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Biomedical subjects

A Stoler

Publications and source records attributed to A Stoler.

9 recordsLinked to original sources
PubMed1992

Part I. Reconstruction after total mandibulectomy with free cranial and microvascular iliac crest grafts as preparation for implants.

A young Ecuadorian girl underwent a total mandibulectomy due to infected fibrous dysplasia. In the subsequent 16 years, she was unable to speak intelligibly or masticate, surviving on liquids alone. After referral to the United States, the patient underwent six major surgical procedures that reconstructed her mandible from cranial and microvascular iliac crest grafts. The reconstruction improved her appearance and prepared her for insertion of dental implants and the eventual construction of a prosthetic device. These resulted in both functional and esthetic benefits.

Adult↗
PubMed1992

Part II. Mandibular reconstruction: combined intra-oral and in vitro placement of osseointegrated implants into a free and vascularized bone graft.

A 28-year-old Hispanic girl underwent a complete mandibular reconstruction many years following full mandibulectomy for fibrous dysplasia. Because of infectious complications, both free cranial and microvascular iliac crest grafts were used. The patient had osseointegrated implants placed directly into the grafted mandible. Osseointegrated implants were also placed into a segment of free iliac crest bone, in vitro, and then grafted laterally onto the reconstructed mandible. Prosthetic reconstruction was then carried out to restore the patient to normal function, health, comfort, and esthetics.

Adult↗
PubMed1989

Unusual patterns of keratin expression in the overlying epidermis of patients with dermatofibromas: biochemical alterations in the epidermis as a consequence of dermal tumors.

Dermatofibromas are frequently associated with acanthosis of the overlying epidermis. Using monospecific antisera and cRNA probes, we have examined the pattern of expression of keratin and keratin mRNA in the affected epidermis of patients with these dermal tumors. Our studies reveal several abnormalities in keratin expression within the thickened areas of overlying epidermis. In two of 15 patients, we detected K6 and K16, keratins which are frequently associated with epidermal diseases of hyperproliferation but are not present in normal epidermis. In both cases, K6 and K16 were found in suprabasal layers, similar to that seen for psoriasis and squamous cell carcinomas. Expression of K6 and K16 in skin samples from patients with dermatofibromas seemed to be dependent upon how near was the tumor to the overlying epidermis, and possibly upon the degree of cellularity within the tumor mass. A second aberration in keratin expression, and one which did not appear to be linked to K6/K16 expression, was the altered expression of the basal epidermal keratin K14. Expression of this keratin and its mRNA was variable, often extending into multiple suprabasal layers and including both basal-like and squamous-like cells. In contrast to the expression of K6/K16, aberrant expression of K14 was a relatively frequent event, occurring in greater than 70% of the dermatofibroma skin samples examined. These observations provide the first biochemical evidence in support of previous morphologic studies, indicating that alterations in epidermal differentiation can occur as a consequence of dermal skin tumors.

Fibroma↗
PubMed1988

Use of monospecific antisera and cRNA probes to localize the major changes in keratin expression during normal and abnormal epidermal differentiation.

We report here the isolation and characterization of three antisera, each of which is specific for a single keratin from one of the three different pairs (K1/K10, K14/K5, K16/K6) that are differentially expressed in normal human epidermis and in epidermal diseases of hyperproliferation. We have used these antisera in conjunction with monospecific cRNA probes for epidermal keratin mRNAs to investigate pathways of differentiation in human epidermis and epidermal diseases in vivo and in epidermal cells cultured from normal skin and from squamous cell carcinomas in vitro. Specifically, our results suggest that: (a) the basal-specific keratin mRNAs are down-regulated upon commitment to terminal differentiation, but their encoded proteins are stable, and can be detected throughout the spinous layers; (b) the hyperproliferation-associated keratin mRNAs are expressed at a low level throughout normal epidermis when their encoded proteins are not expressed, but are synthesized at high levels in the suprabasal layers of hyperproliferating epidermis, coincident with the induced expression of the hyperproliferation-associated keratins in these cells; and (c) concomitantly with the induction of the hyperproliferation-associated keratins in the suprabasal layers of the epidermis is the down-regulation of the expression of the terminal differentiation-specific keratins. These data have important implications for our understanding of normal epidermal differentiation and the deviations from this process in the course of epidermal diseases of hyperproliferation.

Amino Acid Sequence↗
PubMed1986

Coordinate control of anchorage independence, actin cytoskeleton, and angiogenesis by human chromosome 1 in hamster-human hybrids.

A panel of hybrids previously derived from fusions between a chemically transformed hamster cell line and normal human fibroblasts (A. Stoler and N. Bouck, Proc. Natl. Acad. Sci. USA, 82: 570-574, 1985) has been used to test whether or not anchorage independence, lack of actin cables, and angiogenic activity, three characteristics of transformed cells considered necessary but not sufficient for neoplasia, are coordinately regulated. In these hybrids anchorage independence is initially suppressed and those hybrids where it remains suppressed have been shown to retain human chromosome 1. Here we show that suppressed hybrids also display actin microfilament cables characteristic of normal cells and are unable to elicit an angiogenic response in the rat cornea assay. In contrast, those hybrids in which anchorage independence is expressed and which have lost human chromosome 1 have an actin cytoskeleton resembling that of the transformed parent and are potently angiogenic.

Actins↗
PubMed1985

Identification of a single chromosome in the normal human genome essential for suppression of hamster cell transformation.

Normal human fibroblasts were fused to carcinogen-transformed baby hamster kidney (BHK) cells and found to be able to suppress the anchorage-independent transformed phenotype of the hamster cells. This suppression was not due to interspecies incompatibility, for transformation could be effectively expressed in hybrids if either the human or the BHK parent had initially been transformed by a dominantly acting viral genome. Upon growth of suppressed hybrids, loss of human chromosomes was accompanied by the re-expression of transformation. Karyotype analysis indicated that only human chromosome 1 was retained in all hybrids that were suppressed and was lost in all hybrids in which transformation was re-expressed. Cytological evidence for the presence or absence of chromosome 1 was confirmed by electrophoretic identification of the human isozyme for phosphoglucomutase 1. Clones re-expressing transformation were isolated from two suppressed hybrids and in both cases loss of suppression was accompanied by the loss of human chromosome 1. Thus, the maintenance of suppression in these cross-species hybrids appears to require the continued presence of normal human chromosome 1. These findings raise the possibility that the frequent involvement of human chromosome 1 in potentially inactivating aberrations in human tumors may reflect a suppressor role for this chromosome in human malignancy.

Animals↗