Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0677930 (primary tumor)
 20,210 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Squamous, large cell, and adenocarcinoma, collectively termed non-small cell lung cancer (NSCLC), are diagnosed in approximately 75% of patients with lung cancer in the United States. The treatment of these three tumor cell types is approached in virtually identical fashion because, in contrast to small cell carcinoma of the lung, NSCLC more frequently presents with localized disease at the time of diagnosis and is thus more often amenable to surgical resection but less frequently responds to chemotherapy and irradiation. Cigarette smoking is etiologically related to the development of NSCLC in the great majority of cases. Genetic mutations in dominant oncogenes such as K-ras, loss of genetic material on chromosomes 3p, 11p, and 17p, and deletions or mutations in tumor suppressor genes such as rb and p53 have been documented in NSCLC tumors and tumor cell lines. NSCLC is diagnosed because of symptoms related to the primary tumor or regional or distant metastases, as an incidental finding on chest radiograph, or rarely because of a paraneoplastic syndrome such as hypercalcemia or hypertrophic pulmonary osteoarthropathy. Screening smokers with periodic chest radiographs and sputum cytologic examination has not been shown to reduce mortality. The diagnosis of NSCLC is usually established by fiberoptic bronchoscopy or percutaneous fine-needle aspiration, by biopsy of a regional or distant metastatic site, or at the time of thoracotomy. Pathologically, NSCLC arises in a setting of bronchial mucosal metaplasia and dysplasia that progressively increase over time. Squamous carcinoma more often presents as a central endobronchial lesion, while large cell and adenocarcinoma have a tendency to arise in the lung periphery and invade the pleura. Once the diagnosis is made, the extent of tumor dissemination is determined. Since most NSCLC patients who survive 5 years or longer have undergone surgical resection of their cancers, the focus of the staging process is to determine whether the patient is a candidate for thoracotomy with curative intent. The dominant prognostic factors in NSCLC are extent of tumor dissemination, ambulatory or performance status, and degree of weight loss. Stages I and II NSCLC, which are confined within the pleural reflection, are managed by surgical resection whenever possible, with approximate 5-year survival of 45% and 25%, respectively. Patients with stage IIIa cancers, in which the primary tumor has extended through the pleura or metastasized to ipsilateral or subcarinal lymph nodes, can occasionally be surgically resected but are often managed with definitive thoracic irradiation and have 5-year survival of approximately 15%.(ABSTRACT TRUNCATED AT 400 WORDS)
 ...
PMID:Non-small cell lung cancer. Part I: Biology, diagnosis, and staging. 164 34

Formalin-fixed, paraffin-embedded specimens from 110 cases of primary hepatocellular carcinoma were stained for hepatitis B x antigen (HBxAg), hepatitis B surface antigen (HBsAg), and hepatitis B core antigen (HBcAg). Eighty-four % of these patients were HBxAg positive in their tumor cells. Among the 110 cases studied, 80 had adjacent nontumorous tissue in the same block, and 65 of these nontumorous liver tissues stained positive for HBxAg (81%). HBsAg was positive in 19% of cases within tumor tissue and 61% in surrounding nontumorous tissue. HBcAg was positive in 11% of cases within tumor tissue and 26% in surrounding nontumorous tissue. These findings show that HBxAg is a common marker in the liver of patients with hepatitis B virus (HBV)-associated primary hepatocellular carcinoma and that it is closely associated with tumor cells in these individuals. In addition, the finding of HBxAg in the absence of detectable HBsAg and HBcAg in the liver tissues of many HBsAg carriers suggests that HBxAg could be expressed independent of HBV replication and implies that the synthesis of this antigen may be directed from integrated HBV DNA templates. The finding of HBxAg in the nucleus of hepatocytes from primary hepatocellular carcinoma patients with dysplasia, combined with the known trans-activating properties of HBxAg, implies that HBxAg plays one or more important roles in hepatocarcinogenesis. The finding of HBxAg in bile duct epithelium and cholangiocarcinoma tissues is compatible with the hypothesis that HBV may contribute to this other primary tumor type in the liver. Together, these results further implicate HBxAg in the pathogenesis of primary liver cancers.
 ...
PMID:Hepatitis B x antigen in hepatitis B virus carrier patients with liver cancer. 165 8

Squamous, large cell, and adenocarcinoma, collectively termed non-small cell lung cancer (NSCLC), are diagnosed in approximately 75% of patients with lung cancer in the United States. The treatment of these three tumor cell types is approached in virtually identical fashion because, in contrast to small cell carcinoma of the lung, NSCLC more frequently presents with localized disease at the time of diagnosis and is thus more often amenable to surgical resection but less frequently responds to chemotherapy and irradiation. Cigarette smoking is etiologically related to the development of NSCLC in the great majority of cases. Genetic mutations in dominant oncogenes such as K-ras, loss of genetic material on chromosomes 3p, 11p, and 17p, and deletions or mutations in tumor suppressor genes such as rb and p53 have been documented in NSCLC tumors and tumor cell lines. NSCLC is diagnosed because of symptoms related to the primary tumor or regional or distant metastases, as an incidental finding on chest radiograph, or rarely because of a paraneoplastic syndrome such as hypercalcemia or hypertrophic pulmonary osteoarthropathy. Screening smokers with periodic chest radiographs and sputum cytologic examination has not been shown to reduce mortality. The diagnosis of NSCLC is usually established by fiberoptic bronchoscopy or percutaneous fine-needle aspiration, by biopsy of a regional or distant metastatic site, or at the time of thoracotomy. Pathologically, NSCLC arises in a setting of bronchial mucosal metaplasia and dysplasia that progressively increase over time. Squamous carcinoma more often presents as a central endobronchial lesion, while large cell and adenocarcinoma have a tendency to arise in the lung periphery and invade the pleura. Once the diagnosis is made, the extent of tumor dissemination is determined. Since most NSCLC patients who survive 5 years or longer have undergone surgical resection of their cancers, the focus of the staging process is to determine whether the patient is a candidate for thoracotomy with curative intent. The dominant prognostic factors in NSCLC are extent of tumor dissemination, ambulatory or performance status, and degree of weight loss. Stages I and II NSCLC, which are confined within the pleural reflection, are managed by surgical resection whenever possible, with approximate 5-year survival of 45% and 25%, respectively. Patients with stage IIIa cancers, in which the primary tumor has extended through the pleura or metastasized to ipsilateral or subcarinal lymph nodes, can occasionally be surgically resected but are often managed with definitive thoracic irradiation and have 5-year survival of approximately 15%.(ABSTRACT TRUNCATED AT 400 WORDS)
 ...
PMID:Non-small cell lung cancer. Part II: Treatment. 171 39

An 82-year-old woman developed a well-differentiated squamous cell carcinoma that apparently arose in two discrete congenital cysts of the liver. Both cysts were lined predominantly by stratified squamous epithelium with extensive areas of dysplasia and foci of transition to in situ carcinoma and overt exophytic and infiltrating squamous cell carcinoma. A third intrahepatic cyst was lined entirely by bile duct-type epithelium and contained no tumor. The liver was massively infiltrated by the carcinoma, and there were metastases to the lymph nodes, lung, and bone marrow. Since a search for an alternative primary tumor site was unrevealing, the authors interpret this as a unique case of primary squamous cell carcinoma originating in congenital cysts of the liver.
 ...
PMID:Primary squamous cell carcinoma originating in congenital cysts of the liver. Report of a case and review of the literature. 173 27

Seventy-six patients with Barrett's esophagus were cared for during a 10-year period. Fifty-six patients (74%) presented with complications of the disease. There were 20 strictures, 7 giant ulcers, 11 cases of dysplasia, and 29 patients with carcinoma. In patients with benign disease, 93% had mechanically defective sphincters and 83% had peristaltic failure of the lower esophageal body. Esophageal pH monitoring showed excessive esophageal exposure to pH less than 4 in 93% and excessive exposure to pH more than 7 in 34% of the patients tested. Ninety-three per cent of patients with excessive alkaline exposure had complications, compared to only 44% with normal alkaline exposure (p less than 0.01). Gastric pH monitoring, serum gastrin levels, and gastric acid analysis supported a duodenal source for the alkaline exposure. Antireflux surgery was performed using Nissen fundoplication in 30, Belsey partial fundoplication in 3, and Collis-Belsey gastroplasty in 2. Six required resection with colon interposition. Good symptomatic control was achieved in 77% after antireflux surgery. Four patients had symptoms and signs of duodenogastric reflux; three required a bile diversion procedure. Fifteen patients had an en bloc curative resection with colon interposition. One patient with high-grade dysplasia on biopsy was found to have intramucosal carcinoma after simple esophagectomy. Five tumors were intramucosal, seven were intramural, and four were transmural. Lymph node involvement occurred only in the latter two. Actuarial survival 5 years after curative resection was 53%. Median survival time for patients after palliative resection or no resection was 12 months. Study of en bloc specimens indicated that extent of resection should be adapted to extent of disease: esophagectomy for intramucosal disease, en bloc esophagectomy with splenic preservation for intramural and transmural disease. Serum CEA was useful in detecting recurrent disease after surgery when the primary tumor stained positively for CEA.
 ...
PMID:Surgical therapy in Barrett's esophagus. 222 18

A total of 273 male patients underwent radical cystoprostatectomy between 1967 and 1987, 22 of them being regarded as at risk for urethral tumor recurrence. In these 22 primary simultaneous urethrectomy was performed or urethrectomy followed shortly after cystectomy because of the histology of the cystectomy specimen. Of the remaining 251 patients, a urethral tumor recurrence was observed in 23 (9.2%). Another patient with a urethral recurrence had originally been operated on in another hospital. The first urethral tumor recurrence was observed in 1977, but between October 1987 and May 1988, 7 patients were treated for urethral recurrence or rerecurrence, suggesting that this problem will be recorded increasingly often with improved survival rates from the original bladder tumor and longer follow-up of these patients. In 21 of the 24 patients with recurrence, multifocal tumor growth (multiple primary tumors, multifocal carcinoma in situ, unifocal primary tumor with concomitant carcinoma in situ or severe dysplasia) was found in their primary cystectomy specimen. Two had unifocal tumors. The original histology of the patient operated on elsewhere is not known. The data suggest that primary simultaneous urethrectomy should be performed in all patients undergoing cystoprostatectomy for multifocal bladder tumors. All patients in whom the urethra is left in place need regular washout cytologies of the urethra for the rest of their lives to ensure early diagnosis of any urethral tumor recurrences.
 ...
PMID:[Urethral tumor recurrence following radical cystoprostatectomy--an indication for primary cystoprostato-urethrectomy?]. 276 95

We studied the expression of villin, a microfilament-associated, actin-binding protein typical of brush-border microvilli, in a variety of human carcinomas by applying immunofluorescence microscopy to frozen sections and immunoblotting methods to tissue extracts using a rabbit antiserum and a monoclonal antibody specific for villin. All of the 24 primary and metastatic colorectal adenocarcinomas tested were uniformly and strongly positive for villin, with the immunocytochemical labeling concentrated at the luminal cell margin. In poorly differentiated tumor areas, rudimentary tubules were stained. All of the six tubular adenocarcinomas of the stomach studied as well as two adenocarcinomas of the gall bladder and a hepatocellular carcinoma were also villin-positive. Villin was detectable in 12 of 14 adenocarcinomas of the pancreas; in some of these cases, its distribution was heterogeneous. Among 21 renal cell carcinomas investigated, positivity for villin was seen in nine of 13 clear cell tumors (especially those of grade II), and in all four chromophilic cell tumors; however, all four chromophobe cell tumors studied were negative. Four of 11 endometrial but none of nine ovarian carcinomas were (uniformly or focally) villin positive. Of 18 adenocarcinomas of the lung studied, one was uniformly and four focally positive for villin, while the remainder were negative. All of the other epithelial tumors studied, including 12 adenocarcinomas of the breast and seven epithelial or biphasic pleural mesotheliomas, were villin negative. Our results show that the expression of villin in intestinal epithelial cells is consistently maintained in their corresponding carcinomas, even when the organized brush-border structure has been lost. The presence of villin in some endometrial and pulmonary adenocarcinomas--in contrast to its absence in the respective normal epithelia--suggests that this protein is newly expressed during hyperplasia, dysplasia, or carcinogenesis. Determining the presence or absence of villin and its immunocytochemical staining pattern in metastatic adenocarcinomas may be of some help in determining the type and site of the primary tumor.
 ...
PMID:Villin: a cytoskeletal protein and a differentiation marker expressed in some human adenocarcinomas. 289 90

Clinical and demographic data as well as the course of illness were analyzed in a retrospective study of 50 patients with a primary tumor or a malformation of the calvarial bones. The most frequent histological diagnosis was "eosinophilic granuloma of bone" (found in 42% of cases), followed by hemangioma, osteoma, dermoid, epidermoid and malignant tumors, and fibrous dysplasia. Local recurrence was observed in 1 patient with ossifying fibroma and 1 with a dermoid tumor, while further dissemination of illness was observed in 3 patients with "eosinophilic granuloma". In these cases, systemic drug therapy is needed. The necessity of an intensive search for further signs of illness and long follow-up periods in patients with primary localized histiocytosis X is stressed.
 ...
PMID:[Tumors and space-occupying abnormalities of the skull calotte]. 325 4

Positive or negative surgical margins of excision cannot predict the clinical course of patients with squamous cell carcinomas of the head and neck. Local recurrences are increased in frequency and number when invasive or in situ carcinoma or severe dysplasia is present at the margins. Histologic grade of the carcinoma has no influence. In patients with negative margins, 2- and 5-year survivals are dependent on the clinical stage and size of the primary tumor.
 ...
PMID:Surgical margins in squamous cell carcinomas. 335 51

Important tumour markers in tumours of the oral mucosa and salivary glands are intermediate filaments of cytoskeleton, oncofetal and proliferative antigens, lectin receptors and blood group substances, enzymes, metalloproteins and viral antigens. The special occurrence of the following tumour markers was demonstrated: keratin, vimentin, carcinoembryonic antigen (CEA), tissue polypeptide antigen (TPA), lectins (helix pomatia antigen = HPA, peanut agglutinin = PNA), Thomsen-Friedenreich-antigen, blood group substances A and B, amylase, lactoferrin, viral antigens of papilloma virus (group 11 and 16). In oral dysplasia and squamous cell carcinomas, relationships exist between the presence of keratin filaments and cell differentiation. Lectins represent membrane-orientated markers of differentiation. A loss of blood group substances A and B can be observed in oral dysplasias. Papilloma viruses and viral antibodies can be demonstrated in papillomas, leukoplakias and carcinomas. The salivary gland tumours show a distinct pattern of distribution for keratin, vimentin, CEA, TPA, metalloproteins and enzymes. Transplanted human salivary gland tumours in athymic nude mice keep the same tumour marker profile as in the primary tumor.
 ...
PMID:The importance of tumor markers in oral pathology. II. Cell membrane and cytoplasmic antigens as tumour markers. 404 Jun 31


1 2 3 4 5 Next >>