Disease relevance of SCLC1

• A novel sequence (R659Q) was discovered near the ATP binding site in a human small cell lung cancer (SCLC) cell line, H1436 [1].
• Furthermore, c-myc is expressed in increased amounts in some human tumour lines, and in some cases, human small cell lung cancers (SCLC) contain DMs and HSRs [2].
• In contrast, expression of N-myc has been found only in a restricted set of tumours, most of which show neural characteristics; these include human neuroblastoma, retinoblastoma and small cell lung carcinoma (SCLC) [3].
• Rb messenger RNA expression was absent in 60% of the SCLC lines and 75% of pulmonary carcinoid lines, including all samples with DNA abnormalities [4].
• The finding of abnormalities of the Rb gene in SCLC and pulmonary carcinoids (both neuroendocrine tumors) suggests that this gene may be involved in the pathogenesis of a common adult malignancy [4].

Psychiatry related information on SCLC1

• Cannibalistic cells appeared to be of SCCL origin. "Cannibalism" is never observed in serum-free cultures but can be reinduced by serum exposure [5].
• We therefore conclude that 3-dimensional gel-histoculture is a useful means of distinguishing pure SCLC from NSCLC, which may improve treatment decision making [6].
• CONCLUSION: The findings of this study suggest that smoking cessation results in the greatest reductions for SCLC and SQC [7].
• A previous study had shown SCLC patients to have deficits in memory, frontal lobe executive functioning, and motor skills before they received prophylactic cranial irradiation (PCI) [8].
• Since donepezil and vitamin E have been somewhat successful in treating other dementias, this study tested the hypothesis that these agents can prevent cognitive decline in SCLC patients [9].

High impact information on SCLC1

• Transcript A was missing in all SCLC cell lines analysed and in several other cancer cell lines [10].
• We reveal a similar pattern of Hh signalling in airway development during normal differentiation of pulmonary neuroendocrine precursor cells, and in a subset of small-cell lung cancer (SCLC), a highly aggressive and frequently lethal human tumour with primitive neuroendocrine features [11].
• Adhesion of SCLC cells to ECM enhances tumorigenicity and confers resistance to chemotherapeutic agents as a result of beta1 integrin-stimulated tyrosine kinase activation suppressing chemotherapy-induced apoptosis [12].
• Strategies based on blocking beta1 integrin-mediated survival signals may represent a new therapeutic approach to improve the response to chemotherapy in SCLC [12].
• Because neoplastic characteristics such as decreased strand stability9 and ras mutations have been found in the plasma DNA of cancer patients, we looked for microsatellite alterations in the plasma of SCLC patients [13].

Chemical compound and disease context of SCLC1

• In a controlled, randomized study, survival of patients with small cell carcinoma of the lung (SCCL) was prolonged on addition of warfarin sodium to combination chemotherapy plus radiation therapy [14].
• The Lambert-Eaton myasthenic syndrome (LEMS) is a disorder of neuromuscular transmission, often associated with small cell lung carcinoma (SCLC), and characterized by reduced quantal release of acetylcholine from the motor nerve terminals [15].
• BACKGROUND: The combination of etoposide plus cisplatin (EP) is considered to be standard therapy for small-cell lung cancer (SCLC) [16].
• We have characterized the determinants of methotrexate (MTX) responsiveness in eight patient-derived cell lines of small-cell lung cancer (SCLC) [17].
• The biological effects of raf activation in small cell lung cancer cells was determined by transfecting NCI-H209 or NCI-H510 SCLC cells with a gene encoding a fusion protein consisting of an oncogenic form of human Raf-1 and the hormone binding domain of the estrogen receptor (DeltaRaf-1:ER), which can be activated with estradiol [18].

Biological context of SCLC1

• Our data show loss of alleles of chromosome 3p markers in tumour DNA of all nine patients supporting the hypothesis that this region contributes to tumorigenesis in SCLC [19].
• Here we describe a third myc-related gene (L-myc) cloned from SCLC DNA with homology to a small region of both the c-myc and N-myc genes [20].
• A cytogenetic deletion in chromosome 3 (p14-p23) was reported in small-cell lung cancer (SCLC) by Whang-Peng et al [19].
• We used polymorphic DNA probes for chromosome 3p and compared tumour and constitutional genotypes of nine SCLC patients [19].
• Using a molecular-genetic approach, we here present evidence for a consistent deletion at the chromosomal region 3p21, not only in SCLC, but in all major types of lung cancer [21].

Anatomical context of SCLC1

• The cytotoxic activity of N901-bR was tested against both small-cell lung cancer (SCLC) cells and neuroblastoma cells, either alone or among normal bone marrow mononuclear cells, and the efficacy of this treatment to specifically eliminate these cells was evaluated in a limiting dilution assay [22].
• IMPLICATIONS: N901-bR may have clinical utility for purging of neuroblastoma cells and SCLC cells before autologous stem cell transplantation [22].
• None of the antigens defined by these MoAb were expressed on non-SCCL lung tumor cell lines [23].
• Because CD10/NEP modulates peptide-mediated proliferation of small cell carcinomas of the lung (SCLC) and normal fetal bronchial epithelium, we evaluated the enzyme's expression in non-small cell lung carcinomas (NSCLC) [24].
• 125I-[Tyr4]-bombesin binding was unaffected by CT treatment but [Tyr4]-bombesin stimulated phospholipase C activity was decreased in membranes from CT-treated SCLC cells [25].

Associations of SCLC1 with chemical compounds

• These results suggest that warfarin may be useful in the treatment of SCCL and also support the hypothesis that the blood coagulation mechanism may be involved in the growth and spread of cancer in man [14].
• Patients with extensive stage SCLC were randomly treated with standard-dose (n = 46) or high-dose etoposide plus cisplatin (n = 44); poor-risk patients with extensive stage disease (n = 25) were assigned to standard dose etoposide plus cisplatin [26].
• RESULTS: Sensitivities to doxorubicin and etoposide were higher in SCLC cell lines than in NSCLC lines, and the difference was statistically significant [27].
• Before 1986, patients with limited stage SCLC were treated with a cyclophosphamide-based regimen with (n = 47) or without (n = 46) chest radiotherapy [26].
• To determine whether drug intensification improves survival of patients with extensive SCLC, we compared this treatment with a four-drug regimen containing EP plus cyclophosphamide and 4'-epidoxorubicin (PCDE) [16].

Other interactions of SCLC1

• Full length MRP4 cDNA was obtained from SCLC1 and SR-2 [28].
• Both UMC-SCLC-1 and UMC-SCLC-1A demonstrated the deletion of chromosome 3p, amplification and abundant expression of N-myc, and increased expression of c-raf [29].

Analytical, diagnostic and therapeutic context of SCLC1

• Here, we demonstrate that a monoclonal antibody to bombesin binds to the C-terminal region of BLPs, blocks the binding of the hormone to cellular receptors and inhibits the clonal growth of SCLC in vitro and the growth of SCLC xenografts in vivo [30].
• Immunoprecipitation of metabolically labeled cells with antibodies to class I antigens showed most SCLC lines to have synthesized almost no beta 2m and HLA-A,B,C proteins [31].
• METHODS: The study sample included 262 patients with histologically confirmed SCLC treated in clinical trials from 1977 through 1993 [26].
• However, RT-PCR revealed a low level of IGF-I gene expression in one SCLC and one NSCLC cell line only [32].
• METHODS: Gene expression was studied in four small-cell lung cancer (SCLC) and three non-small-cell lung cancer (NSCLC) cell lines using Northern blot analysis and reverse transcriptase polymerase chain reaction (RT-PCR) for IGFBP-1 [32].

References