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James Sciubba

Publications and source records attributed to James Sciubba.

11 recordsLinked to original sources

Cystic metastasis from head and neck squamous cell cancer: a distinct disease variant?

BACKGROUND: Head and neck squamous cell carcinoma (HNSCC) commonly spreads to regional deep cervical nodes. In most cases, these metastases present as firm, solid masses in the designated lymph node chains. A distinct subset of metastatic nodes present as cystic masses, with most of the volume made up of a liquid center surrounded by a thin solid rim. It has been observed that certain squamous cell carcinoma (SCC) subsites are more likely to produce metastases that are cystic. These sites predominantly include primary tumors of tonsil tissue from Waldeyer's ring. In the past, these cystic cancers often have been erroneously diagnosed as branchiogenic carcinomas, that is, a branchial cleft cyst that has undergone malignant degeneration. Today, most authors have concluded that so-called branchiogenic carcinomas are actually cystic metastases in the neck probably arising from an oropharyngeal primary SCC. The purpose of this work is to consider the phenomenon of cystic lymph node metastasis in head and neck cancer in depth. METHODS: A review of the relevant English-language literature linking cystic metastasis and head and neck cancer was performed. RESULTS: These studies indicate that lateral cystic masses in adults often represent an occult primary cancer originating in the epithelium within Waldeyer's ring. CONCLUSIONS: Adult patients who are initially seen with a lateral cystic neck mass must be presumed to have a cancer until proven otherwise. The mass should be biopsied by fine-needle aspiration (FNA). However, negative FNA findings may be misleading; therefore, an excisional biopsy and examination under anesthesia with directed biopsies of Waldeyer's ring and bilateral tonsillectomy should be considered a part of the diagnostic workup.

Animals↗

Mitochondrial DNA content increase in response to cigarette smoking.

An increase in mitochondrial DNA (mtDNA) content and decline in mitochondrial function occurs with aging and in response to DNA-damaging agents, including tobacco smoke. We did a cross-sectional study and quantified changes in mtDNA content in a population of individuals with varied smoking and alcohol exposure. Age, smoking history, ethanol intake, and other demographic data were characterized for 604 individuals participating in a screening study for smoking-related upper aerodigestive malignancy. Total DNA was extracted from exfoliated cells in saliva. DNA from a nuclear gene, beta-actin, and two mitochondrial genes, cytochrome c oxidase I and II (Cox I and Cox II), were quantified by real-time PCR. mtDNA content was correlated with age, exposure history, and other variables using multivariate regression analyses. A significant increase (P<0.001) in mtDNA content was noted in smokers (31% and 29% increase for Cox I and Cox II, respectively) and former smokers (31% and 34%) when compared with never smokers. This association persisted after adjustment for other significant factors including age, alcohol drinking, and income (P<0.001). Increased mtDNA content was positively associated with pack-years of smoking (P=0.02). Despite an average smoking cessation interval of 21 years in former smokers, tobacco cessation interval was not statistically significantly associated with mtDNA content. Smoking is associated with increased mtDNA content in a dose-dependent fashion. Mitochondrial DNA alterations in response to smoking persist for several decades after smoking cessation, consistent with long-term, smoking-related damage.

Actins↗

Lower-extremity liposarcoma metastatic to the larynx: case report.

Distant metastases to the larynx are rare. We describe the case of a 46-year-old man who was referred to our head and neck surgery clinic with a 6-week history of sore throat and otalgia. He was found to have a laryngeal lesion that was consistent with a primary myxoid liposarcoma that had been extirpated from a lower extremity earlier To the best of our knowledge, no case of myxoid liposarcoma metastatic to the larynx has been previously reported in the English-language literature.

Humans↗

Odontogenic ghost cell carcinoma.

BACKGROUND: Odontogenic ghost cell carcinoma (OGCC), a malignant counterpart of the calcifying odontogenic cyst (COC), is exceedingly rare. Previous descriptions of this tumor were based on identification of malignant histologic characteristics such as infiltration, cellular pleomorphism, numerous mitoses, and necrosis concurrent with classical benign COC or its solid benign variant, the odontogenic ghost cell tumor. METHODS: We present a case of a young Asian man who underwent multiple local excisions of a recurring maxillary COC. After one such excision, a rapid onset of painful swelling ensued, and the patient was referred to our institution for definitive surgery. RESULTS: The patient underwent a right subtotal maxillectomy. Intraoperatively, a 5-cm tumor was found to be extending into the right maxillary sinus and nasal cavity. The excised tumor was diagnosed as an OGCC. The tumor was excised with clear margins, and no adjunctive radiotherapy was given. The patient was free of residual or recurrent disease 18 months after surgery. CONCLUSION: On the basis of this case and prior cases found in the literature, OGCCs show a spectrum of growth from slow growing locally invasive tumors to highly aggressive, rapidly growing, infiltrative tumors. Wide local excision with histologically clean margins is the recommended mode of treatment. We recommend close long-term surveillance of recurrent or long-standing benign COCs and OGCC.

Adult↗

Malignant odontogenic tumors: a 22-year experience.

OBJECTIVES/HYPOTHESIS: Malignant odontogenic tumors are exceedingly rare and arise from odontogenic epithelial residues and odontogenic cysts in the jaw bones. Odontogenic malignancies have various origins. Some develop directly from the remnants of odontogenic epithelium left after completion of dental development; others may result from malignant transformation of a benign odontogenic cyst or ameloblastoma. These lesions are usually locally aggressive with radical surgery being the primary mode of treatment. Because of their rarity, much of the existing information about malignant odontogenic tumors with regard to their origin, clinicopathological features, biological behavior, and therapeutics is derived from case reports or small series. The study represents one of the largest series of malignant odontogenic tumors compiled in a single institution. STUDY DESIGN: Retrospective 22-year review from an Academic Medical Center. METHODS: Twenty cases of reported malignant odontogenic tumors were diagnosed in the authors' institution between 1981 and 2002. All pathological slides were reviewed to reconfirm diagnosis. Malignancy was confirmed based on the following criteria: histological findings of infiltrative growth, atypical cytological features, and focal necrosis or clear evidence of distant metastatic spread. Patient age, race, sex, treatment and outcome were recorded on chart review. RESULTS: Of the twenty reported cases, only nine were actually found to be malignant tumors on re-evaluation. These consisted of four cases of malignant ameloblastomas, two cases of ameloblastic carcinoma, one case of malignant Pindborg tumor (calcifying epithelial odontogenic tumor), one case of odontogenic ghost cell carcinoma, and one case of squamous cell carcinoma arising in an odontogenic keratocyst. The racial demographics were six Caucasian patients, one African American patient, and two Asian patients; seven men and two women represented the gender distribution. Tumors of six cases were located in the mandible, and of three cases, in the maxilla. All cases were treated with radical surgical excision. Two patients died of their disease, three patients were alive and free of disease, and four patients were lost to follow-up. CONCLUSION: Malignant odontogenic tumors are rare. They require a multidisciplinary team to determine proper treatment. Long-term surveillance is mandatory and is accomplished by routine physical examinations, along with serial radiographic imaging.

Adult↗

A transcriptional progression model for head and neck cancer.

PURPOSE: A genetic progression model for head and neck squamous cell carcinoma (HNSC) has been established and implies the presence of transcriptional dysregulation as a consequence of accumulation of genetic alterations. Although expression array data have been provided for HNSC, the timing of transcriptional dysregulation in the progression from normal mucosa to dyplastic epithelium to invasive HNSC has not been described. Here, we describe a transcriptional progression model of HNSC. EXPERIMENTAL DESIGN: Expression arrays representing >12,000 genes and expressed sequence tags were used to examine malignant lesions (M), premalignant lesions (PM), distant, histopathologically normal mucosa from patients with premalignant or malignant lesions (MN), and normal mucosa from the upper aerodigestive tract of patients with noncancer diagnoses (N). Significance analysis of microarrays, hierarchical clustering, and principal components analysis was used to identify genes with differential expression patterns. RESULTS: Using a false discovery rate of <5% for significance analysis of microarray, the M group revealed 965 up-regulated and 1106 down-regulated genes relative to the N group. The PM group demonstrated 108 up-regulated and 226 down-regulated genes relative to the N group, whereas the M group demonstrated only 5 up-regulated and 13 down-regulated genes relative to the PM group. Both hierarchical cluster analysis and principal components analysis revealed a consistent separation between the N, PM, and M groups, with a closer association between the PM and M groups. To provide independent validation of the microarray data, quantitative reverse transcription-PCR was performed for a significantly up-regulated gene, integrin alpha 6, correlating well with microarray data (linear regression analysis, P < 0.0001). CONCLUSIONS: Similarly to the genetic progression model of HNSC, this transcriptional model shows that the majority of alterations occurs before the development of malignancy and identifies key targets of transcriptional dysregulation during progression from a normal to a premalignant state and from a premalignant to a malignant state.

Carcinoma↗

Chondroid chordoma of the nasal septum.

Chondroid chordoma is an uncommon malignant tumor of bone that occurs mostly in patients of early middle age. To our knowledge, this tumor has not been previously described in the nasal septum as a primary lesion. We describe a 39-year-old woman who presented with a 1-year history of nasal obstruction. Results of her physical examination and imaging studies demonstrated a nasoseptal mass. We also discuss the histologic and radiographic characteristics of the chondroid chordoma and compare it with other tumors that arise in the nasoseptal area to highlight the different prognoses and approaches to management.

Adult↗

Oral lesions in young children.

Oral lesions in very young children usually have a benign presentation, and only rarely contribute to significant aerodigestive symptomatology. Management begins with early recognition of the pathology and appropriate diagnosis. Hemangiomas, lymphangiomas, and teratomas may present with airway compromise or feeding difficulties, necessitating early intervention.

Child, Preschool↗

Ameloblastic carcinoma of the maxilla.

The maxilla is an unusual site for an ameloblastoma, and certainly for an ameloblastic carcinoma. Ameloblastomas are considered as benign, yet locally aggressive neoplasms in the vast majority of cases. However, very rarely, these tumors demonstrate a clinical course of malignancy. Recently, a classification system was published differentiating between malignant odontogenic carcinoma variants. The two such forms include malignant ameloblastoma, and ameloblastic carcinoma. In the differential diagnosis, the designation of malignant ameloblastoma is reserved for lesions that, despite their benign histology, metastasize as well-differentiated cells. The diagnosis of ameloblastic carcinoma is reserved for tumors that demonstrate a malignant morphologic appearance, regardless of whether metastasis is a proven fact at the time of discovery and treatment. We discuss the presentation, pathology, and treatment of the 18th case of a maxillary ameloblastic carcinoma in the literature.

Aged↗

Progression of microsatellite instability from premalignant lesions to tumors of the head and neck.

The role of microsatellite alterations other than loss of heterozygosity (LOH) in the progression of benign epithelium to head-and-neck squamous cell cancer (HNSCC) has not been previously described. As the severity of the dysplasia increases at the microscopic level, there is an increase in the prevalence of LOH as defined by microsatellite analysis. Other alterations have been detected in the form of microsatellite instability (MSI), represented by insertions or deletions of base pairs. It is unknown, however, whether the prevalence of these alterations likewise increases during these early stages of tumor progression. Using 6 selected markers that demonstrate a high rate of MSI and allelic imbalance in invasive head-and-neck cancer, we examined 111 lesions ranging from hyperplasia without atypia to invasive mucosal HNSCC. Two of 34 (5.9%) of the hyperplasias without atypia, 2/12 (16.7%) of the mild dysplasias, 2/21 (9.5%) of the moderate dysplasias, 7/26 (26.9%) of the high-grade dysplasias/carcinomas in situ and 6/18 (33%) of the HNSCCs demonstrated microsatellite base pair length alterations. Our findings indicate that MSI becomes increasingly more common as early dysplastic lesions progress to fully malignant HNSCC and confirm this as a supplemental detection method in microsatellite analysis.

Base Pair Mismatch↗