• Lung cancer and smoking in Shanghai.

• Cut-off levels of NSE to differentiate SCLC from NSCLC.

• Soluble syndecan-1 and serum basic fibroblast growth factor are new prognostic factors in lung cancer.

• [Randomized controlled trials in Japan--lung cancer]

• [Outpatient chemotherapy for small cell lung cancer in our hospital]

• High-dose chemotherapy in small cell lung cancer.

• Newer techniques of radiation therapy in lung cancer.

• A Phase I-II study of sequential administration of topotecan and oral etoposide (toposiomerase I and II inhibitors) in the treatment of

• Twenty-five years of clinical research for patients with limited-stage small cell lung carcinoma in North America.

• Medical pearl: new views through the microscope.

• Lung cancer.

• Is long term gemcitabine useful in small cell lung cancer?

• Protein kinase C-epsilon promotes survival of lung cancer cells by suppressing apoptosis through dysregulation of the mitochondrial caspase

• Protease inhibitors suppress in vitro growth of human small cell lung cancer.

• Comparative analysis of expression of the proprotein convertases furin, PACE4, PC1 and PC2 in human lung tumours.

• Gene product immunophenotyping of neuroendocrine lung tumors. No linking evidence between carcinoids and small-cell lung carcinomas suggested by

• Nerve growth factor and retinoic acid interactions in the control of small cell lung cancer proliferation.

• Parathyroid hormone-related protein measured at the time of first visit is an indicator of bone metastases and survival in lung carcinoma

• [Demonstration of delta sleep inducing peptide in a strain of human small cell lung cancer by immunocytology]

• Small cell lung cancer: defining a role for emerging platinum drugs.

• Expression of inhibitor of apoptosis proteins in small- and non-small-cell lung carcinoma cells.

1
UI - 2841252
AU - Gao YT; Blot WJ; Zheng W; Fraumeni JF; Hsu CW
TI - Lung cancer and smoking in Shanghai.
SO - Int J Epidemiol 1988 Jun;17(2):277-80
AD - Shanghai Cancer Institute, People's Republic of China.
A case-control study involving interviews with 733 male and 672 female incident lung cancer patients and 1495 population-based controls revealed that cigarette smoking is the dominant cause of lung cancer among men in urban Shanghai. All of the principal cell types were affected, with clear trends of rising risk with increasing intensity and duration of smoking. Far fewer women smoked cigarettes, but the overall risk patterns resembled those among males. Among women, however, smoking accounted for only about one-quarter of all lung cancers and less than 10% of lung adenocarcinomas. The findings lay to rest any doubts about the health hazards of smoking Chinese cigarettes, although smoking is not responsible for the high rates of adenocarcinoma reported among Chinese women.

2
UI - 11956631
AU - Satoh H; Ishikawa H; Kurishima K; Yamashita YT; Ohtsuka M; Sekizawa K
TI - Cut-off levels of NSE to differentiate SCLC from NSCLC.
SO - Oncol Rep 2002 May-Jun;9(3):581-3
AD - Division of Respiratory Medicine, Institute of Clinical Medicine, University of Tsukuba, Tsukuba-city, Ibaraki 305-8575, Japan. hirosato@md.tsukuba.ac.jp
Neuron-specific enolase (NSE) is a specific tumor marker in small cell lung cancer (SCLC) patients, however, it has been reported that serum NSE levels are elevated in some patients with non-small cell lung cancer (NSCLC). To determine the most suitable cut-off level to distinguish between these two types of cancers, NSE levels were measured on serum samples of 417 patients with lung cancer without clinical information. Receiver operating characteristic (ROC) curve showed 14.5 ng/ml as a cut-off level and the 95 percentile serum NSE level in NSCLC was 20.5 ng/ml. None of the NSCLC patients had serum NSE levels more than 70 ng/ml. The measurement of serum NSE provides a discrimination between NSCLC and SCLC. If an NSCLC patient presents with a NSE level >20.5 ng/ml, pathological features must be examined with regard to the neuroendocrine differentiation.

3
UI - 12234986
AU - Joensuu H; Anttonen A; Eriksson M; Makitaro R; Alfthan H; Kinnula V;
TI - Leppa S Soluble syndecan-1 and serum basic fibroblast growth factor are new prognostic factors in lung cancer.
SO - Cancer Res 2002 Sep 15;62(18):5210-7
AD - Department of Oncology, Helsinki University Central Hospital, Haartmaninkatu 4, PO Box 180, FIN-00029 Helsinki. heikki.joensuu@hus.fi
Syndecan-1 is a ubiquitous and multifunctional extracellular matrix proteoglycan,which mediates basic fibroblast growth factor (bFGF) binding and activity. Shedding of syndecan-1 ectodomain from the plasma membrane is highly regulated. We evaluated the influence of soluble syndecan-1 and serum bFGF determined by ELISA on outcome in 184 lung cancer patients (non-small cell lung cancer, n = 138; small cell lung cancer, n = 46). Serum syndecan-1 and bFGF levels were determined from sera taken before treatment. The median follow-up of the patients alive (n = 21) was 8.1 years (range, 6.6-8.9 years). High serum syndecan-1 and bFGF levels tended to occur in the same patients (P = 0.044). When the serum values corresponding to the highest tertile were used as the cutoff value, the median survival time of the patients with a high serum syndecan-1 level (>59 ng/ml) was 4 months [95% confidence interval (CI), 3-6 months] as compared with 11 months (9-16 months) among those with lower serum levels (P = 0.0001), and the median survival time of the patients with a high bFGF level (>3.4 pg/ml) was 5 months (3-8 months) versus 11 months (8-14 months) in those with a lower level (P = 0.023). In general, the prognostic influence of both factors was independent of the histological subtype. Both serum syndecan-1 level (relative risk, 1.8; 95% CI, 1.1-3.1) and serum bFGF level (relative risk, 1.6; 95% CI, 1.0-2.7) had independent influence on survival in a multivariate survival analysis in non-small cell lung cancer. We conclude that high serum syndecan-1 and bFGF levels at diagnosis are associated with poor outcome in lung cancer.

4
UI - 12355937
AU - Ichinose Y
TI - [Randomized controlled trials in Japan--lung cancer]
SO - Gan To Kagaku Ryoho 2002 Sep;29(9):1516-21
AD - Department of Thoracic Oncology, National Kyushu Cancer Center, 3-1-1 Notame, Minami-ku, Fukuoka 811-1395, Japan.
Randomized controlled trials conducted in Japan were reviewed. Using PubMed, 12 papers published after 1990 were selected. Six papers presented at the annual meeting of the American Society of Clinical Oncology from 1999 to 2002 were also added for use in this review. According to the results of those trials, cisplatin plus either irinotecan or docetaxel for advanced non-small cell lung cancer, cisplatin plus irinotecan for small cell lung cancer and concurrent chemoradiotherapy for a localized disease of both small and non-small cell lung cancers have been established as standard treatments. No adjuvant treatment method for resected patients has been proved to be sufficiently effective.

5
UI - 12355957
AU - Minami S; Asai M; Iwahori K; Kouga K; Nishiyama A; Komuta K
TI - [Outpatient chemotherapy for small cell lung cancer in our hospital]
SO - Gan To Kagaku Ryoho 2002 Sep;29(9):1661-4
AD - Dept. of Respiratory Medicine, Osaka Police Hospital.

6
UI - 12195754
AU - Pasini F; Pelosi G; De Manzoni G; Rosti G
TI - High-dose chemotherapy in small cell lung cancer.
SO - Tumori 2002 May-Jun;88(3):179-86
AD - Cattedra di Oncologia Medica, Universita di Verona, Italy.
Improvements in small cell lung cancer (SCLC) therapy with conventional doses of drugs with or without radiotherapy have been poor, and the 5-year survival is discouraging. Since SCLC is highly sensitive to radiotherapy and chemotherapy, some studies have tried to improve survival by increasing the dose of the drugs. Within conventional ranges, dose intensity can be increased with the support of hematopoietic growth factors (G/GM-CSF) and/or shortening treatment intervals (e.g. weekly regimens). However, dose intensity could be increased by only 20-30% and a survival advantage was not definitively obtained. Given its high chemosensitivity already two decades ago, SCLC was one of the first malignancies deemed suitable for maximizing dose and dose intensity with the support of autologous bone marrow transplantation (ABMT). On the whole, results were disappointing and the procedure was nearly abandoned. Nowadays, some interest is emerging again due to the improvements in supportive care such as the availability of hematopoietic growth factors and the peripheral blood progenitor cells (PBPC).

7
UI - 12206473
AU - Rath GK; Sharma DN
TI - Newer techniques of radiation therapy in lung cancer.
SO - Indian J Chest Dis Allied Sci 2002 Jul-Sep;44(3):155-7

8
UI - 12237920
AU - Mok TS; Wong H; Zee B; Yu KH; Leung TW; Lee TW; Yim A; Chan AT; Yeo W;
TI - Chak K; Johnson P A Phase I-II study of sequential administration of topotecan and oral etoposide (toposiomerase I and II inhibitors) in the treatment of patients with small cell lung carcinoma.
SO - Cancer 2002 Oct 1;95(7):1511-9
AD - Department of Clinical Oncology, The Chinese University of Hong Kong, Hong Kong, China. mok206551@cuhk.edu.hk
BACKGROUND: Topotecan (9-dimethylaminomethyl-10-hydroxycampthothecin) is a new topoisomerase I inhibitor with promising efficacy in the treatment of patients with small cell lung carcinoma (SCLC). Combination with a topoisomerase II inhibitor may potentate the therapeutic effect of topotecan, although there has been conflicting preclinical information on the combination. The objectives of this study were to establish the maximum tolerated dose and to determine the efficacy of the sequential combination of intravenous topotecan and oral etoposide in the treatment of patients with SCLC. METHODS: Patients with histologically confirmed, limited or extensive stage SCLC were eligible. The dose escalation scheme of three cohorts (six patients per cohort) started at intravenous topotecan 0.5 mg/m(2) per day for 5 days and oral etoposide 50 mg twice daily for 7 days (21-day cycles). Subsequent dose levels involved escalation of topotecan to 0.75 mg/m(2) per day and 1.0 mg/m(2) per day for 5 days. A Phase II study was conducted at one dose level below the maximum tolerated dose. The authors alternated the drug sequence with each consecutive cycle and compared the hematologic toxicity between the two sequences. RESULTS: Thirty-six patients (21 patients with limited disease and 15 patients with extensive disease) received a total of 173 courses of sequential combination chemotherapy (topotecan --> etoposide, 88 courses; etoposide --> topotecan, 85 courses). The authors identified dose levels for the Phase II study as follows: topotecan, 0.75 mg/m(2) per day for 5 days; and etoposide, 50 mg twice daily for 7 days. The dose-limiting toxicity was neutropenia. At this dose level, the incidence of Grade 3-4 neutropenia and the incidence of Grade 3-4 thrombocytopenia were 25% and 10.9%, respectively. Two patients died from neutropenic sepsis. There was no significant difference in hematologic toxicities between the two sequences. Complete and partial response rates were 5.6% and 55.6%, respectively (limited disease, 9.5% and 66.75%; extensive disease, 0% and 40%, respectively). The median progression free survival was 31.9 weeks (limited disease, 36.1 weeks; extensive disease, 28.9 weeks; 95% confidence interval, 25.6-36.0 weeks), and the median overall survival was 52.4 weeks (limited disease, 54.9 weeks; extensive disease, 30.1 weeks; 95% confidence interval, 39.6-57.7 weeks). CONCLUSIONS: Combination therapy with topoisomerase I and II inhibitors is a safe and effective regimen for patients with SCLC. Future research on this combination should focus on an oral regimen for patients with extensive disease and poor tolerance to cisplatin. The authors recommend an oral dosage of topotecan at 1.2 mg/m(2) per day (equivalent to intravenous topotecan at 0.75 mg/m(2) per day) for 5 days followed by etoposide 50 mg twice daily for 7 days. Copyright 2002 American Cancer Society.DOI 10.1002/cncr.10836

9
UI - 12237922
AU - Janne PA; Freidlin B; Saxman S; Johnson DH; Livingston RB; Shepherd FA;
TI - Johnson BE Twenty-five years of clinical research for patients with limited-stage small cell lung carcinoma in North America.
SO - Cancer 2002 Oct 1;95(7):1528-38
AD - Lowe Center for Thoracic Oncology, Department of Adult Oncology, Dana Farber Cancer Institute, Boston, Massachusetts 02115, USA.
BACKGROUND: To determine the changes in clinical trials and outcomes of patients with limited-stage small cell lung carcinoma (SCLC) treated on Phase III randomized trials initiated in North America between 1972 and 1992. METHODS: Phase III trials from 1972 to 1992 for patients with limited-stage SCLC were identified. Patients with limited-stage SCLC treated during a similar time interval were also evaluated in the Surveillance, Epidemiology, and End Results (SEER) database. Trends were tested in the number of trials, in the number and gender of patients entered on trial, and in survival duration over time. RESULTS: Thirty trials involving 6564 patients were eligible for analyses. Nineteen trials (61%) involving 3626 patients were initiated within the first half of this time period (1972-1981). The median of median survival times of all patients treated on the control arms of the Phase III trials initiated between 1972 and 1981 and between 1982 and 1992 were 12.0 months (range, 10-16 months) and 17.0 months (range, 11-20 months), respectively (P < 0.001). Of 26 studies available for survival analysis, 5 (19%) showed a statistically significant survival prolongation in the experimental arm compared with the control arm with a median prolongation of 3.4 months (range, 1-5.2 months). All five evaluated some aspect of thoracic radiation therapy. Over a similar time period, there was a 6.4-month increase in the median survival of limited-stage SCLC patients listed in the SEER database (P < 0.0001) and a more than doubling of the 5-year survival from 5.2% to 12.1% (P = 0.0001). CONCLUSIONS: Analyses of the patients with limited-stage SCLC treated on Phase III trials in North America initiated between 1972 and 1992 and those listed in the SEER database show significant improvements in median survivals. Furthermore, the 5-year survival of patients with limited-stage SCLC listed in the SEER database has more than doubled over the last 25 years. Further research will be needed to determine the relative contribution of improved therapy, supportive care, and stage migration to this prolongation in survival. Copyright 2002 American Cancer Society.DOI 10.1002/cncr.10841

10
UI - 11423845
AU - Smoller BR
TI - Medical pearl: new views through the microscope.
SO - J Am Acad Dermatol 2001 Jul;45(1):120-1

11
UI - 12230752
AU - Neville A
TI - Lung cancer.
SO - Clin Evid 2002 Jun;(7):1369-83
AD - McMaster University, Hamilton, Canada.

12
UI - 11955659
AU - Dediu M
TI - Is long term gemcitabine useful in small cell lung cancer?
SO - Lung Cancer 2002 May;36(2):217-8

13
UI - 12121973
AU - Ding L; Wang H; Lang W; Xiao L
TI - Protein kinase C-epsilon promotes survival of lung cancer cells by suppressing apoptosis through dysregulation of the mitochondrial caspase pathway.
SO - J Biol Chem 2002 Sep 20;277(38):35305-13
AD - University of Florida Shands Cancer Center and Department of Anatomy & Cell Biology, University of Florida, Gainesville, Florida 32610, USA.
The serine/threonine protein kinase C (PKC) has been implicated in the regulation of drug resistance and cell survival in many types of cancer cells. However, the one or more precise mechanisms remain elusive. In this study, we have identified and determined the mechanism by which PKC-epsilon, a novel PKC isoform, modulates drug resistance in lung cancer cells. Western blot analysis demonstrates that expression of PKC-epsilon, but not other PKC isoforms, is associated with the chemo-resistant phenotype of non-small cell lung cancer (NSCLC) cell lines. Northern blotting and nuclear run-on transcription analysis further reveals that the failure of expression of PKC-epsilon in the chemo-sensitive phenotype of small cell lung cancer (SCLC) cells results from transcriptional inactivation of the gene. Importantly, forced expression of PKC-epsilon in NCI-H82 human SCLC cells confers a significant resistance to the chemotherapeutic drugs, etoposide and doxorubicin. Resistance is characterized by a significant reduction in apoptosis in PKC-epsilon-expressing cells. Treatment of NCI-H82 cells with etoposide induces a series of time-dependent events, including the release of cytochrome c from the mitochondria to the cytosol, activation of caspase-9 and caspase-3, and cleavage of poly(ADP-ribose) polymerase (PARP). All of these events are blocked by PKC-epsilon expression. Furthermore, caspase-specific inhibitors, z-VAD-fmk and z-DEVD-fmk, significantly attenuate the accumulation of sub-G(1) population and block the PARP cleavage in response to etoposide. These results suggest that PKC-epsilon prevents cells from undergoing apoptosis through inhibition of the mitochondrial-dependent caspase activation, thereby leading to cell survival. Finally, down-regulation of PKC-epsilon expression by the antisense cDNA in NSCLC cells results in increased sensitivity to etoposide. Taken together, our findings suggest an important role for PKC-epsilon in regulating survival of lung cancer cells.

14
UI - 7506831
AU - Clark DA; Day R; Seidah N; Moody TW; Cuttitta F; Davis TP
TI - Protease inhibitors suppress in vitro growth of human small cell lung cancer.
SO - Peptides 1993 Sep-Oct;14(5):1021-8
AD - Department of Pharmacology, College of Medicine, University of Arizona, Tucson.
The effect of the protease inhibitors Bowman Birk inhibitor (BBI) and aprotinin on the in vitro clonal growth of two human small cell lung cancer (SCLC) cell lines was investigated. In addition, the effect of BBI on the growth factor processing of proGRP by SCLC cells and on mRNA levels for prohormone convertase 1 and 2 (PC1 and PC2) in SCLC cells was examined. The protease inhibitors BBI and aprotinin significantly decreased growth in both SCLC cell lines studied. In NCI-H345 cells, BBI appears to inhibit the processing of proGRP to GRP, as indicated by Western blot analysis. NCI-H345 cells, when treated with BBI (100 micrograms/ml), also showed highly significant decreases of mRNA for PC1 and PC2 of about 50%. These data suggest that proteases serve an important role in the growth regulation of SCLC and that inhibitors of these proteases may be potent suppressors of SCLC growth at the level of the gene.

15
UI - 9166946
AU - Mbikay M; Sirois F; Yao J; Seidah NG; Chretien M
TI - Comparative analysis of expression of the proprotein convertases furin, PACE4, PC1 and PC2 in human lung tumours.
SO - Br J Cancer 1997;75(10):1509-14
AD - Institut de Recherches Cliniques de Montreal, Universite de Montreal, Quebec, Canada.
Proprotein convertases mediate the production of a variety of peptidic mitogens by limited proteolysis of their precursors. These proteases may also participate in the autocrine production of such mitogens by cancer cells and thus contribute to the unchecked proliferation of these cells. As a step towards defining this contribution, we have examined the levels of four convertase mRNAs in human lung neoplasms using semiquantitative Northern blot analysis. Furin mRNA was expressed in all the tumours; its level in squamous cell carcinomas and adenocarcinomas was on average about threefold higher than in small-cell lung carcinomas (SCLCs). PACE4 transcripts were detected in eight of 14 adenocarcinomas and in seven of 17 squamous cell carcinomas; they were detectable in only two of seven SCLCs. PC1 mRNA was undetected in squamous cell carcinomas and in all but two adenocarcinomas; it was present in four of six SCLCs. PC2 mRNA was found in two adenocarcinomas, in one squamous cell carcinoma and in five of seven SCLCs. This preliminary survey indicates that SCLCs often carry more mRNA for the endocrine convertases PC1 and PC2 and less mRNA for the more ubiquitous furin and PACE4, suggesting inverse roles of these convertases in the development of this neoplasm.

16
UI - 10937049
AU - Sampietro G; Tomasic G; Collini P; Biganzoli E; Boracchi P; Bidoli P;
TI - Pilotti S Gene product immunophenotyping of neuroendocrine lung tumors. No linking evidence between carcinoids and small-cell lung carcinomas suggested by multivariate statistical analysis.
SO - Appl Immunohistochem Mol Morphol 2000 Mar;8(1):49-56
AD - Division of Anatomical Pathology, Istituto Nazionale Tumori, Milan, Italy.
Fifty-three neuroendocrine lung tumors (24 carcinoids, one atypical carcinoid, five large-cell neuroendocrine carcinomas, and 23 small-cell lung carcinomas) were investigated for immunocytochemical expression of several gene products, i.e., p53, Rb, bcl-2, c-kit, mdm-2, cdk-4, p21 proteins, and proliferation index as assessed by MIB-1. The goal of the study was to explore the relationships between histotypes in light of their own gene product-based immunophenotypical profiles. To this aim we applied the multiple correspondence analysis, which is an exploratory statistical multivariate technique that converts a data matrix into a particular type of graphic display in which the rows and columns are depicted as points. Such statistical analysis displayed that some categories of the gene product-based immunophenotyping variables are grouped in the plot identifying three groups: the first group related to carcinoids, the second to small-cell carcinomas, and the third to large-cell neuroendocrine carcinomas. These data support the evidence that carcinoids and small-cell carcinomas are two distinct, apparently immunogenotypically unrelated entities among neuroendocrine lung tumors and that atypical carcinoids and large-cell neuroendocrine carcinomas seem not to represent intermediate steps between them.

17
UI - 12213675
AU - Fiorentini C; Facchetti M; Finardi A; Sigala S; Paez-Pereda M; Sher E;
TI - Spano P; Missale C Nerve growth factor and retinoic acid interactions in the control of small cell lung cancer proliferation.
SO - Eur J Endocrinol 2002 Sep;147(3):371-9
AD - Division of Pharmacology, Department of Biomedical Sciences and Biotechnology, University of Brescia, Via Valsabbina 19, 25124 Brescia, Italy.
OBJECTIVE: Nerve growth factor (NGF) has antiproliferative and differentiating effects in neuroendocrine tumors. In cell lines derived from small cell lung cancer (SCLC), NGF treatment stimulates NGF receptor expression, activates NGF secretion, inhibits proliferation and abrogates invasion. Since these effects are lost upon NGF withdrawal, it is relevant to identify other differentiation factors that may co-operate with the NGF system to control SCLC growth and differentiation. DESIGN: Retinoic acid (RA), which has been shown to inhibit cell transformation and proliferation, modulates the expression of NGF receptors and the sensitivity to NGF in different cell models. In the present study, we have investigated whether NGF and RA may interact to control the proliferation of SCLC cell lines. METHODS: SCLC cells were exposed to 50 ng/ml NGF or 1 microM all-trans RA for different times. Cell proliferation was measured by the [(3)H]thymidine incorporation test and NGF receptor expression was evaluated by immunofluorescence. RESULTS: We found that RA increased the expression of both trkA and p75 NGF receptors in NCI-N-592 and GLC8 cell lines and prevented the loss of both NGF production and NGF receptor expression occurring when NGF treatment was discontinued. As a result, RA, which did not inhibit the proliferation of untreated cells, abolished NGF withdrawal-related increase in cell proliferation both in vitro and in vivo, thus making permanent the antiproliferative effects of NGF. CONCLUSIONS: These data suggest that combined treatments with NGF and RA or mimicking drugs may represent a strategy to be further investigated for the treatment of SCLC.

18
UI - 12365018
AU - Hiraki A; Ueoka H; Bessho A; Segawa Y; Takigawa N; Kiura K; Eguchi K;
TI - Yoneda T; Tanimoto M; Harada M Parathyroid hormone-related protein measured at the time of first visit is an indicator of bone metastases and survival in lung carcinoma patients with hypercalcemia.
SO - Cancer 2002 Oct 15;95(8):1706-13
AD - Department of Medicine II, Okayama University Medical School, Okayama, Japan. ahiraki@md.okayama-u.ac.jp
BACKGROUND: Parathyroid hormone-related protein (PTH-rP) is a major cause of tumor-induced hypercalcemia (TIH) and frequently is found to be elevated in serum of patients with TIH. In the current study, the authors examined the usefulness of PTH-rP measurement at the time of first presentation in the follow-up of lung carcinoma patients with TIH. METHODS: The authors retrospectively studied 23 of 1149 lung carcinoma patients who were found to have TIH at the time of first presentation for the correlation between serum PTH-rP and the development of bone metastases and survival compared with lung carcinoma patients without TIH who were matched by gender, age, Eastern Cooperative Oncology Group performance status, histological type of tumor, and stage of the disease. RESULTS: Twenty-three lung carcinoma patients with TIH demonstrated significantly increased serum levels of PTH-rP (mean +/- standard error [SE], 84.1 +/- 16.5 pmol/L) compared with control patients without TIH (mean +/- SE, 36.2 +/- 2.0 pmol/L) at the time of first presentation, (P < 0.001). In these hypercalcemic patients, patients whose serum PTH-rP was > 150 pmol/L (n = 16) were found to have a significantly increased rate of bone metastases (71.4% vs. 12.5%; P = 0.01) and decreased survival (median survival of 1.4 months vs. 5.4 months; P < 0.015) compared with patients whose serum PTH-rP was < 150 pmol/L (n = 7). CONCLUSIONS: The data from the current study suggest that serum PTH-rP as determined at the time of first presentation is a useful indicator of not only hypercalcemia but also bone metastasis and eventual survival in patients with lung carcinoma. Copyright 2002 American Cancer Society.

19
UI - 1318772
AU - Paulin C; Charnay Y
TI - [Demonstration of delta sleep inducing peptide in a strain of human small cell lung cancer by immunocytology]
SO - C R Acad Sci III 1992;314(6):259-62
AD - C.P. Laboratoire d'Histologie, C.N.R.S.-U.R.A. n. 1454, Faculte de Medecine Lyon Sud, Oullins.
The "delta sleep inducing peptide" (DSIP) is a regulatory peptide localized in the brain, the hypophysis and some endocrine cells of the gut. The present immunological study, performed with a monoclonal antibody to DSIP, provides evidence for the presence of DSIP-like immunoreactivity (DSIP-LI) in a strain of small cell carcinoma. The specificity of the immunoreaction was assessed by the tests using heterologous antigen known to be secreted by these cells. The DSIP could play a role in the course of this disease.

20
UI - 12239444
AU - Schiller JH
TI - Small cell lung cancer: defining a role for emerging platinum drugs.
SO - Oncology 2002;63(2):105-14
AD - University of Wisconsin Hospital, Madison, 53792, USA. jhschill@facstaff.wisc.edu
Small cell lung cancer (SCLC) is characterized by early dissemination and a rapid, aggressive clinical course. It has, however, marked susceptibility to both chemotherapy and radiotherapy, although treatment is complicated by the fact that SCLC tumors invariably develop resistance to multiple chemotherapeutic agents. Local therapy is rarely of benefit in SCLC because three-quarters of patients present with metastatic disease and many of the remaining patients are thought to have micrometastatic disease. Chemotherapy is, therefore, the cornerstone of treatment. Of the many combination regimens used, etoposide/cisplatin or etoposide/carboplatin have emerged as the regimens of choice because they offer a good therapeutic index and can be combined with radiotherapy. Response to second-line therapy remains consistently poor. As the prototype platinum compound, cisplatin has played a major role in the management of SCLC. Although its exact contribution to the treatment of SCLC has been difficult to ascertain, a recent meta-analysis reported a significant 1-year survival advantage of approximately 4% with cisplatin-containing regimens versus regimens without. However, cisplatin is characterized by several serious adverse events and, like other chemotherapeutic agents, is eventually rendered ineffective against SCLC because of acquired resistance. Several new platinum formulations or compounds are showing promising activity in SCLC. The impetus for their development has been to circumvent cisplatin resistance or to improve upon the toxicity profile of cisplatin. If the early promise shown by these compounds is confirmed in the clinic, they may offer a new approach to the treatment of SCLC, including recurrent disease for which limited treatment options are currently available. Copyright 2002 S. Karger AG, Basel

21
UI - 12243753
AU - Ekedahl J; Joseph B; Grigoriev MY; Muller M; Magnusson C; Lewensohn R;
TI - Zhivotovsky B Expression of inhibitor of apoptosis proteins in small- and non-small-cell lung carcinoma cells.
SO - Exp Cell Res 2002 Oct 1;279(2):277-90
AD - Institute of Environmental Medicine, Department of Toxicology, Karolinska Institutet, Box 210, S-171 77, Stockholm, Sweden.
Small-cell lung cancer (SCLC) and non-small-cell lung cancer (NSCLC) cells both initiate apoptotic signaling, resulting in caspase activation, after treatment with anti-cancer agents. However, in contrast to SCLC cells, NSCLC cells do not fully execute apoptosis. The apoptotic process in NSCLC cells seems to be blocked downstream of caspase activation, thus the failure of NSCLC cells to execute apoptosis could result from inhibition of active caspases by inhibitor of apoptosis proteins (IAPs). Here we investigate the mRNA and protein expression of IAPs in a panel of SCLC and NSCLC cell lines. The NSCLC cell lines had a stronger cIAP-2 expression at both mRNA and protein levels, while the SCLC cell lines had a higher level of XIAP protein. Expression of cIAP-1, cIAP-2, and XIAP, the most potent caspase inhibitors, was further investigated in three lung carcinoma cell lines after treatment with 8 Gy of ionizing radiation or etoposide (VP16). In response to treatment, the level of IAPs was not altered in a way that explained the differences in cellular chemo- and radiosensitivity. The intracellular localization of IAPs was analyzed in untreated and treated lung cancer cells. Surprisingly, we found that cIAP-2 was mainly detected in the mitochondrial fraction, although the function of this protein in mitochondria is unknown. No major relocalization of IAPs was observed after treatment. Taken together, these results indicate that IAPs alone are not the main factor responsible for the resistance of NSCLC cells to treatment.

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