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Query: UMLS:C0677930 (primary tumor)
 20,210 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We analyzed 7 patients with so called "maligne lateral cervical cysts" regarding the controversies in the literature. Primary tumors of oropharyngeal sites were discovered in all these cases of "branchiogenic carcinoma" rising the final diagnosis of cystic metastases. Diagnostic tonsillectomy is supposed to be important to solve this problem of differential diagnosis. The issue of malignant transformation in cysts of branchial cleft origin has to be recognized as being an oncological artifact. We argue that the "maligne lateral cervical cyst" does'nt exist as a proper entity. In analogy to the principles of the treatment of oropharyngeal cancer ipsilateral neck dissection and wide local excision of the cyst followed by radiation therapy is the suggested plan of therapeutic management. Search for a possible unknown primary tumor within the oropharynx must be continued over years.
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PMID:[Clinical relevance of malignant lateral branchial cyst]. 149 87

Forty-seven laryngeal and 21 oropharyngeal recurrences were treated with salvage surgery alone or combined with radiotherapy at the ENT Clinic and Radiotherapy Division of the University of Turin, Italy. Primary tumors had been treated with surgery alone in 10 cases (larynx) and in 21 cases (oropharynx), with combined surgery and radiotherapy in 2 and 8 patients, and with radiotherapy alone in 9 and 18 cases. We observed 26/47 (larynx) and 12/21 (oropharynx) recurrences at the site of primary tumor, 20/47 and 9/21 in loco-regional nodes, and 9/47 and 3/21 in locations adjacent to the primary tumor. Salvage treatment employed surgery alone in 12 (oropharynx) and 16 (larynx) cases; radiotherapy was combined in 9 and 31 cases. Five-year actuarial NED survival was 45.5% for laryngeal and 24% for oropharyngeal cancer patients. After salvage surgery, 50% of laryngeal lesions and only 25% of oropharyngeal recurrences were completely cured. In our series, in 2 cases only the complications caused the patient's death, while in the extant cases a prolonged postoperative hospitalization was necessary. Our study was aimed at investigating the curative potentials of secondary therapy for recurrent carcinomas. A review of the literature on the subject is reported. The small amount of published data prevents "universal" treatment protocol from being assessed. The authors suggest the opportunity of employing a multimodal treatment policy for recurrences of head and neck cancers.
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PMID:[Recurrence after radiotherapy and/or surgery of carcinoma of the oropharynx and the pharynx. Possibilities of salvage surgery]. 189 66

A study was designed to determine the influence of certain surgical pathologic findings on tumor spread and survival in patients with cancer of the oral cavity and oropharynx. All patients with the histopathological diagnosis of carcinoma of the oral cavity or oropharynx from 1955 to 1983 were included in the study. Using the Head and Neck Tumor Registry of the department of otolaryngology of the Washington University School of Medicine, information was obtained regarding preoperative evaluation, staging, classification, diagnosis, treatment, surgical pathology parameters, and outcome results. The patient populations consisted of 545 patients with oral cavity cancer and 224 patients with oropharynx cancer, all of whom were eligible for 3-year follow-up. Information from a retrospective analysis of the pretreatment examination records regarding site and size of the primary tumor and neck dissection, and specific treatment, and from surgical pathology reports regarding site, size, tumor spread and resection margins, was correlated with treatment outcome. The database file was analyzed using dbase III and its companion program Framework, and SAS PC (Statistical Analysis Systems for personal computers).
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PMID:Surgical pathology of cancer of the oral cavity and oropharynx. 194 19

This historically controlled study evaluates radiation therapy in 119 patients--with squamous cell carcinomas of the head and neck--who underwent surgery alone (SA) or surgery plus radiation (S + R). The primary tumor control and nodal control, in patients with negative surgical margins who had surgery alone (SA), were 63% in the oral cavity, 60% in the oropharynx, and 67% in the hypopharynx. The same rates for S + R group and negative surgical margins were 100%, 73%, and 100%. Combining the patients with negative and positive surgical margins, control of the tumor and nodal control were the same in the oral cavity for both treatment groups (41% for SA and 44% for S + R) and increased with the addition of radiation in the oropharynx (30% for SA to 65% for S + R) and hypopharynx (33% for SA to 86% for S + R), in spite of higher percentages of T3 and T4 tumor and positive lymph nodes in the S + R group. The lower control rate in patients who had surgery alone could be due (in part) to inadequate surgery at the primary site (42% local excision) and lack of neck dissection (35% for SA vs. 77% for S + R). Postoperative radiation therapy to the primary site and neck is shown to effectively reduce local recurrence in patients with oral cavity and oropharynx cancer, regardless of surgical margins.
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PMID:Value of radiation therapy in addition to surgery for cancer of the head and neck. 308 23

Elective supraomohyoid neck dissection is considered part of standard treatment of oral and oropharyngeal cancer in most institutions, but its role in the treatment of clinically positive neck cancer remains a subject of controversy. The main object of this study is to report the results of 212 consecutive patients who underwent supraomohyoid neck dissections from 1954 to 1990. Most patients had squamous cell carcinoma of the oral cavity. Eighty-six patients (40.6%) had histologically positive lymph nodes in the surgical specimen (sensitivity, 0.55; specificity, 0.53). At the study closing date there were 58.8% actuarial 10-year overall survival rates. Forty-five patients (21.2%) had 50 tumor recurrences (32 local, 13 regional, five distant), and in 40 patients (18.8%) a second primary tumor was diagnosed. A multivariate regression technique based on Cox's proportional hazards model was used, and age (65 years or younger vs older than 65 years) represented the variable with the highest predictive strength with respect to overall survival (relative risk, 2.3). Tumor site, sex, and histologically proved metastasis were also associated with overall survival rates. The same variables were also related to the risk of recurrence. In conclusion, the death rate is mainly related to the control of the primary site tumor and the occurrence of a second primary tumor rather than to neck recurrences. It confirms that supraomohyoid neck dissection is an adequate elective procedure and possibly sufficient in the treatment of a selected group of patients with lip cancer with positive nodes at level 1.
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PMID:Supraomohyoid neck dissection in the treatment of head and neck tumors. Survival results in 212 cases. 835 96

The charts of 173 patients treated by conservation laryngectomy and pharyngolaryngectomy were retrospectively reviewed. The patients treated by endoscopic laser resection were excluded of this study. Glottic carcinoma was diagnosed in 101 patients, supraglottic carcinoma in 44 patients, hypopharyngeal carcinoma in 24 patients and oropharyngeal carcinoma in 4 patients. The median follow-up period was 44 months, 84/101 glottic cancer, 34/44 supraglottic cancer, 23/24 hypopharyngeal cancer and 2/4 oropharyngeal cancer were staged as T1 and T2. A voice-sparing external approach was carried on in 20 patients with locally advanced tumor (T3-T4). At time of the last follow-up, 132 patients (77%) were alive when 41 patients (23%) died. Overall survival rates for patients treated for T1-T2 glottic cancer at 3, 5 and 10 years were 90, 90 and 78% respectively. Overall survival rates for patients treated for T1-T2 supralottic cancer at 3, 5 and 10 years were 73, 68 and 48% respectively. Overall survival rates for patients treated for T1-T2 hypopharyngeal cancer at 3 and 5 years were 74 and 37% respectively. The site of the primary tumor (glottic versus supraglottic or hypopharynx) showed significant impact on survival (P = 0.0025)). Regarding survival, T stage and N stage were not found statistically significant.
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PMID:Conservation surgery for laryngeal and hypopharyngeal cancer. 1063 94

The purpose of this study is to ascertain the role of neck surgery and radiation therapy for cervical lymph node metastasis in oropharyngeal cancer patients. We reviewed 217 previously untreated patients with squamous cell carcinoma of the oropharynx who were treated at the Cancer Institute Hospital in Tokyo between 1971 and 1995. The N stage distribution was; N0: 83(38.2%), N1: 42(19.4%), N2a: 23(10.6%), N2b: 27(12.4%), N2c: 33(15.2%), and N3: 9(4.2%). A predominance of cervical node metastases in level II and III was revealed and there were no skip metastases outside of level II and III. The control rate of cervical metastasis for each N stage was; N0: 96.9%, N1: 90.0%, N2a: 76.5%, N2b: 62.5%, N2c: 50.0%, and N3: 0%. Definitive irradiation provided sufficient treatment for small nodes, when the primary tumor growth was well controlled by radiation therapy. Neck dissection was necessary for more advanced neck metastases. Selective limited neck dissection (level II and III) is recommended for N0 and N1 patients, and modified or classical RND is considered to be better for most cases with N2 and N3.
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PMID:[Treatment strategy for cervical node metastasis from squamous cell carcinoma of the oropharynx]. 1094 53

Second primary tumors (SPTs) are a significant problem in treating oral and oropharyngeal squamous cell carcinoma and have a negative impact on survival. In most studies the definition of SPT is based on the criteria of Warren and Gates, published in 1932. These criteria, however, are ill-defined and lead to confusion. Recent molecular studies have shown that a tumor can be surrounded by a mucosal field consisting of genetically altered cells. Furthermore, evidence has been provided that SPTs (defined by classical criteria) can share some or even all genetic markers with the index tumor, indicating that both tumors have arisen from a common cell clone. We propose that these secondary neoplastic lesions should not be considered SPTs, implying that the present concept of SPT needs revision. This review describes a novel classification of the secondary tumors that develop after treatment of a carcinoma in the oral cavity or oropharynx. On the basis of the molecular analysis of the tumors and the genetically altered mucosal field in between, we propose definitions for a "true SPT," a local recurrence, a "SFT" (second field tumor derived from the same genetically altered mucosal field as the primary tumor), and a metastasis. Considering the etiologic differences of these lesions, we believe that an accurate molecular definition is essential to make headway with the clinical management of oral and oropharyngeal cancer.
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PMID:Second primary tumors and field cancerization in oral and oropharyngeal cancer: molecular techniques provide new insights and definitions. 1189 50

Retinoids are the natural and synthetic derivatives of vitamin A. Epidemiological studies indicate that a low intake of vitamin A is associated with an increased risk of squamous cancer. In vitro studies on cancer cells show that exposure to retinoids results in the inhibition of growth, by blocking the cell cycle or by inducing apoptosis. With respect to the clinical efficacy of retinoids some positive effects have been observed in early stage oral and oropharyngeal cancer. Administration of retinoids has been shown to elicit responses in leukoplakia, a premalignant lesion of the oral mucosa that frequently develops into invasive cancer. Furthermore, it has been possible with a retinoid, 13-cis-retinoic acid, to delay or inhibit the development of second primary tumors in patients who have been curatively treated for a first primary tumor in the oral cavity or oropharynx. Recent trials, however, failed to show protective effects on the development of second primary tumors. Because of the short duration of the response, the intrinsic resistance to retinoids and the toxic side effects, the treatment with this class of compounds has not become a standard therapy. Recent studies have shed light on how preneoplastic and neoplastic cells defend themselves against the growth inhibiting action of retinoids. An increased retinoid breakdown and an inactivation of nuclear retinoid receptor appear to be the cause of acquired or intrinsic resistance. This knowledge can be used to develop novel tumor-selective strategies. This review gives an update on the role of retinoids in oral and oropharyngeal cancer and their precursor lesions. The focus will be on the anticancer activity, the mechanism of action and future directions.
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PMID:Anticancer activity and mechanism of action of retinoids in oral and pharyngeal cancer. 1216 30

Biopsies of oropharyngeal cancer were screened for chromosomal imbalances by comparative genomic hybridization (CGH) performed on 22 primary tumors and morphologically nonmalignant surrounding mucosa. The aim was to determine early chromosomal changes of tumor development and to draw conclusions on the mechanisms leading to multiple tumors. The most prominent chromosomal imbalances observed were over representations of genomic material on 3q, 15q, 8q, and 11q and losses on 9p, 3p, and 11q. In morphologically normal mucosa collected at 1 cm from the primary tumor border (M1), amplifications on 15q and 21q were most frequent. Far fewer gains and losses were found in M1 than in the primary tumor (average 2.2 vs. 6.9). Gains dominated over losses, but a tendency toward an increasing proportion of losses in the primary tumor (PT) was observed (ratio of gains to losses: PT, 4.75; M1, 6.3). Almost all the imbalances in M1 were detected in the primary tumor. No chromosomal alterations were identified with CGH in tissue samples dissected at 2 cm from the primary tumor (M2). In all samples, dysplastic morphologic changes decreased with distance from the primary tumor, which correlates with the observed lower level of genetic changes. We suggest that gains of genetic material on 15q and 21q are early events in malignant progression of squamous cell carcinoma, followed by gains on 3q, 8q, and 11q, and losses on 3p and 9p at later stages. Based on our cytogenetic data, we discuss the monoclonal model followed by lateral epithelial spread as an explanation of multiple head and neck squamous cell carcinomas.
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PMID:Chromosomal aberrations in premalignant and malignant squamous epithelium. 1285 Mar 78


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