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J G Batsakis

Publications and source records attributed to J G Batsakis.

At least 55 records · Page 3Linked to original sources
PubMed1996

Thyroid gland ectopias.

Failures of descent of the medial anlage of the thyroid and incomplete obliteration of its vertical tract lead to midline or near-midline ectopias such as lingual thyroid and thyroglossal cysts. Each poses special diagnostic and therapeutic considerations. "Ectopias" of the thyroid gland lateral to the carotid artery and jugular vein, however, cannot be readily explained by current embryological information. In these instances, and especially for intranodal thyroid tissue, a metastasis from an occult thyroid primary is the mandatory first consideration.

Carcinoma, Papillary↗
PubMed1996

Microsatellite instability in preinvasive and invasive head and neck squamous carcinoma.

To investigate the extent and significance of microsatellite instability in head and neck carcinogenesis we analyzed DNA extracted from normal squamous epithelium, severe dysplasia, and corresponding carcinoma specimens from 20 patients by multiplex polymerase chain reaction. Loci on chromosomes 3p, 5p, 5q, 8p, 9p, 9q, 11q, 17p, 17q, 18p, 18q were selected for analysis. Our results show that three of the dysplasias (15.0%) and six of the invasive carcinoma (30.0%) manifested instability at multiple loci. Two of the dysplastic lesions had identical alterations in the corresponding carcinomas and one showed instability differences in only two of eight loci. Normal squamous epithelium lacked microsatellite instability. No apparent association between smoking, alcohol use, or family history of cancer and instability was found in this small cohort. Invasive carcinomas with instability were relatively more poorly differentiated and had a higher stage and a high proliferative fraction. Our study indicates that microsatellite instability is 1) noted in a small subset of dysplastic lesions of head and neck squamous epithelium and 2) present in approximately one-third of invasive lesions, usually with aggressive characteristics, and may clinically be a late event associated with tumor progression.

Aged↗
PubMed1996

Allelic loss and replication errors at microsatellite loci on chromosome 11p in head and neck squamous carcinoma: association with aggressive biological features.

The frequent loss of heterozygosity (LOH) demonstrated at chromosome 11p regions in several sporadic malignancies has suggested the presence of tumor suppressor genes at these locations. To obtain detailed mapped incidence of the microsatellite alterations at these regions and to investigate the possible correlation between the genotype and the pathobiological characteristics of head and neck squamous carcinoma, we analyzed paired DNA samples from normal mucosa and primary tumor specimens from 56 patients with these tumors. Our results show that 50.9% of the tumors had microsatellite alterations at one or more of these loci. LOH was manifested in 45. 5% and instability in 5.5% of the tumors. 11p15 loci showed more frequent LOH (39.6%) than those of 11p13 (29.3%) and 11p11-12 (18. 8%); the D11S988 (11p15) marker showed the highest single locus incidence of LOH (29.7%). Eight tumors (22.2%) demonstrated simultaneous LOH at both the 11p15 and 11p13 regions. LOH was significantly associated with poor histological differentiation, DNA aneuploidy, and high proliferative activity in these neoplasms. Our study extends the involvement of the 11p13 and 11p15 regions to head and neck squamous tumorigenesis and indicates that the terminal loci of 11p may harbor a tumor suppressor gene(s) associated with the progression of these tumors.

Adult↗
PubMed1995

Heterogeneity of the proliferative fraction and cyclin D1/CCND1 gene amplification in head and neck squamous cell carcinoma.

High proliferative fraction and cyclin D1/CCND1 gene amplification have been associated with certain aggressive features of head and neck squamous carcinoma in some studies, but not in others. The differences may be related to the intratumoral heterogeneity of these factors. Moreover, the interrelationship between these seemingly related factors has not been determined. In order to determine the correlation between tumor proliferative fractions and CCND1 gene amplification, 3 spatially different samples from each of 32 primary head and neck squamous cell carcinomas (HNSCC) were separately analyzed by flow cytometry. A mixture of these specimens was also minced and snap frozen for molecular studies. DNA was extracted from patient lymphocytes, normal appearing squamous epithelium, and tumors. A genomic DNA probe containing the first exon of CCND1 was used for hybridization by Southern technique. A 5.6 kb genomic DNA probe of immunoglobulin heavy chain was used as an internal standard for quantification of CCND1 gene amplification. Our results showed that 30% of the tumor cases manifested intratumoral heterogeneity (> 50% differences) of their proliferative activity. The highest value was used for correlation with gene amplification. Eleven (34.4%) of the 32 tumors showed CCND1 amplification (2-10-fold). When the proliferative fraction was dichotomized into high and low groups based on the mean value (> or = 13%), a highly statistical correlation between CCND1 amplification and tumor proliferation was obtained (P < 0.001). No significant correlation between gene amplification and other clinicopathologic parameters was noted.(ABSTRACT TRUNCATED AT 250 WORDS)

Blotting, Southern↗
PubMed1995

Sequential p53 mutation analysis of pre-invasive and invasive head and neck squamous carcinoma.

Single-stranded conformational polymorphism (SSCP) and direct sequencing were performed on uninvolved mucosa, severe dysplasia and invasive carcinoma samples from 20 patients with head and neck squamous carcinoma. Seven (35%) of the non-invasive lesions and 15 (75%) of the invasive carcinomas manifested p53 mutations. Although the majority of mutations were mis-sense, resulting in single amino acid substitution, a silent mutation encoding for the same amino acid and 2 non-sense mutations encoding a stop codon were also observed. Mutations in invasive carcinoma were mostly in exon 8 and involved codons 296, 288 and 298; non-invasive lesions showed more mutations at exons 5 to 7. Five lesions showed simultaneous mutations in 2 different exons; in 3 both non-invasive and invasive carcinomas showed primary mutation at exons 5 to 7, and invasive carcinoma showed a secondary mutation at exon 8. Different codon mutations in the same exon between dysplastic and the corresponding carcinoma samples were found in 2 cases. p53 alterations were not observed in any of the normal mucosa samples. No apparent association between p53 mutations and conventional clinicopathologic parameters, including DNA content, was found in this cohort. Our study indicates that (i) p53 alteration is an early event in the genesis of a subset of head and neck squamous carcinomas, (ii) normal mucosa within the resected specimens lacked p53 mutation, (iii) sequential mutations of different exons of the p53 gene suggests accumulation of genetic alterations during the neoplastic transformation of these lesions and (iv) the difference in codon mutation of the same exon between dysplastic and corresponding carcinoma suggests an independent clonal development.

Adult↗
PubMed1995

Sequential loss of heterozygosity at microsatellite motifs in preinvasive and invasive head and neck squamous carcinoma.

Studies of sequential molecular alterations in noninvasive and invasive head and neck squamous carcinoma are few in number. Consequently, the genetic changes associated with the neoplastic transformation of these carcinomas have not been defined. To identify chromosomal alterations in preinvasive and invasive head and neck squamous carcinoma, we analyzed DNA from microdissected normal squamous epithelium, severe dysplasia, and invasive carcinoma samples from 20 patients for loss of heterozygosity (LOH) at microsatellite loci by multiplex PCR. Twenty-five microsatellite repeats on chromosomes 3p, 5q, 8p, 9p and 9q, 11q, 17p, 17q, and 18p and 18q regions were used. In informative cases, LOH in noninvasive lesions was observed in 9p (28%), 9q and 18q (10%), 11q and 17p (7%), and 3p and 18p (5%). A high incidence of LOH in invasive carcinoma was observed at 9p (72%), 8p (53%), 3p (47%), 9q (35%), and 11q (33%). LOH was also associated with DNA aneuploidy, high tumor stage, and poor histological differentiation. Our results indicate that: (a) the high incidence of LOH at loci on chromosomes 9p, 8p, 3p, 9q, and 11q implicate these regions in head and neck squamous carcinoma tumorigenesis; (b) 9p loci alterations are manifested in the early development of these tumors; (c) LOH is correlated with poor prognostic clinicopathological factors; and (d) LOH at 8p loci appears to be associated with the tumor's aggressive features.

Adult↗
PubMed1995

p53 and retinoid chemoprevention of oral carcinogenesis.

We studied p53 protein's pattern of expression, association with retinoid response or resistance, and modulation by retinoid intervention in oral premalignancy. These p53 analyses were included in a prospective trial of the retinoid isotretinoin (1.5 mg/kg/day for 3 months) in 40 patients (45 oral premalignant lesions). Seven nonsmoking subjects (eight oral biopsies) were included as a control. Protein levels of p53 were determined separately for the whole epithelium and the basal, parabasal, and superficial layers. A wide range of accumulated p53 protein levels occurred in 40 (89%) of 45 lesions in basal and parabasal but not superficial layers. No p53 protein was detected in any normal controls. Accumulation of p53 increased in direct association with histological grade (P = 0.0004). An inverse relationship occurred between the levels of accumulated p53 protein and response to isotretinoin (P = 0.006). High-dose isotretinoin did not modulate accumulated p53 protein expression.

Adult↗
PubMed1995

Pathology review in an early prostate cancer detection program: results from the American Cancer Society-National Prostate Cancer Detection Project.

Biopsy materials obtained in the American Cancer Society National Prostate Cancer Detection Project were reviewed at the Central Pathology Laboratory at the Armed Forces Institute of Pathology. Of 265 cases submitted, 177 were diagnosed as prostatic carcinoma, 7 as prostatic intraepithelial neoplasia (PIN), 13 as atypical glands or atypical hyperplasia, and the remaining 68 were benign hyperplasias. Irrespective of the means of detectin or the grading system used (Gleason or WHO-Mostofi), a large majority of the cancers were detected as low-grade tumors. Of 27 cases of PIN reported, 20 were associated with cancer, leaving 7 cases with the sole diagnosis of PIN. These data may indicate the increased use of prostate-specific antigen (PSA), digital rectal examination (DRE), and transrectal ultrasound (TRUS) in the United States is shifting the spectrum of prostate cancer pathology toward early low-grade tumors.

Biopsy↗
PubMed1995

c-erbB-2/neu oncogene and Ki-67 analysis in the assessment of palatal salivary gland neoplasms.

To evaluate the role of the Ki-67 proliferation antigen and c-erbB-2/neu oncogene expression in the clinical assessment of salivary gland tumors, we followed up 71 patients with minor salivary tumors of the palate. All benign neoplasms (n = 18) showed low Ki-67 scores (< 12%), whereas 26% (14 of 53) of malignant neoplasms manifested high Ki-67 scores (> 12%). A significant statistical difference between Ki-67 scores for benign and malignant neoplasms was observed (p < 0.001). Ki-67 index also correlated significantly with malignant tumor grade (p = 0.04) and patient survival (p = 0.02). Only 1 of the 18 benign tumors had c-erbB-2/neu oncogene overexpression. A significant difference between c-erbB-2/neu overexpression in benign and malignant tumors was observed (p = 0.01). Overexpression of c-erbB-2/neu oncogene was noted in 38% (16 of 42) of malignant tumors and was significantly associated with aggressive tumor behavior (p < 0.001). Multivariate analysis of significant factors revealed that gender, tumor stage, and c-erbB-2/neu oncogene overexpression were jointly predictive of survival. Our data indicate that although the Ki-67 proliferating antigen and c-erbB-2/neu oncogene expression may reflect certain intrinsic biologic properties of these neoplasms, only c-erbB-2/neu overexpression is significantly associated with their biologic aggression.

Adolescent↗
PubMed1995

Terminal duct adenocarcinomas of the parotid gland.

The major salivary glands are considered to rarely be the sites of primary terminal duct adenocarcinomas, a neoplasm with a considerable predilection for origin from intraoral minor salivary glands. We present a clinicopathological study of 22 terminal duct adenocarcinomas of the parotid gland, the largest single series to date. A comparison between the parotid neoplasms and over 200 minor salivary gland terminal duct adenocarcinomas indicates there is little difference in biological behaviour and confirms the low-grade quality of the carcinomas, regardless of site of origin.

Adenocarcinoma↗
PubMed1995

Epithelial-myoepithelial carcinoma of salivary glands. A clinicopathologic, DNA flow cytometric, and immunohistochemical study of Ki-67 and HER-2/neu oncogene.

Thirty-one salivary gland epithelial-myoepithelial carcinomas from 26 patients were studied by DNA flow cytometry, and immunostaining for Ki-67 and HER-2/neu oncogene product. The results were correlated with clinicopathologic factors and patient outcome. The tumor most commonly involved the parotid gland, and mainly affected patients in their 6th to 8th decades. The clinical course was characterized by a high incidence of local recurrence (50%) and not infrequent distant metastasis (25%). None of the patients in this cohort died of disease. DNA content analysis revealed 21 neoplasms with DNA diploidy and 5 tumors with DNA aneuploidy; all aneuploid cases were near-diploid (hyperdiploidy) and showed low proliferative activity. All aneuploid and 60% of the diploid neoplasms developed recurrences and/or metastases. Immunohistochemical analysis of Ki-67 proliferation markers also showed low overall growth fractions. Interestingly, Ki-67 immunoreactivity was largely restricted to myoepithelial cells, suggesting a central role for this cell in the development of these tumors. HER-2/neu oncogene analysis failed to demonstrate overexpression in any of the tumors examined. This study indicates that epithelial-myoepithelial carcinoma is a low grade malignant neoplasm with a high propensity for recurrence. HER-2/neu oncogene and Ki-67 offer no additional advantages over current factors in the biologic evaluation of these neoplasms. DNA aneuploidy may allow for the identification of a subset of tumors that is more prone to recurrence and metastasis, but further studies with extended follow-up are needed.

Adolescent↗
PubMed1995

Pituitary gland involvement of the sinonasal tract.

Involvement of the upper aerodigestive tract by a pituitary adenoma is due either to downward extension of an intracranial tumor or to a tumor arising from ectopic (Rathke's pouch) remnants. Sites of predilection for the ectopic adenoma are headed by the sphenoid bone and sinus, followed by the soft tissue of the dorsal pharynx and clivus. Both invasive sellar and ectopic adenomas can be destructive, with the extracranial extension of pituitary adenomas being more locally aggressive. There have been no examples of metastasizing ectopic pituitary tumors.

Adenoma↗
PubMed1995

"Inflammatory pseudotumor": what is it? How does it behave?

Inflammatory pseudotumor, as a histologic diagnosis and carrying with it the prospect of a benign clinical course, is rather firmly entrenched as a pulmonary lesion. Extrapulmonic forms, however, are farraginous and, as reported, have included lesions having few, or even none, of the histologic features of those in the lungs. For those more closely aligned with the fibroblastic or myofibroblastic phase of the lung lesions, their biologic behavior can belie their histology in that they can be locally aggressive and metastasize as sarcomas. For those tumors in the upper airway, and especially in the abdomen, pathologists should be very circumspect in the use of inflammatory pseudotumor as a diagnosis, and clinicians should not be lulled into denying the extrapulmonic forms their due respect.

Granuloma, Plasma Cell↗
PubMed1995

Teratomas of the head and neck with emphasis on malignancy.

The great majority of teratomas of the head and neck present in the neonate or infant and are biologically benign and yet with a high mortality because of their space-occupying and obstructive character. Teratomas in the adult neck and sinonasal tract are histologically and biologically malignant, with an often unpredictable response to therapy.

Adult↗
PubMed1995

Bacillary angiomatosis.

The acquired immunodeficiency syndrome and other causes of immunosuppression have ushered in a variety of opportunistic infections. One of these is bacillary angiomatosis, a vasoproliferative lesion whose principal causative agent is Rochalimaea henselae. Bacillary angiomatosis, while preponderantly a cutaneous affliction, can be systemic, including involvement of the head and neck mucous membranes. Molecular technology and epidemiologic studies used to identify the bacterial agent of bacillary angiomatosis have also uncovered R henselae as the organism responsible for most cases of cat-scratch disease. Why the same organism promotes two different histopathologic lesions, as seen in bacillary angiomatosis and cat-scratch disease, is unknown.

Angiomatosis, Bacillary↗
PubMed1995

Mycobacterial disease of the head and neck: current perspective.

The worldwide increase in mycobacterial diseases, tuberculous and nontuberculous, and their association with human immunodeficiency virus infection has had and will continue to have an impact on the practice of otolaryngologist-head and neck surgeons. Epidemiologic and ecologic changes in tuberculosis and nontuberculous mycobacterial diseases tend to blur former clinicopathologic distinctions among these groups, especially in immunocompromised hosts. Diagnosis depends on objective identification of the mycobacterium, a process facilitated by molecular diagnostics.

Adolescent↗
PubMed1995

Oral squamous cell carcinoma and the mandible.

Of the various oral carcinoma subsites, the carcinomas related to the mandibular region (alveolar ridge, floor of mouth, lower retromolar area, lower buccal sulcus) are among those with the highest rate of recurrences. Neoplastic invasion of the mandible is one of the factors promoting the recurrences. Determining the presence and extent of bony involvement is therefore critical in the management of patients. The surgeon has several methods to aid in the determination of margins of invasion: radiology, gross clinical inspection, and intraoperative frozen section. Each has its deficiences and in the end, it is a combination of the methods, tempered by clinical judgment, that produces the best results.

Carcinoma, Squamous Cell↗