Ivan. "The Road From Teratocarcinoma to Human Embryonic Stem Cells." Stem Cell Reviews 1, no. 3 (2005): 273–76. http://dx.doi.org/10.1385/scr:1:3:273.

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50

Skowronski, J., T. G. Fanning, and M. F. Singer. "Unit-length line-1 transcripts in human teratocarcinoma cells." Molecular and Cellular Biology 8, no. 4 (April 1988): 1385–97. http://dx.doi.org/10.1128/mcb.8.4.1385.

Full text

Abstract:

We have characterized the approximately 6.5-kilobase cytoplasmic poly(A)+ Line-1 (L1) RNA present in a human teratocarcinoma cell line, NTera2D1, by primer extension and by analysis of cloned cDNAs. The bulk of the RNA begins (5' end) at the residue previously identified as the 5' terminus of the longest known primate genomic L1 elements, presumed to represent "unit" length. Several of the cDNA clones are close to 6 kilobase pairs, that is, close to full length. The partial sequences of 18 cDNA clones and full sequence of one (5,975 base pairs) indicate that many different genomic L1 elements contribute transcripts to the 6.5-kilobase cytoplasmic poly(A)+ RNA in NTera2D1 cells because no 2 of the 19 cDNAs analyzed had identical sequences. The transcribed elements appear to represent a subset of the total genomic L1s, a subset that has a characteristic consensus sequence in the 3' noncoding region and a high degree of sequence conservation throughout. Two open reading frames (ORFs) of 1,122 (ORF1) and 3,852 (ORF2) bases, flanked by about 800 and 200 bases of sequence at the 5' and 3' ends, respectively, can be identified in the cDNAs. Both ORFs are in the same frame, and they are separated by 33 bases bracketed by two conserved in-frame stop codons. ORF 2 is interrupted by at least one randomly positioned stop codon in the majority of the cDNAs. The data support proposals suggesting that the human L1 family includes one or more functional genes as well as an extraordinarily large number of pseudogenes whose ORFs are broken by stop codons. The cDNA structures suggest that both genes and pseudogenes are transcribed. At least one of the cDNAs (cD11), which was sequenced in its entirety, could, in principle, represent an mRNA for production of the ORF1 polypeptide. The similarity of mammalian L1s to several recently described invertebrate movable elements defines a new widely distributed class of elements which we term class II retrotransposons.

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Journal articles on the topic 'Teratocarcinoma'

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