PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “SCLC”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 145 records · Page 8Linked to original sources
PubMed1985

Single-dose etoposide in combination with vincristine and doxorubicin in the treatment of small-cell lung cancer (SCLC).

From July 1980, 104 consecutive patients with previously untreated small-cell lung cancer (SCLC) received vincristine 1.4 mg/m2, doxorubicin (Adriamycin) 40 mg/m2, and Etoposide (VePesid) 300 mg/m2 intravenously (as a single infusion) every 3 weeks. The overall response rate (complete response plus partial response) was 58%. In 47 patients with limited disease the response rate was 66% with 21/47 (45%) complete responders. Treatment was delivered on an outpatient basis. Toxicity was mild, and in 455 rapid infusions of etoposide, there have been no adverse reactions.

Adult↗
PubMedDate not supplied

Small cell lung cancer (SCLC): a randomized trial of cyclophosphamide, adriamycin, vincristine plus etoposide (CAV-E) or teniposide (CAV-T) as induction treatment, followed in complete responders by alpha-interferon or no treatment, as maintenance therapy.

In this phase III, double-random study, we compared CAV-E to CAV-T combination as induction treatment (1st randomization) for SCLC. Subsequently, patients achieving a complete response (CR) were randomized again (2nd randomization) to receive maintenance treatment with alpha-IFN or no treatment. From June 1990 to June 1992, 75 untreated patients were enrolled in this trial. After stratification according to limited disease (LD) or extensive disease (ED), patients were randomized to receive the following treatment: cyclophosphamide 1000 mg/m2, adriamycin 50 mg/m2, vincristine 2 mg, day 1 i.v., plus etoposide (E) 100 mg/m2 (CAV-E: arm-A) or teniposide (T) 60 mg/m2 on day 2, 3, 4 i.v., every 3 weeks (CAV-T: arm-B). LD patients after 3 cycles of treatment received chest radiotherapy and 2 further cycles, whereas ED patients received 5 consecutive cycles. Patients who achieved a CR entered the 2nd randomization receiving a-IFN (3 x 10(6) I.U., i.m. daily x 9 months) or no treatment. A second-line treatment with carboplatin 300 mg/m2 plus E (if T was initially used) or T (if E was initially used) was also scheduled for patients achieving less than CR to induction treatment. Preliminary results are as follows: 75 patients were randomized, 72 were eligible for survival (arm-A = 37 and arm-B = 35) and 60 were fully evaluable for response (arm-A = 34 and arm-B = 26). In patients with LD the overall response rate was 79% (CR 21%) in arm-A vs 92% (CR 50%) in arm-B. In patients with ED, the overall response rate was 80% (CR 33%) in arm-A vs 84% (CR 7%) in arm-B. At a mean observation time of about 1 year (range 1-25 months), median survival of LD patients was 15 months in arm-A and 13 months in arm-B (Chi-square = 1.55; p > 0.05); in ED patients survival was 10.8 months and 8 months respectively (Chi-square = 2.88; p > 0.05). Cumulative survival probability was identical (12 months) in all patients of both arms. Toxicity was mainly haematologic and gastrointestinal: WHO grade 3-4 myelosuppression and vomiting were observed in 20% and 11% respectively, of cycles delivered in arm-A, compared to 19% and 8%, respectively, of cycles in arm-B. Two septic deaths occurred with CAV-T, while 1 patient discontinued treatment due to persistent myelosuppression with CAV-E. After the first and second-line treatment 20 patients showed a CR.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1995

[A pilot study of combination chemotherapy with cyclophosphamide, adriamycin, chronic daily dosing of oral etoposide for patients with SCLC ineligible for intensive chemotherapy].

Twenty-two patients with small cell lung cancer (SCLC) ineligible for intensive chemotherapy were treated with a combination of cyclophosphamide 800 mg/m2 iv day 1, adriamycin iv 40 mg/m2 day 1, and oral etoposide 40 mg/m2 once daily day 1-21. The overall response rate was 72.7% with 2 complete and 14 partial responders. The median survival time was 272 days in LD and 231 days in ED. The side effects were acceptable but not as mild as expected.

Administration, Oral↗
PubMed1992

Characterization of the submicroscopic deletion in the small-cell lung carcinoma (SCLC) cell line U2020.

The small-cell lung carcinoma cell line U2020 contains a submicroscopic, homozygous deletion that removes a chromosomal segment within 3p13-p14, including the locus D3S3. We have sublocalized 49 additional probes to the 3p13-p14.2 region and have identified 7 new DNA markers that arise from within the U2020 deletion. The estimated size of the deletion, based on marker density, is approximately 4-5 megabases (Mb). Including D3S3, 7 of the 8 markers have been linked by pulsed-field gel (PFG) electrophoresis over an area of approximately 2 Mb. Including the one unlinked marker, PFG analysis accounts for about 3 Mb of the region. The U2020 deletion appears confined to the 3p13-p14.2 region and does not include the candidate tumor suppressor gene, protein-tyrosine phosphatase gamma (PTPG).

Carcinoma, Small Cell↗
PubMed1994

Epitope mapping of SCLC-cluster-2 MAbs and generation of antibodies directed against new EGP-2 epitopes.

Western blot analysis proved that all cluster-2 MAbs recognize identical or overlapping disulfide-bond-dependent epitopes, indicating the presence of a disulfide-bond-stabilized EGP-2 domain carrying highly immunodominant non-linear epitopes. The apparent immunodominance of this domain makes it difficult to generate and select antibodies against other potentially useful EGP-2 epitopes. Using PCR, we have generated mutant EGP-2 cDNA (delta EGP-2) from which the coding sequences for a putative immunodominant 6-kDa intra-chain loop structure has been removed. delta EGP-2 transfected COS-7 cells reacted with MM104, an antibody detecting a linear epitope on EGP-2, but were not recognized by any cluster-2 MAb. To generate new anti-EGP-2 antibodies we constructed another mutant EGP-2 protein (delta EGP-2) from which additional domains, irrelevant for antibody generation (signal peptide, trans-membrane and cytoplasmic domains), were removed. delta EGP-2 was introduced in a prokaryotic expression system that adds a polyhistidine affinity tag to the delta EGP-2 N-terminus, making possible one-step purification by immobilized metal-ion-affinity chromatography (IMAC). Western blot analysis showed that sera derived from mice immunized with purified delta EGP-2 had high-titer antibodies to reduced EGP-2 samples. We conclude that the availability of prokaryotic and eukaryotic EGP-2-expression constructs might facilitate the selection of new anti-EGP-2 MAbs otherwise difficult to obtain.

Amino Acid Sequence↗
PubMed1995

Acquisition and enhanced expression of the metastatic phenotype following transfections of genomic mouse tumor DNA containing human SCLC gene sequences.

Previous primary and secondary co-transfections of genomic DNA from a metastatic human small cell lung cancer cell line into NIH/3T3 cells resulted in a murine fibrosarcoma cell line (Tx93B) that produced frequent spontaneous lung metastases in subcutaneously injected tumor-bearing nude mice. In order to transfer the acquired metastatic behavior to additional cell lines that could then be tested in syngeneic immunocompetent animals, DNA from Tx93B cells was transfected without additional neo gene into Balb/c embryo fibroblasts, which led to the isolation of a tertiary transfectant cell line (D3) of low spontaneous metastatic potential in normal Balb/c mice. Subsequent cell lines established serially from lung metastases in mice injected with D3, and metastatic descendants of D3 (all selected for the original neo marker in G-418), resulted in three generations of metastatically variant cell lines capable of causing pulmonary metastases in 11.1%, 54.6%, and 89.5%, respectively, of subcutaneously injected animals, and in 100% of normal mice injected intraperitoneally. There was no apparent ras-family oncogene participation in the metastatic behavior of either of the two DNA donor cell lines or in the metastatically variant tertiary transfectants. Gelatin zymography indicated that the secretion of gelatinolytic enzymes in vitro by the variant cell lines was inversely proportional to their metastatic capability. Human Alu repeat gene sequences detected in the metastatic variants suggested that co-transfected metastasis-associated genes present in the original human DNA donor cell may have contributed to acquisition of the metastatic phenotype by the tertiary transfectant cell lines. The increase in metastatic potential observed in successive generations of the D3-derived tumor cell lines, further suggested that selection for cells having increased metastatic capability had occurred during passage in vivo accounting for the phenotypic change. Because of their common origin and progressively metastatic nature these cell lines may prove useful in the identification of metastasis-associated genes accessible through the use of differential expression cloning strategies.

3T3 Cells↗
PubMed1988

Unexpected high toxicity in a phase II study of teniposide (VM-26) in elderly patients with untreated small cell lung cancer (SCLC).

Teniposide (VM 26) as a single agent has shown promising results in the treatment of patients with small cell lung cancer. We treated 32 (30 evaluable) non-pretreated elderly and poor prognosis patients with small cell lung cancer with teniposide 100 mg/day (30 min infusion) days 1-5, every 3-4 weeks. Overall initial performance status was poor (WHO 2 or 3 in 62%). Extensive disease (ED) was documented in 50% including five patients with CNS metastases all of whom received simultaneous cranial irradiation. There was an unexpected high early death rate of 30% (9/30) including five patients with early toxic death due to severe bone marrow suppression leading to fatal septicaemia. The overall response rate was only 33% with no complete response. Where appropriate non-responding or relapsing patients received second line treatment with multidrug regimens +/- radiotherapy. The overall median survival was 5.6 months [ED: 1.7, limited disease (LD): 7.5 months]. Median response duration was 5.4 months (ED: 5.1, LD: 6.7 months). For responding patients median survival was 8.8 months (ED) and 11.5 months (LD). We conclude that in elderly and poor performance status patients single agent teniposide as used in this study has an unacceptable high early death rate and that the response rate is inferior to modern standard multidrug regimens.

Aged↗