OBJECTIVE: The purpose of this study was to evaluate our experience with the diagnosis and management of tumors of the parapharyngeal space (PPS), with particular emphasis on the evolving role of magnetic resonance imaging (MRI). METHODS: A case series review of 51 patients with parapharyngeal tumors who underwent surgical excision between 1980 and 1992 were analyzed with regard to presenting signs and symptoms, histologic diagnosis, imaging technique (computed tomography [CT] versus MRI), surgical approach, and outcome. RESULTS: Fifty-one patients underwent surgical excision of a parapharyngeal tumor of which the vast majority (78%) were benign neoplasms. Compared with benign neoplasms, the malignant tumors were much more likely to be associated with pain, trismus, and a cranial nerve deficit. MRI was able to locate the tumor in 20 of 21 patients (95%), while CT was able to localize the tumor in 32 of 38 patients (84%). CONCLUSIONS: MRI, because of its superior soft-tissue resolution and ability to provide imaging in multiple planes, is the imaging modality of choice to diagnose neoplasms of the parapharyngeal space. Because most of these tumors are benign, MRI allows the surgeon to select the surgical approach with the least morbidity.

Adolescent↗

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Inhibition of lung colonization at two different steps in the metastatic sequence.

Two immunomodulatory protocols were evaluated for their ability to inhibit lung colonization by mouse mammary tumor line 4T07. Preimmunization with tumor cells or pretreatment with poly I:C were equally effective at inhibiting lung colonization but a clonogenic tumor cell assay demonstrated that the treatments reduced tumor cell burden at different steps during the metastatic process. Poly I:C pretreatment accelerated tumor cell clearance based on the recovery of clonogenic tumor cells from lungs dispersed within 6 h post-arrest. Preimmunization inhibited the subsequent replication of tumor cells which survived and established in the lung, as indicated by the expansion of clonogenic cell numbers between 1 day and 7 days post-arrest. Histologic examination of serial sections of lungs demonstrated that very few (6%) of the tumor cells were extravascular 6 h post-tumor cell injection. By 24 h and 168 h the percentages of tumor cells which were extravascular had increased to 62% and 86%, respectively. Thus, poly I:C pretreatment appears to enhance killing of tumor cells prior to extravasation, whereas preimmunization appears to inhibit tumor cells after extravasation.

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Managing the aspirating patient.

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Cricoid Cartilage↗

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The superiorly based flap long-term tracheostomy in pediatric patients.

PURPOSE: Tracheostomy is commonly used to provide control of the upper airway in pediatric patients. The traditional approach, which uses a midline vertical incision in the anterior tracheal wall, is associated with relatively high rates of complications when it is used on a long-term basis. Alternative approaches, such as removing tracheal window or creating tracheal flaps, have been avoided in the pediatric patient because of the risk of tracheal stenosis and the potential for the subsequent effect on tracheal growth. The superiorly based flap tracheostomy (SBFT) has greatly reduced these risks in adults and offers better stomal maintenance, safety, and patient acceptance, but it has not been widely evaluated in pediatric patients. METHODS: We reviewed 21 superiorly based flap tracheostomies performed in children at our institution between 1986 and 1993. Routine follow-up assessments included fixed and flexible laryngotracheoscopy. Average follow-up was 17 months. RESULTS: The most common indication for performing the SBFT was bilateral vocal cord paralysis. Short-term complications included wound infection and granuloma in 2 patients. Long-term complications were not observed. One patient died from lower respiratory tract causes. Five of the patients were eventually decannulated, and the stoma closed without laryngotracheal stenosis. Morbidity rates were less and mortality was comparable to those of traditional tracheostomy. CONCLUSION: We conclude that the SBFT is promising a technique for establishing long-term control of the airway in pediatric patients.

Child↗

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Heterogeneity in p53 mutations in mouse mammary tumor subpopulations with different metastatic potential from the orthotopic site.

We have found that p53 expression is altered with progression to the metastatic phenotype of a series of neoplastic subpopulations of a single mouse mammary tumor. Single strand conformation polymorphism (SSCP) analysis of p53 transcripts indicate that the expressed p53 genes in each of the subpopulations contain one or more differences from wild type p53. Although the mutations in the coding sequence of p53 are different in each of the sublines, suggesting that independent mutational events have occurred, the mutations are clustered in exons 2-4 and in exon 6. In the metastatic subpopulations, there is either a complete loss of p53 transcriptional activity or accumulation of transcripts with an additional alteration in exons 4-5.

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Correlation of differences in modulation of ras expression with metastatic competence of mouse mammary tumor subpopulations.

The ras family of cellular oncogenes is one of the most frequently detected families of transformation-inducing genes in human solid tumors. The capacity of breast cancers to grow and metastasize have been related to enhanced expression of normal p21ras rather than the mutant form. Transformation in tumours that lack the mutant p21ras has been suggested to result from transcriptional deregulation of ras. cis-Acting sequence elements that participate in the regulation of gene expression in normal tissues and that could serve as potential targets for the deregulation of expression in tumors have been localized in several genes including c-myc and N-ras. Using a mouse mammary metastasis model system of closely related tumor subpopulations that vary in metastatic potential and with defined deficiencies, we show that c-Ha-ras plays a prominent role as a metastasis-modulating gene in this system. We have identified a highly conserved cis-acting sequence element in the first intron of the mouse and rat, and in the first exon of Ha- and Ki-ras genes of human, mouse and rat. This regulatory sequence confers strong transcription enhancer activity that is differentially modulated by steroid hormones in metastatic and nonmetastatic subpopulations. Our results indicate that perturbations in the regulatory activities of cis-acting sequences such as the one we have identified may play an important role in governing oncogenic potency of Ha-ras through transcriptional control mechanisms.

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Growth factors in mouse mammary cell interactions in vitro.

Paracrine interactions may be important in homeostasis of mammary gland. We have previously reported that normal mammary epithelial cells and stromal cells stimulate the growth of mammary tumor cells in 3-dimensional cultures in collagen gels. We now describe the ability of EGF, TGF beta, bFGF, aFGF, and PDGF to directly affect growth of tumor cells in 3-dimensional cultures in collagen gels. In addition, we assessed the ability of neutralizing antibodies against each growth factor to disrupt interactions between normal mammary cells and mammary tumor cells. Only bFGF and PDGF directly stimulated growth of the mouse mammary tumor cells. However, neither anti-bFGF nor anti-PDGF abrogated the stimulation of tumor cells by normal mammary epithelial cells or normal mammary stromal cell.

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Activated c-Ha-ras is not sufficient to produce the preneoplastic phenotype of human breast cell line MCF10AT.

MCF10AT cells are human breast epithelial cells which are able to establish preneoplastic lesions in immune deficient mice. Although, the preneoplastic phenotype was observed following transfection with a mutated c-Ha-ras (codon 12 valine), clones of MCF10AT are unable to form lesions in vivo. Restriction size fragment analysis was used to confirm that a clone unable to form the preneoplastic lesions retained the activated c-HA-ras and confirmed that the insertion site of the activated c-Ha-ras was the same for the clone as for MCF10AT1 which was selected for its ability to form lesions in vivo. Western blotting with antibody specific for the codon 12 valine c-Ha-ras demonstrated that p21 protein was comparable as well. Thus, the activated c-Ha-ras is not sufficient for the preneoplastic phenotype of human breast stem cell line MCF10AT.

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Transforming and oncogenic potential of activated c-Ha-ras in three immortalized human breast epithelial cell lines.

The ability of activated c-Ha-ras (codon 12 valine) to transform human breast epithelial cells varied for three different immortalized normal human breast epithelial cell lines established from two different women. Although activated c-Ha-ras may transform and induce a preneoplastic phenotype in MCF10A cells, activated c-Ha-ras was not sufficient to transform MCF10-2A cells. Only two of three MCF10-2A clones which expressed mutant p21 protein acquired the ability to form colonies in soft agar. When xenografted into nude beige mice, two MCF10-2A clones formed squamous carcinomas and one formed no lesions at all. The ability to form tumors did not correlate with growth in soft agar. All three activated c-Ha-ras-transfected clones of MCF-12A formed colonies in soft agar but only two produced squamous carcinomas in nude beige mice. Unlike activated c-Ha-ras-transfected MCF10A cells, none of the activated c-Ha-ras-transfected MCF10-2A or MCF-12A clones formed ducts in xenografts. Rather, initial xenograft lesions consisted of nests of cells with squamous differentiation. These observations illustrate that additional events are involved in the transformation and progression of human breast epithelial cells with activated c-Ha-ras.

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