Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0242379 (lung cancer)
 71,905 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Several recent studies based on restriction fragment length polymorphism analysis have supported the concept that the accumulation of multiple genetic alterations converts a normal cell to a malignant cell. Activation of oncogenes and/or inactivation of tumor suppressor genes have been observed during tumor progression in colorectal cancer, lung cancer, and breast cancer. To investigate the possibility that multiple genes are altered during the progression of renal cell carcinoma, we have used restriction fragment length polymorphism markers throughout the genome to test for loss of heterozygosity in 38 renal cell carcinomas. Nearly 64% of the tumors had lost heterozygosity on the short arm of chromosome 3. We also observed loss of heterozygosity averaging about 30% at informative loci on six other chromosomal arms (chromosomes 5q, 6q, 10q, 11q, 17p, and 19p). These results lead us to suspect the existence of several tumor suppressor genes associated with carcinogenesis of renal cell carcinoma.
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PMID:Allelotype of renal cell carcinoma. 167 Sep 99

We have isolated and mapped 75 new DNA markers including 52 restriction fragment length polymorphism (RFLP) markers on human chromosome 3. Clones were mapped by nonisotopic in situ hybridization, in which discrete fluorescent signals can be detected on prometaphase R-banded chromosomes. Thirty-seven markers were mapped to each arm of chromosome 3, and one was localized to the centromere. Five markers defined variable number of tandem repeat (VNTR) loci. Although the 75 clones were scattered throughout the chromosome, they were concentrated in the R-positive bands. This physical map of chromosome 3 will contribute to the characterization of the chromosomal and molecular aberrations involved in renal cell carcinoma, small-cell lung cancer, and other malignancies and in single-gene disorders such as von Hippel-Lindau disease and autosomal dominant retinitis pigmentosa.
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PMID:Isolation and mapping of 75 new DNA markers on human chromosome 3. 167 99

We examined Southern blot analysis of genomic DNAs from 70 patients with sporadic renal cell carcinoma, using the human L-myc oncogene fragment as a hybridization probe. Our purpose was to study the relationship between the restriction fragment length polymorphism (RFLP) of the L-myc and the frequencies of metastasis. The patients were classified into 3 genotypes according to the polymorphic patterns defined by two alleles (L-L:17, L-S:31, S-S:22). The relative ratios of the 3 genotypes in the renal cancer patients were similar to those seen in healthy Japanese. However, of 20 patients who exhibited distant metastases at diagnosis, only 2 belonged to the L-L type. The incidence of distant metastasis in L-L type patients was significantly lower than that in L-S and S-S patients (p = 0.068, by Fisher's exact probability test). These results basically correspond to the previous findings in the lung cancer patients [Kawashima et al.: Proc. natn. Acad. Sci. USA 85: 2353-2356, 1988]. On the other hand, L-myc RFLP analysis in 50 prostatic cancer patients revealed that the incidence of metastasis at diagnosis did not correlate with L-myc genotypes. L-myc RFLP seems to be less promising in prostatic cancer than in lung or kidney cancer.
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PMID:Restriction fragment length polymorphism of the L-myc gene and susceptibility to metastasis in genitourinary cancers. 168 40

Bleomycin is an agent with significant antitumor efficacy whose major dose limiting toxicity is pulmonary fibrosis. Attempts have thus been made to identify congeners with reduced toxicity and with comparable or greater antitumor activity. Tallysomycin S10b is a bleomycin analogue possessing significantly greater potency, equal or reduced lung toxicity, and slightly greater antineoplastic activity when compared to the parent compound in preclinical studies. This report describes our experience with tallysomycin S10b in 30 patients with a variety of non-hematologic neoplasms. Pulmonary toxicity, occurring in 4 patients, was the major toxicity. The recommended cumulative dose of tallysomycin S10b was difficult to establish from the results of this study, as pulmonary toxicity appeared to be more idiosyncratic than dose- or schedule-dependent. The employment of more sensitive methods for detecting pulmonary toxicity in this study suggest that tallysomycin S10b may have reduced pulmonary toxicity compared to the parent compound. Both bleomycin and tallysomycin S10b have similar t1/2 beta half-lives of 2-4 h. Six patients had prolonged terminal elimination half-lives of tallysomycin S10b, but no clear relationship between this phenomenon and efficacy or toxicity was evident. No complete or partial responses occurred. Disease stabilization occurred in 4 of 15 patients with diagnoses of renal cell carcinoma, rectal cancer and lung cancer. Five of eight patients with non-measurable disease had stable disease, including one with mesothelioma, one with carcinoma of the head and neck, two with renal cell cancer and one with colon carcinoma.
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PMID:Phase I trial of tallysomycin S10b, a bleomycin analogue. 169 67

Aminoacylase-1 (ACY1, EC 3.5.1.14) is a cytosolic enzyme with a wide range of tissue expression and has been postulated to function in the catabolism and salvage of acylated amino acids. ACY1 has been assigned to chromosome 3p21, a region reduced to homozygosity in small-cell lung cancer and renal cell carcinoma, and has been reported to exhibit reduced or absent expression in small-cell lung cancer cell lines and tumors. Using monoclonal antibodies to human ACY1, we have isolated cDNA clones from a liver lambda gt11 cDNA library. As proof of identity, the fusion protein encoded by a putative ACY1 cDNA displayed ACY1 enzymatic activity. Additionally, it was determined that the putative ACY1 cDNA clones hybridize to an EcoR1 restriction fragment that has been mapped to chromosome 3p. Both ACY1 activity and this restriction fragment have been further demonstrated to be syntenic to distal 3p21.1 through the use of a panel of human-rodent somatic cell hybrids containing fragments of chromosome 3. An additional EcoR1 restriction fragment to which the probe hybridizes has been assigned to chromosome 18. The major mRNA species to which the ACY1 cDNA hybridizes is 0.9 kb; faint hybridization to a 4.2-kb mRNA species is also detected. These studies further refine a region of interest in the investigation of gene inactivation in small-cell lung cancer and provide a new marker on chromosome 18.
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PMID:Human aminoacylase-1: cloning, regional assignment to distal chromosome 3p21.1, and identification of a cross-hybridizing sequence on chromosome 18. 170 30

Thirty-seven patients with tracheobronchial lesions by malignant tumor were treated with Nd-YAG laser. Thirty-seven patients were twenty-three males and fourteen females and ages ranged from 34 to 79 years. Diseases included were primary tracheal tumor in 3 cases, lung cancer in 16 (8 squamous cell carcinoma, 5 adenocarcinoma, 2 large cell carcinoma, 1 small cell carcinoma), cancer of adjacent organs in 9 (5 thyroid cancers, 4 esophageal cancers), and metastatic cancer to the lung or mediastinal lymph nodes in 9 (4 renal cell carcinoma, 2 thyroid cancer, one patient respectively, colon cancer and breast cancer). Intermittent irradiation of YAG laser was done for 0.5 second at 30-40 Watt through flexible bronchoscope under local anesthesia. It was repeated 1 to 41 times (mean 4.1 times) and energy amount was 148 Joules to 18,513 Joules (mean 3,305 J). The result was; stenosis disappeared in 22 cases (59.4%), improved in 14 (37.8%), and in one case YAG laser therapy discontinued due to intractable bleeding. The Nd-YAG laser therapy for tracheobronchial lesions by malignant tumor is very useful to improve dyspnea or atelectasis.
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PMID:[Nd-YAG laser therapy of tracheobronchial lesions by malignant tumor]. 173 32

Two cases of necrotic myelopathy are presented. This is a very rare paraneoplasic syndrome. One patient had clear cell renal carcinoma and other had lymphatic metastasis of malignant melanoma without filiation of the primary tumor. The complete spinal study (MNR, CT, myelography) proved normal. Diagnosis is possible when all other causes of spinal disease have been discarded. Nowadays, it is possible to diagnose this disease premortem. The international literature reviewed showed 31 cases published since 1903, associated mainly to malignant diseases such as lymphomas, lung cancer, renal carcinoma, breast cancer, leukemias, etc. The differential diagnosis appears in the comments, as well as the presentation and evolution of the cases described up until now.
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PMID:[Necrotizing myelopathy associated with neoplasia. A clinico-pathological study of 2 cases and a review of the literature]. 175 90

Constitutional chromosome abnormalities that may predispose a group of individuals to develop certain neoplasms have been reported for some human solid tumors. Deletions of 13q in retinoblastoma, 11p in Wilms' tumor, 1p in neuroblastoma, 3p in renal cell carcinoma, 5q in colorectal carcinoma and 22q in meningioma are examples of such anomalies. In breast carcinoma, a specific cytogenetic defect has not been conclusively identified. We have studied Phytohemagglutinin-stimulated lymphocytes of 76 breast cancer patients, 68 predisposed family members, 40 controls, and 30 additional controls with lung cancer to determine whether nonrandom chromosome defects are present. From each sample 100, G-or Q-banded metaphase spreads were studied for rearrangements. A marked clustering of alterations in the long arm of chromosome no. 1 (q11-22) was seen in breast cancer patients and in some predisposed family members. Alterations in 1q were present in 1% to 3% of metaphases, and included translocations to chromosomes 3, 6, 7, 9, 12, 15, 17, 18, 21 and the X; deletion of 1q, or pericentric inversion. Twelve out of 62 (19.3%) familial cases, 3 out of 14 (21.4%) sporadic cases, 9 out of 68 (13.2%) predisposed cases and 2 out of 40 (5%) control cases showed 1q alterations. None of the 30 lung cancer patients showed chromosome 1 anomaly in this region. This is consistent with the reports on primary breast tumor tissues, cell lines and pleural effusions where 1q defects have been reported. We conclude that chromosome 1q rearrangement might be one of the primary lesions specifically associated with the development of breast cancer.
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PMID:Chromosome anomalies in human breast cancer: evidence for specific involvement of 1q region in lymphocyte cultures. 188 38

This paper describes the cellular and tissue distribution of P-glycoprotein (P-GP) (mdr1 gene product), the role of P-GP in vivo and immunodiagnosis of multi-drug-resistant cancers. We mainly used MRK 16 monoclonal antibody (MAb) reactive with P-GP. P-GP was found to be expressed very strongly in the adrenal cortex of adults and strongly in the renal tubules of the kidney, capillary blood vessels of the brain, and also in placenta. Interestingly, P-GP was not distributed in fetal and neonatal adrenals, and thus may be closely related to adrenal maturation. A high level of P-GP expression was also seen in all cases of functional hormone-producing adrenal tumor, one case of insulinoma, two cases of untreated colonic cancer, one case each of untreated lung cancer, gastric cancer and breast cancer, six cases of renal cell carcinoma and 17 cases of bladder cancer. Using flow cytometry and immunocytochemistry, we investigated the reactivity of MRK 16 MAb with peripheral human mononuclear cells (mainly blastic cells and lymphocytes) from 31 patients with leukemia or malignant lymphoma. Reactivity with MRK 16 MAb was observed in five cases. Some cases reflected the prior administration of adriamycin, vincristine and VP-16, which are known to induce P-GP expression. P-GP-MRK 16-protein A-Sepharose complex derived from human adrenal possessed marked ATPase activity. These data suggest that P-GP may play a physiological role in the human adrenal. Finally, diagnostic criteria of multi-drug-resistant cancers are presented.
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PMID:Expression and functions of P-glycoprotein (mdr1 gene product) in normal and malignant tissues. 197 61

The sternum is known as a common site of bone metastasis in a variety of neoplasms. Sternal metastasis is usually visualized as hot spot on bone scintigraphy. However, photon deficiency in the sternum on bone scintigraphy is reported in few cases with malignancy. We undertook a retrospective analysis to clarify the clinical significance of photon deficiency in the sternum in 12 patients with malignancy. Twelve patients (five breast cancer, two multiple myeloma, one lung cancer, one renal cell cancer, one hepatocellular carcinoma, one malignant lymphoma, and one thyroid cancer) showing cold sternal metastasis on bone scintigraphy were identified among 9,430 patients in whom bone scintigraphy was performed. Except for two cases with pathologically confirmed sternal metastasis, all patients showed lytic change in the sternum on tomography or CT scan. Six cases of solitary sternal metastasis showed partial effect of systemic therapy (chemotherapy, humoral therapy, and radiation therapy) and surgical treatment. It is necessary to keep in mind that this type of lesion may occur as a manifestation of metastatic disease.
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PMID:Photon-deficient finding in sternum on bone scintigraphy in patients with malignant disease. 207 33


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