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Abramson Cancer CenterNCI CANCERLIT® Search: Small Cell Lung Cancer - October 2001
National Cancer Institute®
Last Modified: November 21, 2001
Table of Contents
1
UI - 21230209
AU - Rodriguez-Salas N; Palacios J; de Castro J; Moreno G; Gonzalez-Baron M;
TI -
Gamallo C
Beta-catenin expression pattern in small cell lung cancer: correlation
with clinical and evolutive features.
SO - Histol Histopathol 2001 Apr;16(2):353-8
AD - Department of Medical Oncology, La Paz Hospital, Autonomous University
of Madrid, Spain.
Beta-catenin expression in small cell lung carcinomas (SCLC) was
investigated by immunohistochemical method using antibodies against
beta-catenin. 50 pre-treatment biopsies were examined and the
relationship between beta-catenin expression and the patients' relevant
clinical characteristics, response to chemotherapy, time to relapse or
progression, and overall survival, were analyzed. Beta-catenin
expression exhibited different intensity within each sample,
predominantly localized in the cytoplasm, and no sample showed nuclear
expression. There was cytoplasmic hyperexpression in 14 cases,
hypoexpression in 15 cases, and normal expression in 21 cases. We did
not find any association between beta-catenin expression and clinical
data. Our results show, however, correlation between beta-catenin
cytoplasmic hyperexpression with a shorter time to progression
(p=0.0437) as well as with a shorter overall survival (p=0.0253).
Beta-catenin hyperexpression could have prognostic significance in SCLC.
2
UI - 21356554
AU - Lewinski T; Zulawski M; Turski C; Pietraszek A
TI -
Small cell lung cancer I--III A: cytoreductive chemotherapy followed by
resection with continuation of chemotherapy.
SO - Eur J Cardiothorac Surg 2001 Aug;20(2):391-8
AD - Department of Lung and Thoracic Tumors, The Maria Sklodowska--Curie
Memorial Cancer Center and Institute of Oncology, Warsaw, Poland.
OBJECTIVES: To define the place for surgery in combined modality
treatment of small cell lung cancer patients. The endpoint was: does
complete resection reduce the risk of local failure? METHODS: Between
with a bulky cN2 tumor at presentation, were exposed to VP-16 based
cytoreductive chemotherapy. After three courses of induction treatment,
46 patients underwent thoracotomy and 35 of them had resection. RESULTS:
There were two sudden deaths (pulmonary embolism). No other
complications were observed. In six cases (6/35 = 16%), no residual
tumor was found in the resected specimen. Four weeks after surgery,
chemotherapy was resumed. Three patients experienced local relapse
(3/33), among them, the single patient with incomplete resection, and
two other patients developed local and distant failure (2/33). Thus, the
local relapse rate was 15% (5/33). Eight patients, mainly with
chemotherapy induced surgicopathological complete remission (pCR) and
with lymph nodes free of tumor in surgical specimens (pN0), are alive,
tumor-free, at a median of 136 + months. Two patients died tumor-free at
65 and 147 months. One patient died of unrelated causes at 21 months
with no evidence of disease at autopsy. The median survival in the cN0 +
N1 subsets was 25.09 months, whereas in cN2 disease, this was 13.75
months. There were no long-term survivors among the patients with
persistent N2 disease. The median survival in all 35 patients using the
Kaplan--Meier method was 18 months; the 5-year tumor-free survival rate
was 29% and the 10-year tumor-free survival rate was 23%. CONCLUSIONS:
Satisfactory local tumor control confirmed the assumption of the study.
No residual tumor in the resected specimen (pCR) is the most favorable
prognostic factor and determinant of long-term survival. Surgery should
not be performed in the patients with persistent N2 disease.
3
UI - 21385130
AU - Lui WO; Tanenbaum DM; Larsson C
TI -
High level amplification of 1p32-33 and 2p22-24 in small cell lung
carcinomas.
SO - Int J Oncol 2001 Sep;19(3):451-7
AD - Department of Molecular Medicine, Endocrine Tumor Unit, CMM L8:01,
Karolinska Hospital, SE-171 76 Stockholm, Sweden. weng-onn.lui@cmm.ki.se
Small cell lung cancer (SCLC) is a frequently occurring, highly
aggressive tumor with a generally poor clinical outcome. In order to
approach the genetic mechanisms behind the tumor progression, a general
screen for DNA copy number alterations was performed using comparative
genomic hybridization (CGH). In the series of 23 cases analyzed, CGH
alterations were frequently detected ranging from 9 to 22 abnormalities
in the individual tumors. The most frequent losses were detected on
chromosome arms 3p (23/23), 13q14-21 (23/23), 4p (20/23), 4q (20/23),
and 2q22-24 (18/23), while gains preferentially involved chromosome arms
19p (18/23), 19q (17/23), 1p31-35 (15/23), 17q22-25 (11/23), and
5p14-15.3 (9/23). In addition, high level amplification at chromosome
arms 1p32-33 and 2p22-24 were found in three and two cases,
respectively. Candidate genes for these amplifications include the l-MYC
(1p32) and n-MYC (2p24.1) oncogenes, which have been previously found to
be overexpressed in SCLC. Taken together, the findings demonstrate a
high level of chromosomal instability in SCLC, which is well in
agreement with the highly malignant phenotype of this tumor type.
Subchromosomal regions involved in gains and losses were delineated and
the amplifications of 1p32-33 and 2p22-24 were demonstrated, thus
providing starting points for the exact characterization of molecular
events involved in SCLC tumor progression.
4
UI - 21436106
AU - Cioffi M; Vietri MT; Gazzerro P; Magnetta R; D'Auria A; Durante A; Nola
TI -
E; Puca GA; Molinari AM
Serum anti-p53 antibodies in lung cancer: comparison with established
tumor markers.
SO - Lung Cancer 2001 Aug-Sep;33(2-3):163-9
AD - Istituto di Patologia Generale e Oncologia, Facolta di Medicina e
Chirurgia Seconda Universita degli Studi di Napoli, Via S. Andrea delle
Dame 2-80138, Napoli, Italy. rialab@usa.net
As reported earlier, p53 antibodies are detected in the sera of patients
with different types of cancer, including lung cancer. In contrast, in
the serum of healthy subjects the presence of anti-p53 antibodies is
extremely rare. We collected the venous blood samples of 109 patients
affected with lung cancer (LC): 57 patients (46 M, 11 F) with
non-small-cell carcinoma (NSCLC), 52 others (40 M, 12 F) with small-cell
carcinoma (SCLC). Serum p53 antibodies were assayed using ELISA method
and all positive sera were confirmed by Western-blot method. In
addition, using IRMA methods we assayed serum CEA, TPA, CYFRA21-1 and
NSE. Serum p53Ab are detectable (p53Ab-positive) in 35/109 (32.1%)
patients with lung cancer. About 17/57 (29.8%) patients affected with
NSCLC and 18/52 (34.6%) with SCLC were p53Ab-positive. CEA, TPA,
CYFRA21-1 and NSE sensitivity in LC patients (NSCLC+SCLC) is 50.5%,
58.7%, 42.2%, 35.8%, respectively. The lower sensitivity (32.1%) of
serum p53Ab is connected with the higher specificity and diagnostic
accuracy (100% and 69%, respectively). Out of 35 patients
p53Ab-positive, five (14.3%) exhibit only serum p53Ab, while serum
values of the established tumor markers were lower than cut-off. Serum
p53Ab assessment is a simple and a low-cost assay with a good
specificity and diagnostic accuracy that in LC patients can be used at
least in association with established tumor markers.
5
UI - 21436110
AU - Radzikowska E; Roszkowski K; Glaz P
TI -
Lung cancer in patients under 50 years old.
SO - Lung Cancer 2001 Aug-Sep;33(2-3):203-11
AD - III Department of Tuberculosis and Lung Diseases, National Tuberculosis
and Chest Diseases Research Institute, Warsaw 01-138, Plocka 26 St.,
Poland. e.radzikowska@igichp.edu.pl
PURPOSE: The community based lung cancer registry was set up and the
results were analysed to assess the differences in clinicopathological
parameters and survival between patients under and over 50 years of age.
PATIENTS AND METHODS: The Pulmonary Outpatient Clinics supplied the data
on 5404 lung cancer patients diagnosed in Poland in 1995. Data regarding
demographic, smoking, histology, clinical stage, performance status,
family history of cancer, therapy and survival were obtained. RESULTS:
At time of diagnosis 757 (14%) patients were under 50 years of age. In
this group the frequency of females was higher as compared to this in
the group of older patients (24.2% vs. 12.1%; P<0.001). Also the
incidence of adenocarcinoma (12.6% vs. 7.6%; P<0.001) and small cell
lung cancer (22.9% vs. 14.8%; P<0.001) were significantly higher in
younger patients. Young patients had better performance status (55.4%
vs. 46.6%; P<0.001) than old. The incidence of cancer in families of
younger patients was higher both among the mothers (4.7% vs. 3.0%;
P<0.001) and among the fathers (7.6% vs. 4.1%, P<0.001). Surgery or
chemotherapy were more often applied to patients under 50 years in
comparison to older ones (P<0.001). Young patients had better prognosis.
Higher percentage of them survived one year (32.6% vs. 28.9%; P<0.049).
In multivariate analysis, age over 50 at diagnosis, male gender,
diagnosis of small cell lung cancer, advanced stage of the disease, bad
performance status, and non-surgical therapy were independent negative
prognostic factors. CONCLUSION: Among young patients, overrepresentation
of women, subjects with positive family history of cancer, with better
performance status, with adenocarcinoma and small cell lung cancer were
noticed. Young patients were treated more aggressively and had better
prognosis than patients over 50 years of age.
6
UI - 21436111
AU - Thomas CR Jr; Giroux DJ; Janaki LM; Turrisi AT 3rd; Crowley JJ; Taylor
TI -
SA; McCracken JD; Shankir Giri PG; Gordon W Jr; Livingston RB; Gandara
DR
Ten-year follow-up of Southwest Oncology Group 8269: a phase II trial of
concomitant cisplatin-etoposide and daily thoracic radiotherapy in
limited small-cell lung cancer.
SO - Lung Cancer 2001 Aug-Sep;33(2-3):213-9
AD - Department of Radiation Oncology, San Antonio Cancer Institute,
University of Texas Health Science Center, San Antonio, TX, USA
PURPOSE: To report the long-term follow-up of Southwest Oncology
Group-8269, a phase II North American cooperative group trial of
concurrent cisplatin, etoposide, vincristine (PEV), and thoracic
radiotherapy (TRT) for limited small-cell lung cancer (L-SCLC). METHODS:
114 eligible patients from 47 institutions enrolled between April, 1985
consisted of three cycles of PEV. TRT was administered at 1.8
Gy/fraction in 25 daily fractions to a total dose of 45 Gy, to begin
concomitantly. Consolidative chemotherapy included two cycles of
vincristine, methotrexate, etoposide, doxorubicin and cyclophosphamide.
Prophylactic cranial irradiation (PCI) was concurrent with the 3rd cycle
of chemotherapy. The PCI dose was 30 Gy in 15 fractions of 2
progression-free with a minimum follow-up interval of 13.2 years, as of
patients died of causes other than SCLC and five patients are still
alive and progression-free. Of the remaining 71 patients dying of SCLC,
local failure (LF) occurred in 24% (17 patients), distant metastasis
(DM) occurred in 35% (25 patients), simultaneous LF and DM occurred in
25% (18 patients), and was indeterminate in 16% (11 patients). Thus, LF
was a component of failure in 49%. Twenty patients had the CNS as the
initial site of failure. Eleven patients (10%) developed fatal second
primary cancers, including two with acute myelogenous leukemia, two with
squamous cell lung cancer, one each with breast, pancreas, prostate,
renal cell, and myelodysplasia. One patient developed both a melanoma
and non-Hodgkin's lymphoma. CONCLUSION: There are long-term survivors
with concomitant TRT and PEV. LF and DM are common. Pattern of failure
suggests needs to improve local and systemic control.
7
UI - 21436114
AU - Miller AA; Niell HB
TI -
Phase I and pharmacologic study of sequential topotecan, carboplatin,
and etoposide.
SO - Lung Cancer 2001 Aug-Sep;33(2-3):241-8
AD - Veterans Affairs Medical Center- Memphis, 1030 Jefferson Avenue,
Memphis, TN 38104, USA. aamiller@wfubmc.edu
Inhibition of topoisomerase I by topotecan results in a compensatory
increase in topoisomerase II levels associated with increased in vitro
sensitivity of tumors to etoposide. Maximum synergy has been observed
for the sequence of topotecan followed by etoposide. This is the
pharmacologic rationale for the sequence of topotecan 0.4 mg/m(2) per
day for 7 days continuous i.v. infusion, carboplatin i.v. on day 8, and
etoposide 50 mg per day p.o. days 9 through 20. The carboplatin dosage
was escalated from an AUC of 4 to 5 to 6 (Calvert formula). Up to six
treatment cycles were administered at 28-day intervals. Eligible
patients had metastatic non-small cell lung cancer (NSCLC) or extensive
disease small lung cell lung cancer (SCLC), no prior chemotherapy,
performance status 0-2, and adequate organ function. Follow-up was twice
weekly in the first cycle for CBC and for topotecan and etoposide
concentrations. Follow-up, thereafter, was weekly. Tumor response was
assessed after two and six cycles and then as clinically indicated. At
carboplatin AUCs of 4 and 5, no NCI grade 4 toxicity was observed in
cycle 1 in cohorts of three patients each. At the AUC of 5, two patients
experienced dose-limiting events after cycle 3, one grade 4 neutropenia
lasting >3 days (no fever) and one failure to recover an absolute
neutrophil count >1500/microl by day 35. This was, therefore, deemed the
maximal tolerable dose. Number of treatment cycles per patient ranged
between 1 and 6, and three patients completed six cycles. All patients
were male, age 47-71, with NSCLC in one and SCLC in six. The patient
with NSCLC had progressive disease after one cycle. One complete and
three partial responses were observed in five patients with SCLC. Mean
steady-state plasma concentrations during topotecan infusion ranged from
0.73 to 1.69 ng/ml, and mean etoposide concentrations ranged from 60 to
230 ng/ml. This sequence of topotecan, carboplatin, and etoposide
appeared tolerable and active. Neutropenia was the dose-limiting
toxicity.
8
UI - 21436115
AU - Videtic GM; Fung K; Tomiak AT; Stitt LW; Dar AR; Truong PT; Yu EW;
TI -
Vincent MD; Kocha WI
Using treatment interruptions to palliate the toxicity from concurrent
chemoradiation for limited small cell lung cancer decreases survival and
disease control.
SO - Lung Cancer 2001 Aug-Sep;33(2-3):249-58
AD - The Department of Radiation Oncology, London Regional Cancer Center,
University of Western Ontario, London, Ontario, Canada.
greg.videtic@lrcc.on.ca
BACKGROUND AND PURPOSE: We analyzed the impact on survival outcomes of
treatment interruptions due to toxicity arising during the concurrent
phase of chemotherapy/radiotherapy (ChT/RT) for our limited-stage
small-cell cancer (LSCLC) population over the past 10 years. MATERIALS
AND METHODS: From 1989 to 1999, 215 patients received treatment for
LSCLC, consisting of six cycles of alternating
cyclophosphamide/doxorubicin or epirubicin/vincristine (CAV; CEV) and
etoposide/cisplatin (EP). Thoracic RT was started with EP at either the
second or third cycle (85% of patients). RT dose was either 40 Gy in 15
fractions over 3 weeks or 50 Gy in 25 fractions over 5 weeks, delivered
to a target volume encompassing gross disease and suspected microscopic
disease with a 2 cm margin. Treatment breaks arising during concurrent
ChT+RT were used to manage severe symptomatic or hematologic toxicities.
We used the interruptions in thoracic RT as the 'marker' for any
concurrent break and measured 'break duration' by the total length of
time (in days) RT was interrupted, since that also signaled that ChT
could be re-initiated. Patient results were analyzed for the impact of
interruptions/treatment prolongation on overall and disease-free
survival. RESULTS: For all patients, 2-year and 5-year overall and
disease-specific survivals were 22.7 and 7.2, 27.6 and 9.3%,
respectively; overall and disease-specific median survivals were 14.7
months each. A total of 56 patients (26%) had treatment breaks due to
toxicity. Hematologic depression caused the majority of breaks (88%).
The median duration of breaks was 5 days (range 1-18). Patients with and
without interruptions were compared for a range of prognostic factors
and were not found to have any significant differences. Comparing
interrupted/uninterrupted courses, median survivals were 13.8 versus
15.6 months, respectively, and 5-year overall survivals were 4.2 versus
8.3%, respectively. There was a statistical difference between overall
survival curves which favored the uninterrupted group (P=0.01). When
comparing a series of prognostic variables, multivariable analysis found
that the most significant factor influencing survival in the present
study was the presence of treatment breaks (P=0.006). There was a trend
for development of any recurrence in the patients with breaks (P=0.08).
When controlling for the use of prophylactic cranial irradiation (PCI)
in the two groups, the rate of failure in the chest was higher in the
patients with RT breaks (58 vs. 33%). The rate of failure in the brain
was dependent on the use of PCI only. CONCLUSIONS: Interruptions in
treatment to palliate the toxicity from concurrent chemoradiation result
in poorer local control and decreased survival.
9
UI - 21436121
AU - Trillet-Lenoir V; Lotz JP; Le Cesne A; Roy P; Avallet L; Edouard A
TI -
Reflexions from the experience of the French CLEOPATRE program and
concerns about the status of clinical research on small cell lung
cancer.
SO - Lung Cancer 2001 Aug-Sep;33(2-3):303-7
AD - Medical Oncology Unit, Centre Hospitalier Lyon Sud, 69495 Pierre Benite
Cedex, France. veronique.trillet-lenoir@chu-lyon.fr
10
UI - 21387836
AU - Macbeth F; Price A
TI -
Reviews should be more systematic.
SO - Radiother Oncol 2001 Aug;60(2):225-7
11
UI - 21424851
AU - Knippel SL
TI -
Surgical therapies for lung carcinomas.
SO - Nurs Clin North Am 2001 Sep;36(3):517-25, x-xi
AD - Department of Thoracic and Cardiovascular Surgery, The University of
Texas MD Anderson Cancer Center, Houston, Texas 77030-4095, USA.
Lung cancer is the leading cause of cancer-related death for men and
women in the world today. Surgical resection of early stage non-small
cell lung cancer is the recommended treatment option and offers the
patient the best chance for survival. Nurses are instrumental in lung
cancer prevention, early detection, delivery of quality perioperative
care, and maximizing long-term patient survival.
12
UI - 21443280
AU - Tang D; Phillips DH; Stampfer M; Mooney LA; Hsu Y; Cho S; Tsai WY; Ma J;
TI -
Cole KJ; She MN; Perera FP
Association between carcinogen-DNA adducts in white blood cells and lung
cancer risk in the physicians health study.
SO - Cancer Res 2001 Sep 15;61(18):6708-12
AD - Division of Environmental Health Sciences, Joseph L. Mailman School of
Public Health, Columbia University, New York, New York 10032, USA.
In this matched case-control study nested within the prospective
Physicians' Health Study, we evaluated whether DNA damage in blood
samples collected at enrollment significantly predicted risk, consistent
with our hypothesis that cases have greater biological susceptibility to
polycyclic aromatic hydrocarbons and other aromatic tobacco carcinogens.
The subjects were 89 cases of primary lung cancer and 173 controls, all
males, matched on smoking, age, and duration of follow-up. Aromatic-DNA
adducts were measured in WBCs by the nuclease P1-enhanced
(32)P-postlabeling method that primarily detects smoking-related
adducts. Among current smokers, but not former or nonsmokers, there was
a significant increase in mean adduct levels of cases compared with
controls (11.04 versus 5.63; P = 0.03). "Healthy" current smokers who
had elevated levels of aromatic DNA adducts in WBCs were approximately
three times more likely to be diagnosed with lung cancer 1-13 years
later than current smokers with lower adduct concentrations (odds ratio,
2.98; 95% confidence interval, 1.05-8.42; P = 0.04). We were not able to
discern case-control differences in former smokers and nonsmokers. The
findings are of interest because they suggest that individuals who
become cases have greater biological susceptibility to tobacco
carcinogens, a biological difference, which manifests most clearly while
exposure is ongoing.
13
UI - 21381728
AU - Kelly K; Lovato L; Bunn PA Jr; Livingston RB; Zangmeister J; Taylor SA;
TI -
Roychowdhury D; Crowley JJ; Gandara DR; Southwest Oncology Group
Cisplatin, etoposide, and paclitaxel with granulocyte colony-stimulating
factor in untreated patients with extensive-stage small cell lung
cancer: a phase II trial of the Southwest Oncology Group.
SO - Clin Cancer Res 2001 Aug;7(8):2325-9
AD - University of Colorado, Denver, CO 80262, USA.
PURPOSE: This study was designed to determine the efficacy and toxicity
of cisplatin, etoposide, and paclitaxel (PET) in patients with
extensive-stage small cell lung cancer (ES-SCLC). EXPERIMENTAL DESIGN:
Chemo-naive adult patients with a performance status (PS) of 0-2 and
adequate organ function were eligible. Patients received cisplatin 80
mg/m(2) i.v., etoposide 80 mg/m-2 i.v., and paclitaxel 175 mg/m(2) i.v.
over a 3-h period on day 1 followed by etoposide 160 mg/m(2) p.o. on
days 2 and 3 every 21 days for six cycles. G-CSF 5 microg/kg was
injected s.c. on days 4-14. RESULTS: Eighty-eight patients were
assessable. The median age was 60 years; 50% were male, 78% had PS of
0-1, 28% had PS of 2, 53% had multiple sites, and 13% had brain
involvement. The overall response rate was 57% with 10 (12%) of 84
patients achieving a complete response. Median progression-free survival
was 6 months [95% confidence interval (CI), 5-7 months] with a median
survival of 11 months (95% CI, 8-13 months) and a 1-year survival rate
of 43% (95% CI, 33-54%). Six patients (7%) died from toxicity. Grade 5
toxicity occurred in 3 (14%) of 22 patients (with a PS of 2) versus 3
(5%) of 61 patients (with a PS of 0-1; P, not significant). Grade 4
neutropenia developed in 40% of patients. Grade 3 nonhematological
toxicities were primarily nausea (20%), vomiting (16%), and fatigue
(14%). CONCLUSION: The survival result achieved was superior to prior
SWOG experiences; however, the toxic death rate was unacceptably high in
PS-2 patients. These results provide the largest database for the
ongoing randomized Intergroup trial comparing PET to cisplatin+etoposide
in PS-0-1 patients with ES-SCLC.
14
UI - 21456676
AU - Kayser G; Gunzenhauser I; Becker HD; Herth F; Kayser K
TI -
[Proliferation rate of small cell lung carcinoma. A cytomorphometric
parameter with prognostic significance]
SO - Pathologe 2001 Sep;22(5):326-32
AD - Abteilung Pathologie, Thoraxklinik, Amalienstrasse 5, 69126 Heidelberg.
klkayser@lung.de
AIM: Evaluation of prognosis-associated parameters in patients with
small cell lung carcinoma. MATERIAL AND METHODS: Biopsies of 46 patients
suffering from a non-treated small cell lung carcinoma were stained with
Feulgen and immunohistochemically with Ki-67 antibody. The integrated
optical density (IOD) and proliferation rate was measured by syntactic
structure analysis and correlated with survival. RESULTS: About 85% of
patients had a smoking history (46 pack years on average). The median
survival time was 13.5 months, the proliferation rate (Ki-67 positive
tumor cell nuclei) 68.2% and S-phase percentage 9.2%. Ot average, 25
proliferating tumor cell nuclei formed clusters (mean diameter 95
microns). The prognosis was associated with the proliferation rate (p <
0.04), tumor stage (stage I versus lib, p < 0.05), at threshold limits
with S-phase rate (p < 0.07) and serum levels of LDH and NSE (p < 0.06
and p < 0.07 respectively). CONCLUSIONS: Immune histochemical
determination of the Ki-67 protein is a useful method to estimate the
prognosis of patients with small cell lung carcinoma.
15
UI - 21487552
AU - Marchevsky AM; Gal AA; Shah S; Koss MN
TI -
Morphometry confirms the presence of considerable nuclear size overlap
between "small cells" and "large cells" in high-grade pulmonary
neuroendocrine neoplasms.
SO - Am J Clin Pathol 2001 Oct;116(4):466-72
AD - Department of Pathology, Cedars-Sinai Medical Center, UCLA School of
Medicine, Los Angeles, CA, USA.
We morphometrically evaluated 5-micron H&E-stained sections from 28
surgically resected high-grade pulmonary neuroendocrine neoplasms,
including 16 small cell lung carcinomas (SCLCs) and 12 large cell
neuroendocrine carcinomas (LCNECs). For each case, 200 tumor nuclei and
20 to 100 normal lymphocytes were measured. The frequency distributions
of tumor cell/lymphocyte (TC/L) size ratios were plotted in bins ranging
from 1 to 6, classified into 6 histogram types with TC/L size ratio
peaks ranging from 2 to 6 (A-E) and a histogram with a wide distribution
(F). SCLCs fit histograms A through E; LCNECs, A through F. Morphometry
demonstrated considerable nuclear size overlap in high-grade neoplasms.
Approximately one third of SCLCs exhibited considerable numbers of
neoplastic cells that were larger than 3 normal lymphocytes, while 4 of
12 LCNECs had a predominant number of small cells. Ten tumors exhibited
a B histogram with a "borderline" peak TC/L of 3. The rule that a TC/L
size ratio larger than 3 helps distinguish "large" from "small"
neoplastic cells was confirmed in only 9 of 28 cases. The use of more
generic terminology such as "high-grade neuroendocrine carcinoma" or
"grade III neuroendocrine carcinoma" for SCLC and LCNEC is discussed.
16
UI - 21291609
AU - Mavroudis D; Papadakis E; Veslemes M; Tsiafaki X; Stavrakakis J;
TI -
Kouroussis C; Kakolyris S; Bania E; Jordanoglou J; Agelidou M;
Vlachonicolis J; Georgoulias V; Greek Lung Cancer Cooperative Group
A multicenter randomized clinical trial comparing
paclitaxel-cisplatin-etoposide versus cisplatin-etoposide as first-line
treatment in patients with small-cell lung cancer.
SO - Ann Oncol 2001 Apr;12(4):463-70
AD - Department of Medical Oncology, School of Medicine, University of Crete,
Greece. georgoul@med.uch.gr
BACKGROUND: Previous phase I-II studies have shown that the combination
of paclitaxel-cisplatin-etoposide (TEP) is very active and well
tolerated in patients with small-cell lung cancer (SCLC). In order to
compare the TEP combination to cisplatin etoposide (EP) regimen as
front-line treatment in patients with SCLC, we conducted a randomised
multicenter study. PATIENTS AND METHODS: One hundred thirty-three
chemotherapy-naive patients with histologically proven limited or
extensive stage SCLC were randomised to receive either paclitaxel 175
mg/m2 i.v. three-hour infusion on day 1 and cisplatin 80 mg/m2 i.v. on
day 2 and etoposide 80 mg/m2 i.v. on days 2-4 with G-CSF support (5
mcg/kg s.c. days 5-15) or cisplatin 80 mg/m2 i.v. on day 1 and etoposide
120 mg/m2 i.v. on days 1-3 in cycles every twenty-eight days. RESULTS:
Due to excessive toxicity and mortality observed in the TEP arm, an
early interim analysis was performed and the study was closed. Sixty-two
patients received two hundred sixty-one cycles of TEP and seventy-one
patients three hundred twenty-three cycles of EP The two patient groups
were well balanced for age, sex, performance status, stage of disease
and the presence of abnormal LDH at diagnosis. In an intention-to-treat
overall analysis both regimens were equally active with a complete and
partial response rate of 50% (95% confidence interval (CI): 37.5%-62.4%)
for TEP and 48% (95%) CI: 36.2%-59.5%) for EP (P = 0.8). The median time
to disease progression was 11 months for TEP and 9 months for EP (P =
0.02). The duration of response, one-year survival and overall survival
were similar in the two arms. Similarly, in an intention-to-treat
subgroup analysis of patients with limited or extensive stage disease,
there was no difference in the activity between the two regimens except
of a longer median time to disease progression in the extensive stage in
favour of the TEP regimen, eight versus six months (P = 0.04). However,
there were eight toxic deaths in the TEP arm versus none in the EP arm
(P = 0.001). Moreover, the TEP regimen was associated with more severe
toxicity than the EP regimen in terms of grade 4 neutropenia (P = 0.04),
grade 3-4 thrombocytopenia (P = 0.02), febrile neutropenia (P = 0.08),
grade 3-4 diarrhea (P = 0.01), grade 3-4 asthenia (P = 0.05) and grade 3
neurotoxicity (P = 0.06). CONCLUSIONS: In this early terminated study,
the TEP regimen was significantly more toxic than the EP regimen. The
TEP regimen is associated with significant toxicity and mortality, and
should not be used outside of a protocol setting. For future
investigations, dose and schedule modifications are necessary to reduce
toxicity.
17
UI - 21291624
AU - van der Lee I; Smit EF; van Putten JW; Groen HJ; Schlosser NJ; Postmus
TI -
PE; Schramel FM
Single-agent gemcitabine in patients with resistant small-cell lung
cancer.
SO - Ann Oncol 2001 Apr;12(4):557-61
AD - Department of Pulmonology, St. Antonius Hospital, Nieuwegein, The
Netherlands.
OBJECTIVE: This study was conducted to assess the activity and toxicity
ofgemcitabine in patients with resistant small-cell lung cancer (SCLC).
PATIENTS TAND METHODS: Forty-one patients with limited- or
extensive-stage SCLC, who were previously treated with at least one
chemotherapeutic regimen and progressed during or within three months of
finishing the last regimen, were treated with 1000 mg/m2 gemcitabine on
days 1, 8, and 15 of a four-week cycle. RESULTS: Thirty-eight patients
were evaluable for response. Five partial and no complete responses were
seen, for an overall response rate of 13% (95% confidence interval (CI):
6%-27%). Time to progression varied from 4 to 20 weeks, with a median of
8 weeks. Median survival was 17 weeks (range 4-84 weeks). Hematological
toxicity mainly consisted of NCI-CTC grade 3 thrombocytopenia (29% of
patients) and, to a lesser extent, grade 3 leukopenia (18% of patients).
Non-hematological toxicity was mild, with nausea being the most commonly
reported event. CONCLUSIONS: Gemcitabine has modest activity in patients
with resistant SCLC. There is some non-cross resistance to most agents
against SCLC.
18
UI - 21447015
AU - Oliver E; Killen J; Kiebert G; Hutton J; Hall R; Higgins B; Bourke S;
TI -
Paschen B
Treatment pathways, resource use and costs in the management of small
cell lung cancer.
SO - Thorax 2001 Oct;56(10):785-90
AD - MEDTAP International, 20 Bloomsbury Square, London WC1A 2NA, UK.
BACKGROUND: Small cell lung cancer (SCLC) represents about 20% of
primary lung tumours and the costs associated with the management of
SCLC can be significant. The main objective of this study was to obtain
information on current patterns of care and associated resource use and
costs for patients with SCLC from initial diagnosis and treatment phase,
throughout disease progression and terminal care. METHODS: A 4 year
retrospective patient chart analysis (1994-7) was conducted on a
consecutive series of 109 patients diagnosed with SCLC in two Newcastle
hospitals. For this consecutive series of patients all details about
care received including tests and procedures, treatment, and medication
from diagnosis till death were recorded. Pathways of care and forms were
designed to enable resource use to be captured for different disease
phases. Unit costs were determined from a variety of sources including
the Newcastle Hospitals NHS Trust Finance Department and the British
National Formulary. RESULTS: The average total cost per patient
calculated for the full cohort of 109 patients was pound 11,556. Initial
treatment was the most resource use intensive constituting 48.2% of the
total cost. The major cost element throughout all disease phases was
hospitalisation. Twenty eight percent of the total costs of care occur
after recurrence of the disease until death, of which 73% are generated
by terminal care. CONCLUSION: The results of this retrospective medical
chart analysis show that the costs of care of SCLC are considerable,
although the variability between patients in terms of the type and
quantity of resource use is very high. Analyses such as this provide a
useful insight into resources used in actual clinical practice.
19
UI - 21487499
AU - Thiberville L; Bota S
TI -
[Small cell bronchial cancers: epidemiology, pathologic anatomy,
etiology, diagnosis, course, treatment]
SO - Rev Prat 2001 Sep 1;51(13):1465-72
AD - Clinique pneumologique, centre hospitalier et universitaire de
Rouen-hopitaux de Rouen, hopital Charles-Nicolle, 76031 Rouen.
20
UI - 21487046
AU - Arriagada R; Pignon JP; Le Chevalier T
TI -
Initial chemotherapeutic doses and long-term survival in limited
small-cell lung cancer.
SO - N Engl J Med 2001 Oct 25;345(17):1281-2
21
UI - 21441424
AU - Lebitasy MP; Hedelin G; Purohit A; Moreau L; Klinzig F; Quoix E
TI -
Progress in the management and outcome of small-cell lung cancer in a
French region from 1981 to 1994.
SO - Br J Cancer 2001 Sep 14;85(6):808-15
AD - Service de Pneumologie Lyautey, CHU de Strasbourg, 1 rue des Canonniers,
67100 Strasbourg, France.
Recent analyses of series of small-cell lung cancer (SCLC) patients
included in clinical trials have shown improved survival over time, but
it has been impossible to determine whether this was due to selection
biases, stage migration, or true therapeutic improvement. To determine
if there has been a true improvement of survival over time, we reviewed
the medical records of all consecutive patients diagnosed with SCLC
between 1981 and 1994 in the Bas-Rhin in France. Among the 787 patients
(median age 63), there was no significant period effect for sex, age, or
stage. Staging work-ups became increasingly thorough (significant period
effect). The mean number of investigations and of tumour sites detected
correlated significantly. The chemotherapy rate increased (from 76.4% in
1981-1983 to 91.7% in 1993-1994, P = 10(-5)) and mediastinal irradiation
decreased (to roughly 25% of patients after 1983). Median survival time
increased for the overall population from 6.6 months in 1981-1983 to
11.3 months in 1993-1994 (P = 10(-5)), for patients with limited disease
(LD) from 9.2 (P = 0.002) months to 14.0 months, and for those with
extensive (ED) disease from 3.5 months to 9.6 months (P = 10(-5)).
Significant independent prognostic factors were disease extent, clinical
trial participation, period, type of chemotherapy, and mediastinal
irradiation in LD. Survival time has truly improved as 'state of the
art' management of SCLC has changed. Copyright 2001 Cancer Research
Campaign http://www.bjcancer.com.
22
UI - 21489949
AU - Borg C; Ligneau B; Trillet-Lenoir V
TI -
[Dose intensity of chemotherapy in small-cell lung carcinoma]
SO - Bull Cancer 2001 Sep;88(9):863-70
AD - Unite fonctionnelle d'oncologie medicale, Centre hospitalier Lyon-Sud,
69495 Pierre-Benite Cedex.
Small cell lung cancer accounts for 20% of the primitive lung
carcinomas. The pronostic is unfavourable, since two thirds of the
patients present with extensive stage at diagnosis. The median survival
without treatment is less than 3 months. Chemotherapy is the standard
front line therapy. In selected patients, chest irradiation and
so-called prophylactic cerebral irradiation are current options. Small
cell lung cancer is a chemosensitive disease. Indeed, the response rate
is around 80-95% of in limited disease patients of which 50-60% are
complete responses. Despite these results, the median survival does not
exceed 16 months. Early recurrences after initial response probably
reflect various resistances mechanisms. Furthermore, small cell lung
cancer is associated with a high fraction of dividing cells. It is a
clinical model where the dose-response relationship concept is worth
testing, and dose-intensity may be integrated into the therapeutic
strategies. Therefore, many clinical trials have assessed these
principles during the past 20 years. We present here the different
methods of therapeutic intensification in small cell lung cancer: with
or without hematopoietic supports, using initial high dose of cytotoxic
drugs, either at the beginning or at the end of induction treatment, or
by increasing the dose-density.
23
UI - 21538316
AU - Hosomi Y; Shibuya M
TI -
[Combination chemotherapy with VP-16 in the treatment of lung cancer and
malignant lymphoma]
SO - Gan To Kagaku Ryoho 2001 Oct;28(10):1352-6
AD - Fourth Department of Internal Medicine, Nippon Medical School, 1-1-5
Sendagi, Bunkyo-ku, Tokyo 113-8603, Japan.
Many investigators have reported the dose and schedule of VP-16
administration, but as yet they remain undetermined. VP-16 is one of the
most active agents for several carcinomas and usually administered
intravenously over 3 to 5 consecutive days in combination with other
agents. Although, the development of new drugs recently reduces the use
of VP-16 administration, VP-16 is still an important drug for the
treatment of lung cancer and malignant lymphoma. In this paper, the
combination therapy with VP-16, especially in the treatment of lung
cancer and malignant lymphoma, are reviewed.
The above citations and abstracts reflect those newly added to CANCERLIT for the month and topic listed in the title. The citations have been retrieved from CANCERLIT using a predefined search strategy of indexed subject terms. Although the search strategy has been refined as best as possible, citations may appear that are not directly related to the topic, and occasionally relevant references may be omitted.
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