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Query: UMLS:C0684249 (lung carcinoma)
 23,830 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Type beta transforming growth factor (TGF-beta) was shown to be the serum factor responsible for inducing normal human bronchial epithelial (NHBE) cells to undergo squamous differentiation. NHBE cells were shown to have high-affinity receptors for TGF-beta. TGF-beta induced the following markers of terminal squamous differentiation in NHBE cells: (i) increase in Ca ionophore-induced formation of crosslinked envelopes; (ii) increase in extracellular activity of plasminogen activator; (iii) irreversible inhibition of DNA synthesis; (iv) decrease in clonal growth rate; and (v) increase in cell surface area. The IgG fraction of anti-TGF-beta antiserum prevented both the inhibition of DNA synthesis and the induction of differentiation by either TGF-beta or whole blood-derived serum. Therefore, TGF-beta is the primary differentiation-inducing factor in serum for NHBE cells. In contrast, TGF-beta did not inhibit DNA synthesis of human lung carcinoma cells even though the cells possess comparable numbers of TGF-beta receptors with similar affinities for the factor. Epinephrine antagonized the TGF-beta-induced inhibition of DNA synthesis and squamous differentiation of NHBE cells. Although epinephrine increased the cyclic AMP levels in NHBE cells, TGF-beta did not alter the intracellular level in NHBE cells in either the presence or absence of epinephrine. Therefore, epinephrine and TGF-beta appear to affect different intracellular pathways that control growth and differentiation processes of NHBE cells.
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PMID:Type beta transforming growth factor is the primary differentiation-inducing serum factor for normal human bronchial epithelial cells. 287 53

Computed tomography of the thorax and abdomen, from the thoracic inlet to the renal hila, was performed as part of initial staging in 51 patients with small cell carcinoma of the lung (SCCL). The computed tomographic (CT) scans were repeated after completion of chemotherapy, as part of routine restaging and assessment of response to therapy. To identify the ways in which CT scanning uniquely benefited evaluation of initial disease extent in comparison to other diagnostic studies exclusive of CT scan, all diagnostic and clinical data were reviewed. CT scan identified more advanced intrathoracic disease than chest radiography in 82% of patients. Mediastinal node involvement not appreciated by chest radiography was seen in 61% of patients. Adrenal and retroperitoneal node involvement, not suspected by other studies, was identified by CT scan in 31% and 12% of patients, respectively. Thirty percent of the patients staged as limited disease (LD) were advanced to extensive disease (ED) by CT scan findings. While confirmation, by biopsy, of positive CT findings was not consistently accomplished, restaging CT scans provided indirect confirmation by displaying improvement or worsening that correlated with disease regression or progression. Thoraco-abdominal CT scanning more accurately identifies the extent of small cell carcinoma than other imaging procedures. This has important implications for reporting results by extent of disease. In addition, CT more accurately identifies the magnitude of intrathoracic primary and nodal tumors, which may influence the choice and conduct of local treatment--surgery and/or radiation therapy--in combination with systemic chemotherapy.
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PMID:Computed tomography in the staging of small cell lung cancer: implications for combined modality therapy. 298 64

Previous studies have suggested that ectopic production of adrenocorticotropic hormone (ACTH) or antidiuretic hormone (ADH) may occur commonly in patients with small cell carcinoma of the lung (SCCL) and that evidence of such production may be elicited only by provocative tests of water excretion and adrenal function. We studied 28 patients with SCCL and 29 patients with other cancers. Adrenal function, assessed by measuring the 8 am plasma cortisol, the 8 am to 4 pm diurnal variation in plasma cortisol, and the suppressibility of the 8 am plasma cortisol following administration of 1 mg of dexamethasone, was found to be abnormal in 28.5, 71, and 25 percent, respectively, of the patients with SCCL, compared with 18, 65, and 29.5 percent in patients with other types of cancer (P greater than 0.3). The possibility of ectopic ADH secretion was assessed by a standard water loading test, which showed excretion impairment in 60 percent of patients with SCCL and 68 percent of patients with other cancers (P greater than 0.9). Neither the stage of neoplastic disease, sites of metastatic deposits, nor performance status of the patients correlated with abnormalities of water and cortisol metabolism, indicating that such abnormalities are common in patients with all types of cancer. These data do not suggest that subclinical disturbances of adrenal function or water excretion are characteristic of any histologic type of cancer. The precise mechanism(s) underlying these abnormalities are unknown.
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PMID:Frequency of abnormalities of cortisol secretion and water metabolism in patients with small cell carcinoma of the lung and other malignancies. 628 Sep 29

Adrenal 4 binding protein (Ad4BP) is a transcription factor that regulates the expression of the steroidogenic enzymes and is expressed primarily in steroidogenic cells. We immunolocalized Ad4BP in adrenocortical carcinoma (eight cases) and various malignancies that histologically simulate an adrenocortical carcinoma to evaluate the value of Ad4BP as an immunohistochemical marker of adrenocortical carcinoma. These malignancies examined were renal cell carcinoma (20 cases), hepatocellular carcinoma (10 cases), malignant melanoma (eight cases), ovarian (six cases) and uterine (three cases) clear cell carcinoma, large cell carcinoma of the lung (five cases), and pheochromocytoma (three cases). Nuclear Ad4BP immunoreactivity was observed only in adrenocortical carcinoma cases but not in other tumors examined. Almost all of the adrenocortical carcinoma cells were immunohistochemically positive for Ad4BP including cells associated with bizarre nuclei. These results show that application of Ad4BP immunostain can contribute greatly to the differential diagnosis of adrenocortical carcinoma.
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PMID:Transcription factor adrenal 4 binding protein as a marker of adrenocortical malignancy. 755 51

The purpose of this study was to determine the patterns of iodine-131 6 beta-iodomethylnorcholesterol (NP-59) imaging and the correlation with computed tomography (CT)-guided adrenal biopsy and follow-up in patients with bilateral adrenal masses. To this end we investigated a consecutive sample of 29 euadrenal patients with bilateral adrenal masses discovered on CT for reasons other than suspected adrenal disease. Adrenal scintigraphy was performed using 1 mCi of NP-59 injected intravenously, with gamma camera imaging 5-7 days later. In 13 of the 29 patients bilateral adrenal masses were the result of metastatic involvement from lung carcinoma (5), lymphoma (3), adrenocarcinoma of the colon (3), squamous cell carcinoma of the larynx (1), and anaplastic carcinoma of unknown primary (1). Among these cases the NP-59 scan demonstrated either bilaterally absent tracer accumulation (in eight, all with bilateral metastases proven by CT-guided biopsy or progression on follow-up CT) or marked asymmetry of adrenocortical NP-59 uptake (in five). Biopsy of the adrenal demonstrating the least NP-59 uptake documented malignant involvement of that gland in five of five patients. In two patients an adenoma was found simultaneously in one adrenal with a contralateral malignant adrenal mass. In each of these cases, the adenoma demonstrated the greatest NP-59 uptake. In 16 patients diagnosis of adenoma was made on the basis of (a) CT-guided adrenal biopsy of the gland with the greatest NP-59 uptake of the pair (n = 4), or (b) adrenalectomy (n = 2), or (c) absence of change in the size of the adrenal mass on follow-up CT scanning performed 6 months to 3 years later (n = 10).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Scintigraphy of incidentally discovered bilateral adrenal masses. 760 61

Five patients with adrenal insufficiency and large adrenal glands at presentation are reported. Addison's disease was due to adrenal tuberculosis in three patients, with important changes in adrenal configuration on CT reflecting the natural history of the disease. Adrenal infiltration by non-Hodgkin lymphoma and metastatic carcinoma of the lung was the cause of the disease in the fourth and fifth patients, respectively, who developed signs of adrenal insufficiency before the diagnosis of the primary lesion became apparent. Histologic confirmation was established after unilateral adrenalectomy in three patients. In two patients with adrenal tuberculosis, long clinical and laboratory follow-up confirmed the diagnosis. This report indicates that Addison's disease is not infrequently associated with adrenal enlargement. Adrenal size is related to the cause and duration of the various disease states leading to adrenal insufficiency. Moreover, adrenal insufficiency associated with enlarged adrenal glands can be the presenting manifestation of lymphoma or metastasis.
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PMID:Adrenal insufficiency with enlarged adrenals. 866 67

Adrenal metastasis is only seen on CT scan is less than 5% of patients with otherwise resectable NSCLS, but this diagnosis has a major impact on treatment and prognosis. We present a case of a patient with NSCLC and an adrenal metastasis, which was diagnosed by EUS/FNA of an enlarged adrenal gland, who had false-negative CT scan for adrenal metastasis. PET was not performed. Prospective studies are needed to assess the incremental yield of EUS/FNA over upper abdominal CT scan and PET for detecting left adrenal metastasis in patients with suspected or proven otherwise respectable NSCLC.
Lung Cancer 2005 May
PMID:Transesophageal endoscopic ultrasound/fine-needle aspiration diagnosis of a malignant adrenal gland in a patient with non-small cell lung cancer and a negative CT scan. 1582 25