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J G Batsakis

Publications and source records attributed to J G Batsakis.

At least 19 recordsLinked to original sources
PubMed2001

Schneiderian papillomas and carcinomas: a review.

The ectodermally derived Schneiderian mucosa gives rise to an extremely varied collection of benign and malignant neoplasms. Prototypical of these are the Schneiderian papillomas (inverted, fungiform, and cylindrical cell) and their malignant counterparts. Human papilloma virus (HPV) is currently the leading candidate as a cofactor in the pathogenesis of the papillomas. Carcinomas arise in association with the papillomas in about a 10% frequency. The carcinomas may be synchronous or metachronous. Recurrences of the papillomas are the bane of surgeons. The magnitude of the recurrences is directly proportional to the completeness of removal with the best results obtained by techniques that afford the best operative exposure. A comparison of results by different surgical procedures is presented. Histologic features sought to predict recurrences or malignant transformation have, by and large, not been helpful. Keratinization and hyperkeratosis in papillomas, however, are suggested to be sufficiently ominous as to warrant further study.

Carcinoma, Transitional Cell↗
PubMed2001

Molecular and biomarker analyses of salivary duct carcinomas: comparison with mammary duct carcinoma.

Salivary duct carcinoma (SDC) is a rare high-grade aggressive neoplasm that manifests close histologic features with invasive ductal carcinoma of the breast (IDC). In contrast to SDC, extensive molecular studies have been performed on IDC and led to the identification of certain biological markers. To investigate the underlying molecular and biologic characteristics of SDC, we performed molecular analyses using microsatellite markers on chromosomal arms 6q, 16q, 17p, and 17q, DNA flow cytometry and immunohistochemical staining for androgen receptor (AR) and p53 expression on 28 examples of these tumors in comparison to 24 IDC cases. Our results show that generally similar allelic alterations, elevated p53 and androgen receptor expressions, and high frequency of DNA aneuploidy are manifested in both SDCs and IDCs. Differences at certain markers on 6q, 17p and 17q chromosomal loci, however, were observed between the two entities. Certain loci on 6q were more frequently altered in SDC than IDC which loci on chromosomes 17p and q arms were more seen in IDCs than SDCs. The majority of SDCs had high AR expression while most of IDCs were AR negative. Our study indicates that: i) SDC may share some genetic alterations with IDC, ii) high AR expression in SDC may play a role in tumor progression, and iii) p53 overexpression and DNA aneuploidy in both entities reflect their aggressive behavior.

Adult↗
PubMed2000

Papillary squamous cell carcinomas of the upper aerodigestive tract: a clinicopathologic and molecular study.

BACKGROUND: The limited studies and the small number of published cases of papillary squamous cell carcinoma have precluded accurate assessment of the biologic characteristics of this lesion. METHODS: Thirty-eight of the carcinomas were studied. In-situ hybridization and polymerase chain reaction were performed to detect human papilloma virus (HPV) and p53 expression. RESULTS: HPV was found in 4 of 14 assessable carcinomas by in-situ hybridization and in 5 of 14 by polymerase chain reaction. The most frequently identified HPVs were HPVs in 6/11 and 16/18 patients. In general, a reciprocal relationship was found between p53 and HPV prevalence. The most lethal site for this tumor was the sinonasal tract, whereas patients with papillary squamous cell carcinomas of the larynx had the best outlook. Eleven of 25 (44%) assessable patients died of disease (mean time interval, 2 year). CONCLUSIONS: Papillary squamous cell carcinoma of the upper aerodigestive tract is a distinct variant of squamous cell carcinoma. As such and because of its putative association with HPV, papillary squamous cell carcinoma could be an informative model for defining how viral oncogenes cooperate with other factors in genomic instability, carcinogenesis, and tumor development.

Adult↗
PubMed2000

Mucosal melanomas: a review.

Mucosal melanomas, far fewer in number than melanomas of the skin, manifest a far more aggressive and more rapid life-consuming biologic course. This behavior attends melanomas at any mucosal site, upper aerodigestive tracts, anorectum, and male and female genital tracts. Prognostic factors for both groups of melanoma are similar, but most mucosal melanomas have reached the dangerous limits, e.g., depth of invasion or thickness of melanoma at the time of diagnosis. In general, the mucosal melanomas are also more refractory to therapeutic modalities. In part, this may be due to anatomic restrictions of site and the large size of tumor when first discovered. This review presents a contemporary assessment of melanomas at all of the major mucosal sites.

Anus Neoplasms↗
PubMed2000

Sarcomatoid carcinomas of the upper aerodigestive tracts.

Sarcomatoid carcinoma of the upper aerodigestive tract continues to be one of the most difficult diagnostic challenges for surgical pathologists. Histogenesis has been settled in favor of a divergent (mesenchymal) differentiation of a carcinoma, most often a squamous cell carcinoma. Finding the carcinoma and/or its immunohistochemical marker in the metaplastic cells establishes the diagnosis. There are, however, lesions that can simulate sarcomatoid carcinomas to varying degrees, and in which neither a definable carcinoma nor immunohistochemical evidence of one can be found. Such lesions fall into several categories: 1. benign reactive lesions, 2. inflammatory myofibroblastic tumors, 3. sarcomas, usually low-grade, 4. atypical pseudosarcomatous proliferation. The clinicopathologic considerations of sarcomatoid carcinomas are presented in this context and include immunohistochemical findings, prognostic factors, and biologic course.

Carcinosarcoma↗
PubMed2000

Molecular genetic alterations in carcinoma ex-pleomorphic adenoma: a putative progression model?

To determine the genetic changes associated with the development of carcinoma ex-pleomorphic adenoma (Ca Ex-PA), we analyzed 15 microsatellite loci at chromosome arms 8q, 12q, and 17p on DNA from 26 neoplasms (including 8 microdissected benign and malignant components), and 13 pleomorphic adenomas for comparison. Pleomorphic adenomas and the adenoma component of Ca Ex-PAs showed a higher incidence of loss of heterozygosity (LOH) at chromosome arms 8q (52%) and 12q (28%) than at 17p (14%) loci. In the carcinoma component, the combined LOH at chromosome arm 8q, 12q, and 17p regions was 69%, 50%, and 69%, respectively; within these chromosomal regions, 8q11.23-q12 (42%), 12q23-qter (39%), 17p13 (41%), and 17p11 (45%) loci manifested the highest incidence of LOH. Eight carcinomas (30.7%) showed loss at all three chromosomal arms tested. Of the eight microdissected Ca Ex-PAs analyzed, four adenoma and corresponding carcinoma components (50%) had the same LOH at 12q loci and additional LOH at 17p loci only in carcinomas. Chromosome arm 17p alterations correlated significantly with high disease stage and an increased proliferative rate in these tumors. Our results indicate that alterations at regions on chromosome arms 8q and/or 12q may constitute early events associated with pleomorphic adenomas; that LOH at 12q loci may identify a subset of adenoma with potential progression to carcinoma; that acquisition of additional alterations at chromosome arm 17p loci might represent an event preceding malignant transformation and progression; and that 8q, 12q, and 17p regions may harbor tumor suppressor genes involved in the genesis of PA and Ca Ex-PA. Genes Chromosomes Cancer 27:162-168, 2000.

Adenocarcinoma↗
PubMed1999

Superimposed histologic and genetic mapping of chromosome 9 in progression of human urinary bladder neoplasia: implications for a genetic model of multistep urothelial carcinogenesis and early detection of urinary bladder cancer.

The evolution of alterations on chromosome 9, including the putative tumor suppressor genes mapped to the 9p21-22 region (the MTS genes), was studied in relation to the progression of human urinary bladder neoplasia by using whole organ superimposed histologic and genetic mapping in cystectomy specimens and was verified in urinary bladder tumors of various pathogenetic subsets with longterm follow-up. The applicability of chromosome 9 allelic losses as non-invasive markers of urothelial neoplasia was tested on voided urine and/or bladder washings of patients with urinary bladder cancer. Although sequential multiple hits in the MTS locus were documented in the development of intraurothelial precursor lesions, the MTS genes do not seem to represent a major target for p21-23 deletions in bladder cancer. Two additional tumor suppressor genes involved in bladder neoplasia located distally and proximally to the MTS locus within p22-23 and p11-13 regions respectively were identified. Several distinct putative tumor suppressor gene loci within the q12-13, q21-22, and q34 regions were identified on the q arm. In particular, the pericentromeric q12-13 area may contain the critical tumor suppressor gene or genes for the development of early urothelial neoplasia. Allelic losses of chromosome 9 were associated with expansion of the abnormal urothelial clone which frequently involved large areas of urinary bladder mucosa. These losses could be found in a high proportion of urothelial tumors and in voided urine or bladder washing samples of nearly all patients with urinary bladder carcinoma.

Chromosome Aberrations↗
PubMed1999

Genetic alterations in oral squamous cell carcinoma of young adults.

The underlying molecular abnormalities associated with head and neck squamous cell carcinoma in young adults (< 40 years) are unknown. We analyzed DNA extracted from paired microdissected samples of normal squamous epithelia and invasive oral squamous cell carcinomas from 36 young adults at microsatellite loci commonly found in older patients and correlated the results with clinicopathologic parameters and outcome. Our results showed that 30 of the 36 (83%) tumors manifest loss of heterozygosity (LOH) in at least one marker. Microsatellite instability was manifested in only six tumors (< 17%). The highest incidences of alterations were noted at markers D9S168 (9p23-22), TP53 (17p13), and D17S799 (17p11) on the short arms of chromosomes 9 and 17. In general, the incidences of LOH at 3, 9 and 17p regions in young adults were similar to those found in older patients. No correlation between LOH at chromosomes 3, 9, and 17p and clinicopathologic parameters was found. Our study indicates that chromosomal regions with frequent genetic alterations involved in young adult squamous tumorigenesis are similar to those reported in older patients. Further studies of other chromosomes in this population are underway to define the novel molecular features of these tumors.

Adult↗
PubMed1999

Proliferative verrucous leukoplakia and its related lesions.

Proliferative verrucous leukoplakia (PVL) is a unique type of clinical oral leukoplakia. Enigmatic in etiology, PVL behaves in a far more aggressive fashion than other forms of leukoplakia. Its aggressiveness relates not only to a high recurrence rate, but more so to a very high level of and relentless progression from a localized simple keratosis to extensive oral disease and squamous carcinomas of verrucous, or conventional squamous cell type. Diagnosis is often late in the protracted course of PVL with the disease in an advanced stage when it is especially refractory to treatment. Within the histologic spectrum that is seen in PVL, usually as a function of time, are: (1) verrucous hyperplasia (VH), a histologically defined lesion; (2) varying degrees of dysplasia; and (3) three forms of squamous cell carcinoma: verrucous, conventional and, according to some, papillary squamous cell carcinoma. Each of these are discussed both within and outside the context of PVL. VH is a forerunner of verrucous carcinoma and the transition is so consistent that the hyperplasia, once diagnosed, should be treated like verrucous carcinoma. VH is not only an oral lesion; it can occur in the upper airway (sinonasal tract and larynx) where it is not usually found within a maternal soil of PVL. Papillary squamous cell carcinoma has been a loosely defined neoplasm, more often considered a verrucal type of malignancy. It nonetheless is a distinct clinicopathologic entity, separate from verrucous carcinoma and without a predilection for the oral cavity or an association with PVL.

Carcinoma, Squamous Cell↗
PubMed1999

Surgical excision margins: a pathologist's perspective.

The histopathologic status of excisional margins of malignant neoplasms has long been used as a potential indicator for recurrences and prognosis. The predictive ability of the margin, however, is far from satisfactory. Perhaps nowhere else in oncologic pathology has the significance of these margins been as intensively studied as in squamous cell carcinomas of the upper aerodigestive tracts. This review is, in part, a critique of current applications and the clinical implications of surgical margins for the removal of squamous cell carcinomas in these tracts. Specific points addressed in this article are: 1) postremoval (artifactual) changes in measurements; 2) the impact of margin status, as currently assessed, on recurrence and patient outcome; 3) margins and conservation surgery of the larynx; 4) margins and bone (mandible) invasion; and 5) molecular (p53 and eIF4E) margins.

Carcinoma, Squamous Cell↗
PubMed1999

Myoepithelium in salivary and mammary neoplasms is host-friendly.

This commentary relates to ameliorative effects of myoepithelial cells in carcinomas of salivary glands and the breast as viewed not only by proliferative characteristics, but also by laboratory experiments and clinicopathologic evidence. The tumor suppressor action of myoepithelium is, in part, associated with its matrix-synthesizing and proteinase inhibitor properties. Loss of the myoepithelial phenotype yields a more aggressive carcinoma with enhanced invasive and metastatic capability.

Adenocarcinoma↗
PubMed1998

Localization of chromosome 8p regions involved in early tumorigenesis of oral and laryngeal squamous carcinoma.

We analysed 30 primary invasive oral and laryngeal squamous carcinomas (SC), with concurrent dysplastic lesions, for genetic alterations at 15 microsatellite loci on the short arm of chromosome 8. Overall, loss of heterozygosity (LOH) was observed, in at least one informative locus, in 27% of the dysplastic lesions and in 67% of the invasive carcinomas. The highest frequency of allele losses in dysplasia (20% and 17%), and invasive carcinoma (40% and 48%) were detected in the same D8S298 and LPL-tet loci located on chromosomes 8p21 and 8p22 respectively. The minimal region with LOH was limited to 4.6 megaBases (mBs) at 8p22 and 7.1 mBs at 8p21. In addition, allelic losses in both dysplastic and corresponding invasive specimens were noted at the same loci in some tumors suggesting their emergence from a common preneoplastic clone. Allele losses correlated significantly with male gender, oral and laryngeal sites and high proliferative index. The data suggest that inactivation of tumor suppressor gene(s), within these loci, may constitute an early event in the evolution of oral and laryngeal SC.

Adult↗
PubMed1998

The prognostic significance of the biomarkers p21WAF1/CIP1, p53, and bcl-2 in laryngeal squamous cell carcinoma.

BACKGROUND: The clinical course of laryngeal squamous cell carcinoma (LSCC) varies considerably among patients. New biologic markers are needed to facilitate the stratification of individual patients within the conventional clinicopathologic stages of LSCC. METHODS: Eighty-three LSCCs from an equal number of patients who received at least 10 years of follow-up were investigated for p53, p21WAF1/CIP1, and bcl-2 protein expression by immunohistochemical techniques. The results were correlated with various clinicopathologic parameters, DNA content, and patient outcome by univariate and multivariate statistical analyses. RESULTS: Stage IV disease, large tumor size (>3 cm), positive lymph node status, extranodal extension, and p53 overexpression (in > 75% of cells) correlated significantly with prognosis in univariate analysis. There was no correlation between patient outcome and age, gender, race, histologic differentiation, or expression of bcl-2 or p21WAF1/CIP1. In multivariate analysis, lymph node status and p53 overexpression were the only factors significantly associated with survival. CONCLUSIONS: High p53 expression and positive lymph node status were independent predictors of the outcomes of patients with LSCC. These factors may assist in prognostication and better classification of patients for treatment.

Adult↗
PubMed1998

Genetic alterations in acinic cell carcinoma of the parotid gland determined by microsatellite analysis.

We investigated, for the first time, the genetic alterations at certain chromosomal loci in 25 primary parotid acinic cell carcinomas to define the most frequently altered chromosomal regions and their association with pathologic features and DNA content analysis. Our results showed that 21 (84.0%) of the tumors had alteration in at least one of the loci tested. In general, chromosomal regions at chromosomes 4p, 5q, 6p, and 17p were more frequently altered than those on chromosomes 1p and 1q, 4q, 5p, and 6q. Certain markers at 4p15-16, 6p25-qter, and 17p11 regions showed the highest incidence of LOH, suggesting the presence of tumor suppressor genes associated with the oncogenesis of these tumors. LOH was significantly associated only with tumor grade. No apparent correlation between LOH and other clinicopathologic and DNA content characteristics was identified. Our study broadly defined the chromosomal arms and loci that may be targeted for further localization of the minimally deleted regions involved in the tumorigenesis of these tumors.

Adult↗
PubMed1998

Mucosal melanomas of the head and neck.

Mucosal melanomas of the head and neck, as a group, are rapidly lethal neoplasms with site-specific differences in survival. They are preponderantly thick melanomas and as a consequence can present with cervical lymph node metastasis with or without distant spread. Long-term survival is unusual to rare; 5-year survival is poor, and 10-year survival, dismal. Whether this life-consuming nature is due to a biologic characteristic or related to late discovery is unknown. Because of the accelerated course and obvious differences in epidemiology, mucosal melanomas should be considered separate from melanomas of the skin.

Humans↗
PubMed1998

Leukoplakia: still a gallimaufry or is progress being made?--A review.

Leukoplakia as a medical term has been encumbered by a hodgepodge of synonyms and interpretations. It also has been a term associated with strong emotions with respect to an implied malignant potential. It now is regarded as potentially malignant, with varying degrees of risk for transformation. Leukoplakia at its major anatomic site of occurrence, the oral cavity, recently has been redefined, classified, and staged as a preamble to a more rational approach to the clinicopathologic study of leukoplakia. These changes are presented, as are current assessments of proliferative verrucous leukoplakia, verrucous hyperplasia, palatal white lesions, effects of smokeless tobacco on the oral mucosa, hairy leukoplakia, and lichen planus.

Carcinoma, Papillary↗
PubMed1997

Superimposed histologic and genetic mapping of chromosome 17 alterations in human urinary bladder neoplasia.

Multistep alterations of chromosome 17 in the progression of human urinary bladder neoplasia were studied by superimposed histologic and genetic mapping. The p53 gene was included in the analysis as a model tumor suppressor gene that is frequently involved in urothelial carcinogenesis. The strategy provided a systematic approach to the study of multistep genomic alterations that occur as neoplasia progresses from precursor intraurothelial conditions to invasive cancer. This was accomplished by sampling the entire mucosa of the organ and displaying microscopically identified invasive cancer and precursor conditions in the form of a histologic map. Subsequent isolation of DNA provided a set of samples in which the search for genetic alterations was performed and superimposed on the histologic map. This approach disclosed multifocal allelic losses of chromosome 17 in the early preinvasive phases of urothelial neoplasia. The alterations were predominantly confined to the p12-13, q22-11 and q24-25 regions. Mutations and allelic losses of the p53 gene were mapped to early preinvasive phases of urothelial neoplasia. The data provide detailed analysis of chromosome 17 allelic losses that occur in the development and progression of urothelial neoplasia and represent the first step for genome-wide modeling of multistep human urothelial carcinogenesis.

Alleles↗