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K Huebner

Publications and source records attributed to K Huebner.

233 records · Page 13Linked to original sources

Chromosomal locations of mouse immunoglobulin genes.

The chromosomal locations of the structural genes coding for the constant portions of mouse heavy (H) and light chain immunoglobulins were studied by molecular hybridization techniques. Complementary DNA probes containing the constant-region sequences of kappa and lambdaI light chain and alpha, gamma2b, and mu heavy chain mRNAs were annealed to a large excess of DNA from a series of eight mouse-human hybrid cell lines that are deficient for various mouse chromosomes. The lines were scored as positive when a high proportion of a probe annealed and negative when an insignificant proportion annealed. Some lines were clearly negative for H and lambda and clearly positive for kappa. Others were positive or intermediate for lambda, positive for kappa and negative for H. Still others, including a line that was selected for the absence of the mouse X chromosome, were positive for all immunoglobulin species. These results demonstrate that the Clambda, Ckappa, and CH genes are located on different autosomes in the mouse. In contrast, the three heavy-chain families exhibited consistently uniform hybridization results, suggesting that the genes for Calpha, Cgamma, and Cmu are located on the same chromosome. A comparison of karyotypic data with hybridization data has limited the possible locations of the Ig genes to only a few chromosomes.

Animals↗

Suppression of replication of SV40 and polyoma virus in mouse-human hybrids.

Mouse-human heterokaryons are permissive for the replication of both SV40 virus and polyoma virus. If the hybrids which develop from these heterokaryons segregate human chromosomes (mouse greater than human hybrids), the hybrids are permissive for replication of polyoma virus but not for replication of SV40 virus. If the subsequent hybrids segregate mouse chromosomes (human greater than mouse hybrids), such hybrids support the replication of SV40 virus but not the replication of polyoma virus, even when the hybrids contain at least one copy of each mouse chromosome. This indicates that during the transition from heterokaryon to hybrid cell, suppression of expression of species-specific function(s) required for the replication of these species-specific viruses occurs in parallel with the direction of chromosome loss and suppression of nucleolus organizer activity.

Animals↗

Production of B-tropic murine leukemia virus by somatic cell hybrids between mouse peritoneal macrophages and simian virus 40-transformed human cells.

Simian virus 40 (SV40)-transformed human cells (LN-SV) were fused with BALB/c peritoneal macrophages (BALB/c X LN-SV) and with C57BL peritoneal macrophages (C57BL X LN-SV) and hybrid clones, all of which had segregated human chromosomes and contained the entire complement of mouse chromosomes, were isolated. All 15 BALB/c X LN-SV hybrid clones were producing varying titers (10 to 10(6) plaque-forming units/ml) of B-tropic murine leukemia virus, whereas none of the nine C57BL X LN-SV hybrid clones was producing detectable ecotropic murine leukemia virus.

Animals↗

Genetics of cell transformation by simian virus 40.

The results described in this paper indicate that the integration of the SV40 genome into human chromosome 7 results in the transformation of the human cells and in the expression of SV40-induced antigens. If integration of the SV40 genome in human chromosomes other than 7 ever occurs, it does not result in cell transformation and the expression of the virus-induced antigens. The expression of the SV40 T antigen in different monkey cells transformed by an adeno 7-SV40 hybrid is also related to a specific monkey chromosome. Somatic cell hybrids between normal nondividing mouse cells and SV40-transformed human cells behave as transformed cells and contain, without exception, the human chromosome 7 carrying the SV40 genome. Since no segregation into SV40 T antigen-negative hybrid clones was observed in these hybrids, it is inferred that the presence of the human chromosome 7 carrying the SV40 genome in the hybrids is mandatory for cell division.

Antigens, Neoplasm↗

Chromosome assignment of the T-antigen gene of simian virus 40 in African green monkey cells transformed by adeno 7-SV40 hybrid.

Somatic cell hybrids between mouse cells deficient in thymidine kinase [ATP:thymidine 5'-phosphotransferase (EC 2.7.1.75)] and two different monkey cell lines transformed by an adeno 7-SV40 hybrid have been produced using both a semiselective and a double selective procedure. Concordant segregation of the expression of SV40 T antigen with a specific monkey chromosome has been observed in all the mouse-monkey hybrid clones examined. Subcloning of three SV40 T antigen positive hybrid clones resulted in their segregation into SV40 T antigen-positive and negative subclones. Positive correlation between the SV40 T antigen and the same monkey chromosome has been observed in all the subclones examined.

Adenoviridae↗

Suppression of the normal mouse c-myc oncogene in human lymphoma cells.

In Burkitt's lymphoma, which carries the t(8;14) chromosome translocation, the c-myc oncogene normally located on band q24 of human chromosome 8 (refs 1-3) translocates to the heavy-chain locus on chromosome 14 (refs 1, 4, 5); this results in transcriptional deregulation of the translocated c-myc oncogene, which is transcribed constitutively at elevated levels, while the normal c-myc oncogene on the uninvolved chromosome 8 is either silent or expressed at very low levels (A.ar-R. and C.M.C., unpublished results). We have now introduced the active c-myc oncogene of proliferating mouse spleen cells into human lymphoma cells carrying the t(8;14) chromosome translocation by hydridization, and have examined the hybrids for expression of the human and murine c-myc oncogene. The results of this analysis, reported here, indicate that the active mouse myc gene is shut off at the transcriptional level in the human lymphoma cells, implying that human B cells at the stage of differentiation of lymphoma cells used in this study are nonpermissive for normal c-myc transcription.

Animals↗

Cerebral phaeohyphomycosis caused by an Exophiala species.

A 45-year-old woman was found to have cerebral phaeohyphomycosis caused by an Exophiala species. The portal of entry of the fungus remained unknown. Despite surgery and antimycotic therapy the patient died from circulation failure. The fungus is compared to several related Exophiala species.

Brain↗

FHIT gene expression in human urinary bladder transitional cell carcinomas.

BACKGROUND: Our purpose was to investigate the expression of FHIT (Fragile Histidine Triad) gene product in a series of 110 urinary bladder TCCs, and its eventual relationship with histological grade, clinical stage, recurrences and patients' survival. MATERIALS AND METHODS: We performed immunohistochemistry in archival material of formalin-fixed, paraffin-embedded tissues, using the anti-Fhit antibody and the Streptavidin-biotin peroxidase method. RESULTS: In 30 out of 110 cases (27.27%) Fhit protein was absent whereas in 32 cases (29.08%) it was abnormally expressed. In 48 cases (43.63%) Fhit protein was diffusely expressed in all tumor cells. A statistically highly significant correlation (p < 0.001) was noticed between Fhit protein absence or reduction and clinically advanced tumors. Conversely, abnormal Fhit protein expression was not associated with age, histological grade, tumor size, number of recurrences, and clinical outcome in terms of patients' survival. CONCLUSIONS: These results confirm that FHIT gene inactivation is a late event in urinary bladder carcinogenesis. Fhit protein reduced expression or complete absence correlates with advanced clinical stage of the disease, and does not seem to correlate with tumor recurrences and patient survival.

Acid Anhydride Hydrolases↗

Fhit protein expression in oral epithelium: immunohistochemical evaluation of three antisera.

BACKGROUND: A number of studies have shown that the Fhit tumour suppressor protein is abundantly expressed in normal epithelial cells of human organs and that this expression is lost or reduced in the majority of cancers arising in these epithelial tissues. A variety of antiFhit sera have been used but a systematic comparison of the different antisera has not yet been reported. MATERIALS AND METHODS: We compared the Fhit expression pattern in the epithelium of fibrous epuli, oral lichen planus, oral epithelial dysplasia and oral squamous cell carcinomas (OSCC) using three different Fhit antisera. RESULTS: The antigstFhit sera from two sources gave very similar results for all types of oral lesions except for lichen planus and showed that about 60% of OSCCs have lost Fhit expression. CONCLUSION: Although different staining patterns were found for the three antisera, all three could be used for evaluation of Fhit expression in OSCC.

Acid Anhydride Hydrolases↗

FHIT RNA and protein expression in oral squamous cell carcinomas.

BACKGROUND: To investigate the possible role of FHIT, a possible tumour suppressor gene, in oral carcinogenesis, we examined 17 oral squamous cell carcinomas (OSCCs) for genetic alterations. MATERIALS AND METHODS: Fresh tissue was obtained during surgery, snap-frozen in liquid nitrogen and stored at -70 degrees C. Nested PCR amplification to examine the integrity of FHIT mRNA was performed on the reverse transcribed complementary DNA obtained from the frozen normal and tumour tissue. Immunohistochemistry was done on formal in-fixed paraffin-embedded tissue protein from the same cases using a polyclonal antiserum against the full length Fhit. RESULTS: Twelve out 17 (71%) OSCCs showed reduced or absent Fhit protein and half of the cases with reduced Fhit protein exhibited aberrant RT-PCR products. CONCLUSION: Immunohistochemical detection of Fhit protein expression in OSCCs is the more sensitive method to determine the status of Fhit in these tumours, in agreement with previous studies of other tumour types.

Acid Anhydride Hydrolases↗