Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0007095 (carcinoid)
 6,990 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Activation of ras oncogenes is commonly found in human neoplasms. We have investigated 280 human lung cancer specimens for ras activation, including 38 that have not been reported previously, using an oligonucleotide detection assay. From a total of 141 adenocarcinoma samples from smokers, 41 tested positive for a point mutation in codon 12 of K-ras (30%), while three tumors had another type of ras activation. Only two of 40 cases from nonsmokers had a K-ras mutation (5%), suggesting that K-ras mutations may be directly caused by exposure to carcinogens in tobacco smoke. The majority of the point mutations in adenocarcinomas were guanine to thymine transversions in codon 12 of the K-ras oncogene. Occasional point mutations in ras oncogenes were detected in adenosquamous carcinomas (one of five cases) and large cell carcinoma (one of 24 cases), but no ras activations were found in small cell carcinomas (six cases), squamous carcinomas (48 cases), carcinoid carcinomas (15 cases), or thymoma (one case). Analysis of the clinical and pathological features of the adenocarcinoma cases showed no apparent associations between the K-ras activation and age at diagnosis, sex, disease stage, and the occurrence of other neoplasms. K-ras-positive adenocarcinomas tended to be less differentiated than the K-ras-negative ones (P = 0.044, chi 2 test for trend). K-ras mutations identify a subgroup of patients with adenocarcinoma of the lung who have a very poor prognosis despite radical resection of their tumor. Although K-ras has been proposed as a target for antitumor therapy, its major clinical significance could be to aid in the selection of patients for specific therapeutic interventions, such as adjuvant chemotherapy.
 ...
PMID:Clinical significance of ras oncogene activation in human lung cancer. 156 97

We have previously reported complete responses and long-term survival following cisplatin-based combination chemotherapy in some patients with advanced poorly differentiated carcinomas of unknown primary site. In order to better define the clinical and pathologic characteristics of the chemotherapy-responsive subgroup, we have reviewed the case histories of our 32 patients who achieved complete response to combination chemotherapy. Initial light microscopic diagnoses were as follows: poorly differentiated carcinoma (23 patients), poorly differentiated adenocarcinoma (eight patients), or poorly differentiated large cell carcinoma (one patient). The median age was 37 years (range, 19-70); 25 of 32 patients were male. All patients had unresectable neoplasms at the time of diagnosis. Twenty-two patients had metastases at two or more locations. In 27 of 32 patients (84%), the predominant site of tumor involvement was either in the mediastinum, retroperitoneum, lymph nodes, or lungs. Six patients were assigned more specific diagnoses at some time during their clinical course on the basis of further pathologic evaluation, additional biopsy material, or autopsy: germinal tumors, two patients; adenocarcinoma of the lung, one patient; carcinoid tumor of the lung, one patient; and malignant melanoma, two patients. Eighteen patients (56%) remain continuously disease free at a median of 77 months following diagnosis and are considered unlikely to recur. All patients with poorly differentiated carcinomas and tumor location in the mediastinum, retroperitoneum, lungs, or lymph nodes should be considered for treatment with intensive cisplatin-containing combination chemotherapy, since some of these patients have potentially curable malignancies.
 ...
PMID:Curative combination chemotherapy for patients with advanced poorly differentiated carcinoma of unknown primary site. 245 81

Twenty cases of metastatic neoplasms in the breast were identified in a series of 1,034 fine-needle aspirations (FNAs) of the breast, of which 389 were malignant. Patients with breast carcinomas in whom metastasis to the contralateral breast developed were excluded from this study. This series consisted of 17 women and 3 men, ranging in age from 28 to 63 years (mean, 49 years). The tumors included oat cell carcinoma (three), melanoma (three), ovarian serous carcinoma (one), bronchogenic adenocarcinoma and squamous carcinoma (four and two, respectively), lymphoma (two), carcinoid (two), transitional cell carcinoma (one), plasma cell myeloma (one), and rhabdomyosarcoma (one). In two patients, the breast mass was the first manifestation of an extramammary cancer (two adenocarcinoma of the lung). Eleven patients died of disseminated cancer shortly after the breast metastasis was diagnosed. In most cases, the aspirates displayed the cytologic features characteristic of the primary tumors, thereby establishing the metastatic nature of the neoplasm. In four cases (two carcinoids, one myeloma, and one rhabdomyosarcoma), the cytologic features were difficult to differentiate from a primary breast carcinoma; however, the final diagnosis was established by electron microscopic examination and immunocytochemical studies on the aspirates. One case (adenocarcinoma of the lung) was misdiagnosed as primary breast carcinoma on both FNA and mastectomy specimen. Because metastatic neoplasms in the breast may mimic primary breast tumors, the authors recommend the following: (1) Evaluation of FNA of breast should be done with complete knowledge of the patient's clinical history. (2) The possibility of metastasis should be suspected in lesions with unusual cytologic patterns. (3) Ancillary studies on FNA can be helpful in interpreting selected cases.
 ...
PMID:Fine-needle aspiration cytology of metastatic neoplasms in the breast. 275 Jul 5

To define the role of cellular oncogenes in human cancers, we studied the prevalence of mutational activation of ras oncogenes in untreated non-small-cell lung cancer. Genomic DNA was extracted from 39 tumor specimens obtained by thoracotomy and was examined for activating point mutations in codons 12, 13, and 61 of the H-ras, K-ras, and N-ras genes. A novel, highly sensitive assay based on oligonucleotide hybridization following an in vitro amplification step was employed. The K-ras gene was found to be activated by point mutations in codon 12 in 5 of 10 adenocarcinomas. Two of these tumors were less than 2 cm in size and had not metastasized. No ras gene mutations were observed in 15 squamous-cell carcinomas, 10 large-cell carcinomas, 1 carcinoid, 2 metastatic adenocarcinomas from primary tumors outside the lung, and 1 small-cell carcinoma. An approximately 20-fold amplification of the unmutated K-ras gene was observed in a tumor that proved to be a solitary lung metastasis of a rectal carcinoma. We conclude that mutational K-ras activation may be an important early event in the pathogenesis of adenocarcinoma of the lung but that amplification of ras genes or mutational activation of H-ras or N-ras does not play a major part in non-small-cell lung cancer.
 ...
PMID:Mutational activation of the K-ras oncogene. A possible pathogenetic factor in adenocarcinoma of the lung. 304 Dec 18

Antineoplaston A10 injections were administered to 18 patients diagnosed with 19 types of neoplastic disease. The patients' diagnoses included: adenocarcinoma of the rectum and colon, Stage IV (8 cases); adenocarcinoma of the pancreas (4 cases); adenocarcinoma of the breast, Stage IV (3 cases) and single cases of adenocarcinoma of the lungs, Stage III; adenocarcinoma of the stomach, Stage IV; chondrosarcoma of the nose and right maxillary sinus; and carcinoid. The treatment was administered from 52 to 640 days. The highest dosage taken was 2210.5 mg/kg/24 h. Most of the patients were taking from 206.9 to 387.1 mg/kg/24 h. The treatment was associated with minimal side-effects including febrile reactions, muscle and joint pain, muscle contraction in the throat, abdominal pain of short duration and single incidences of nausea, dizziness and headache. Desirable side-effects included increase of platelet count and white blood cell count. Objective response to the treatment was noticed in 8 patients including one patient diagnosed with intraductal carcinoma of the breast, Stage IV, 2 patients with adenocarcinoma of the sigmoid, Stage IV, 1 patient with adenocarcinoma of the rectum, Stage IV, 2 patients with adenocarcinoma of the pancreas, 1 patient with adenocarcinoma of the lung, Stage III, and 1 chondrosarcoma.
 ...
PMID:Toxicology studies on antineoplaston A10 injections in cancer patients. 374 80

This Phase I-II trial evaluated vinzolidine (VZL), a semisynthetic vinblastine derivative administered on a five-day oral schedule every 21 days, with 60% of the total dose on day 1 followed by 10% of the total on each of the following four days. Forty-four patients with advanced malignancies were entered in this study and 34 were evaluable for response. Three patients responded, with complete remissions in patients with adenocarcinoma of the lung (39+ weeks) and adenocarcinoma of the pancreas (20+ weeks) and a minor response in a patient with metastatic carcinoid (6 weeks). Myelosuppression was the dose-limiting toxicity, and was remarkable for its unpredictability among patients and even in the same patient receiving a constant dose of vinzolidine. There was one drug related death associated with myelosuppression. This study was closed because of the erratic myelotoxicity of oral vinzolidine. However, the activity observed with vinzolidine merits future trials, using a parenteral formulation which may have more predictable toxicity.
 ...
PMID:Five-day schedule of vinzolidine, an oral vinca alkaloid, in a variety of tumors. 609 87

Diethylnitrosamine is known to cause squamous cell carcinoma and adenocarcinoma of the lung in Syrian golden hamsters. Sections of lungs obtained from hamsters treated with the systemic carcinogen diethylnitrosamine revealed a significant increase in the number of argyrophilic cells of neuroepithelial bodies. These affected cells also exhibited enhanced survival in vitro. After 7 days in culture, argyrophilia, dense-core vesicles, and corticotropin-like immunoreactivity were observed in many of the cells derived from the lungs of carcinogen-exposed hamsters by dissociation with pronase. In addition, nuclei of argyrophilic cells in neuroepithelial bodies of the exposed hamsters were labeled at 60 min following administration of [3H]thymidine. This suggests that the carcinogen stimulates the pulmonary neuroendocrine-like cells to divide. Normally, the component cells of neuroepithelial bodies may originate from nonargyrophilic precursor cells in the surrounding epithelium, as in control hamsters the argyrophilic cells of neuroepithelial bodies appeared labeled only at 8 days after the administration of thymidine. The relationship of the diethylnitrosamine-induced reactions to bronchial carcinoid tumors or small-cell carcinomas of the lung remains to be established.
 ...
PMID:Effects of diethylnitrosamine on lung neuroendocrine cells. 618 6

Diethylnitrosamine is known to cause squamous cell carcinoma and adenocarcinoma of the lung in Syrian golden hamsters. Sections of lungs obtained from hamsters treated with the systemic carcinogen diethylnitrosamine showed a significant increase in the number of argyrophilic cells of neuroepithelial bodies. The hyperplastic response was retained at least 4 weeks after cessation of treatment. To examine whether these affected cells exhibited enhanced survival in vitro, lung cells were dissociated with Pronase and grown in culture. After 7 days, argyrophilia, dense-cored vesicles, and corticotropin-like immunoreactivity were observed in many of the cells derived from hamsters treated for 5 or 8 weeks. These findings suggest that the endocrine-like cells of neuroepithelial bodies are affected by diethylnitrosamine as evidenced by a numerical increase in vivo and by the properties exhibited by cells in vitro. The relationship of this diethylnitrosamine-induced reaction to bronchial carcinoid tumors or small-cell carcinoma of the lung remains to be established.
 ...
PMID:Lung endocrine-like cells in hamsters treated with diethylnitrosamine: alterations in vivo and in cell culture. 694 63

Advances in molecular biology have increased our knowledge of the biology of preneoplastic lesions in the human lung. The recently published WHO lung tumour classification defines three separate lesions that are regarded as preinvasive neoplasia. These are (1) squamous dysplasia and carcinoma in situ (SD/CIS), (2) atypical adenomatous hyperplasia (AAH), and (3) diffuse idiopathic pulmonary neuroendocrine cell hyperplasia (DIP-NECH). SD/CIS is graded in four stages (mild, moderate, severe, and CIS), based upon the distribution of atypical cells and mitotic figures. Most airways showing SD/CIS demonstrate a range of grades; many epithelia are hard to assess and the reproducibility of this complex system remains to be established. Detailed criteria are, however, welcome and provide an objective framework on which to compare various molecular changes. Alterations in gene expression and chromosome structure known to be associated with malignant transformation can be demonstrated in CIS, less so in dysplasias, but also in morphologically normal epithelium. The changes might be sequential, and their frequency and number increase with atypia. Less is known of the "risk of progression" of SD/CIS to invasive "central" bronchial carcinoma. It may take between one and 10 years for invasion to occur, yet the lesion(s) may be reversible if carcinogen exposure ceases. AAH may be an important precursor lesion for peripheral "parenchymal" adenocarcinoma of the lung: the "adenoma" in an adenoma-carcinoma sequence. There is good morphological evidence that AAH may progress from low to high grade to bronchioloalveolar carcinoma (BAC; a non-invasive lesion by definition). Invasion then develops within BAC and peripheral lung adenocarcinoma evolves. The molecular events associated with this progression are not well understood and studies are hampered by a lack of clear criteria to distinguish high grade AAH from BAC. Nonetheless, as with SD/CIS, the patterns of expression of tumour associated genes are consistent with neoplastic progression. We have little idea of the incidence of AAH in the normal or "smoking" populations. It is found more frequently in cancer bearing lungs, especially in those with adenocarcinoma, and is more common in women. No data are available on the risk of progression of AAH. DIPNECH is an exceptionally rare lesion associated with the development of multiple carcinoid tumours. Almost nothing is known of its biology. Knowledge of these lesions will be crucial in the design and understanding of lung cancer screening programmes, where it is likely that the morphological and, more importantly perhaps, the molecular characteristics of these lesions will provide useful targets for detection and possibly even treatment.
 ...
PMID:Pulmonary preinvasive neoplasia. 1130 41

We report a case of synchronous tumors consisted of bronchial carcinoid and adenocarcinoma of the lung. A 58-year-old female was referred to our hospital after screening, because an abnormal shadow was noted in the right lung on her computed tomography (CT) of the chest. CT scans showed a peripheral pulmonary mass in the right middle lobe and a nodule around the right lower lobe bronchus. The nodular lesion like swollen lymph node was diagnosed as bronchial carcinoid originated in B6 by bronchoscopy. The pulmonary mass was diagnosed as adenocarcinoma by using core needle biopsy during operation. Right middle and lower bilobectomy and mediastinal lymph node dissection were performed. Coincidence of a bronchial carcinoid and an adenocarcinoma of the same side of the lung is a rare occurrence.
 ...
PMID:[Synchronous tumors consisted of bronchial carcinoid and adenocarcinoma of the lung]. 1205 55


1 2 Next >>