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NCI CANCERLIT® Search: Malignant Mesothelioma - June 2002
National Cancer Institute®
Last Modified: June 1, 2002
- Asbestos and its lethal legacy.
- Phosphatase and tensin analog gene overexpression engenders cellular death in human malignant mesothelioma cells via inhibition of AKT
- Overexpression of peroxiredoxins I, II, III, V, and VI in malignant mesothelioma.
- Immunohistochemical MIB-1 and p27 as prognostic factors in pleural mesothelioma.
- Pemetrexed for diffuse malignant pleural mesothelioma.
- The quantitative risks of mesothelioma and lung cancer in relation to asbestos exposure: the Wittenoom data.
- The quantitative risks of mesothelioma and lung cancer in relation to asbestos exposure.
- Asbestos and cancer risk.
- Fairchild and the "guilty" fibre.
- [Primary peritoneal tumors: report on a series of eight cases and review of the literature]
- [Incidence of malignant mesothelioma (1980-1999) and asbestos exposure in 190 cases diagnosed among residents of the province of Brescia]
- Assessment of the mutations of p53 suppressor gene and Ha- and Ki-ras oncogenes in malignant mesothelioma in relation to asbestos exposure: a
- Malignant mesothelioma: immunohistochemistry and DNA ploidy analysis as methods to differentiate mesothelioma from benign reactive mesothelial
- A phase II EORTC study of temozolomide in patients with malignant pleural mesothelioma.
Table of Contents
1
UI - 12001992
AU - Tweedale G
TI -
Asbestos and its lethal legacy.
SO - Nature Rev Cancer 2002 Apr;2(4):311-5
AD - Centre for Business History, Business School, Manchester Metropolitan
University, UK. G.Tweedale@mmu.ac.uk
Asbestos has become the leading cause of occupationally related cancer
death, and the second most fatal manufactured carcinogen (after
tobacco). In the public's mind, asbestos has been a hazard since the
1960s and 1970s. However, the knowledge that the material was a mortal
health hazard dates back at least a century, and its carcinogenic
properties have been appreciated for more than 50 years.
2
UI - 11923140
AU - Mohiuddin I; Cao X; Ozvaran MK; Zumstein L; Chada S; Smythe WR
TI -
Phosphatase and tensin analog gene overexpression engenders cellular
death in human malignant mesothelioma cells via inhibition of AKT
phosphorylation.
SO - Ann Surg Oncol 2002 Apr;9(3):310-6
AD - Section of Thoracic Molecular Oncology, Department of Thoracic and
Cardiovascular Surgery, The University of Texas M. D. Anderson Cancer
Center, Houston, Texas 77030, USA.
BACKGROUND: Abnormal phosphatase and tensin analog (PTEN) gene
expression has been noted in neoplasms. The PTEN protein cleaves
phosphate groups from cellular growth kinases, inhibiting tumor
propagation. A downstream target of PTEN is AKT, a serine-threonine
kinase that when activated inhibits apoptosis. We sought to determine
whether PTEN overexpression in mesothelioma cells would engender
hypophosphorylation of AKT and apoptosis. METHODS: Human malignant
mesothelioma cell lines REN and I-45 were transfected with adenoviral
vectors AdPTEN and AdBgal (marker gene) at various multiplicities of
infection (MOI). Cell viability was measured using a colorimetric assay,
and apoptosis was assessed by morphology and subG1
fluorescence-activated cell sorter (FACS) analysis. PTEN protein and AKT
phophorylation were evaluated by Western blot, and AKT kinase activity
was evaluated by functional assay. RESULTS: Increased cellular killing
was noted with AdPTEN gene transfer. The ratio of cell killing with
AdPTEN to AdBgal widened with increasing MOI and was statistically
significant at all MOI. Cells demonstrated apoptosis by morphologic and
subG1 FACS analyses. Cells overexpressing PTEN demonstrated decreased
phosphorylated (active) AKT and AKT kinase activity compared with
controls. CONCLUSIONS: Overexpression of PTEN engenders apoptosis in
mesothelioma by AKT hypophosphorylation. The forced overexpression of
PTEN may prove useful clinically in this treatment-resistant neoplasm.
3
UI - 11857495
AU - Kinnula VL; Lehtonen S; Sormunen R; Kaarteenaho-Wiik R; Kang SW; Rhee
TI -
SG; Soini Y
Overexpression of peroxiredoxins I, II, III, V, and VI in malignant
mesothelioma.
SO - J Pathol 2002 Mar;196(3):316-23
AD - Department of Internal Medicine, Pulmonary Division, University of Oulu
and Oulu University Hospital, Kajaanintie 50A, 90220 Oulu, Finland.
vuokko.kinnula@oulu.fi
Peroxiredoxins (Prxs) are a recently characterized group of
thiol-containing proteins with efficient antioxidant capacity, capable
of consuming hydrogen peroxide in living cells. Altogether six distinct
Prxs have been characterized in mammalian tissues. Their expression was
investigated in histological samples of mesothelioma and in cell lines
established from the tumours of mesothelioma patients. Four cases with
histopathologically healthy pleura from non-smokers were used as
controls. Healthy pleural mesothelium was negative or very weakly
positive for all Prxs. In mesothelioma, the most prominent reactivity
was observed with Prxs I, II, V, and VI. Prx I was highly or moderately
expressed in 25/36 cases, the corresponding figures for Prxs II-VI being
27/36 (Prx II), 13/36 (Prx III), 2/36 (Prx IV), 24/36 (Prx V), and 30/36
(Prx VI). Positive staining was observed both in the cytosolic and the
nuclear compartment, with the exception of Prx III, which showed no
nuclear reactivity. The staining pattern of Prxs III and V was granular.
Immunoelectron microscopic localization of Prxs was in accordance with
the immunohistochemical findings, showing diffuse cytoplasmic
localization for Prxs I, II, IV, and VI and distinct mitochondrial
labelling for Prxs III and V. There was no significant association
between the extent of staining and different Prxs. It appeared that Prxs
may not have prognostic significance, but being prominently expressed in
most mesotheliomas these proteins, at least in theory, may play a role
in the primary drug resistance of this disease. Copyright 2002 John
Wiley & Sons, Ltd.
4
UI - 11795837
AU - Beer TW
TI -
Immunohistochemical MIB-1 and p27 as prognostic factors in pleural
mesothelioma.
SO - Pathol Res Pract 2001;197(12):859
5
UI - 12023790
AU - Manegold C; Aisner J
TI -
Pemetrexed for diffuse malignant pleural mesothelioma.
SO - Semin Oncol 2002 Apr;29(2 Suppl 5):30-5
AD - Department of Medical Oncology/Internal Medicine, Thoraxklinik
Heidelberg, gGmbH, Heidelberg, Germany.
The treatment of diffuse malignant pleural mesothelioma (MPM) is
currently less than satisfactory. Survival statistics are best for the
epithelial subtype and for tumors that can be completely removed by
surgery. Radiotherapy provides no survival benefit and is used only to
palliate symptoms or to prevent growth along needle tracks and
incisions. The response to chemotherapeutic agents is poor, and to date
there is no standard cytotoxic treatment. Antimetabolites may have some
activity, and one trial of high-dose methotrexate has suggested a
moderate response rate. There is also no evidence that any chemotherapy
regimen given as a part of multimodality treatment, including
radiotherapy and surgery, can improve survival. Recently, a renewed
interest in MPM led to clinical trials with promising preliminary
results for several agents alone or in combination, including
gemcitabine, raltitrexed, vinorelbine, and pemetrexed. Pemetrexed, a
folate-based inhibitor of thymidylate synthase and other enzymes, is
currently under investigation in multiple malignancies. A phase I study
of pemetrexed in combination with cisplatin showed a remarkable response
rate of approximately 50% in patients with the epithelial subtype of
MPM. This led to a large international study of the combination of
pemetrexed plus cisplatin. Copyright 2002, Elsevier Science (USA). All
rights reserved.
6
UI - 12005126
AU - Rogers A; Major G
TI -
The quantitative risks of mesothelioma and lung cancer in relation to
asbestos exposure: the Wittenoom data.
SO - Ann Occup Hyg 2002 Jan;46(1):127-8; discussion 128-9
7
UI - 11108782
AU - Hodgson JT; Darnton A
TI -
The quantitative risks of mesothelioma and lung cancer in relation to
asbestos exposure.
SO - Ann Occup Hyg 2000 Dec;44(8):565-601
AD - Epidemiology and Medical Statistics Unit, Health and Safety Executive,
Magdalen House, Stanley Precinct, L20 3QZ, Bootle, UK.
john.hodgson@hse.gsi.gov.uk
Mortality reports on asbestos exposed cohorts which gave information on
exposure levels from which (as a minimum) a cohort average cumulative
exposure could be estimated were reviewed. At exposure levels seen in
occupational cohorts it is concluded that the exposure specific risk of
mesothelioma from the three principal commercial asbestos types is
broadly in the ratio 1:100:500 for chrysotile, amosite and crocidolite
respectively. For lung cancer the conclusions are less clear cut.
Cohorts exposed only to crocidolite or amosite record similar exposure
specific risk levels (around 5% excess lung cancer per f/ml.yr); but
chrysotile exposed cohorts show a less consistent picture, with a clear
discrepancy between the mortality experience of a cohort of xhrysotile
textile workers in Carolina and the Quebec miners cohort. Taking account
of the excess risk recorded by cohorts with mixed fibre exposures
(generally<1%), the Carolina experience looks uptypically high. It is
suggested that a best estimate lung cancer risk for chrysotile alone
would be 0.1%, with a highest reasonable estimate of 0.5%. The risk
differential between chrysotile and the two amphibole fibres for lunc
cancer is thus between 1:10 and 1:50.Examination of the inter-study dose
response relationship for the amphibole fibres suggests a non-linear
relationship for all three cancer endpoints (pleural and peritoneal
mesotheliomas, and lung cancer). The peritoneal mesothelioma risk is
proportional to the square of cumulative exposure, lung cancer risk lies
between a linear and square relationship and pleural mesothelioma seems
to rise less than linearly with cumulative dose. Although these
non-linear relationships provide a best fit ot the data, statistical and
other uncertainties mean that a linear relationship remains arguable for
pleural and lung tumours (but not or peritoneal tumours).Based on these
considerations, and a discussion fo the associated uncertainties, a
series of quantified risk summary statements for different elvels of
cumulative exposure are presented.
8
UI - 11414251
AU - Howie RM
TI -
Asbestos and cancer risk.
SO - Ann Occup Hyg 2001 Jun;45(4):335-6; discussion 336-8
9
UI - 12024881
AU - Waldron HA
TI -
Fairchild and the "guilty" fibre.
SO - Med Leg J 2002;70(Pt 2):87-8
10
UI - 12016043
AU - Clippe C; Freyer G; Bizollon MH; Raudrant D; Gilly F; Vitrey D; Ligneau
TI -
B; Trillet-Lenoir V
[Primary peritoneal tumors: report on a series of eight cases and review
of the literature]
SO - Bull Cancer 2002 Apr;89(4):430-6
AD - Unite fonctionnelle d'oncologie medicale, centre hospitalier Lyon-Sud,
69495 Pierre-Benite Cedex, France.
Primary peritoneal tumors are rare and yet not well-known malignancies.
We report here the clinical cases of 8 patients who were referred to our
institution with a primary peritoneal tumor, 4 serous carcinomas (PSC)
and 4 malignant mesotheliomas (PMM). Diagnosis was available in all
cases and reviewed by two pathologists. A battery of various
immunomarkers contributed to confirm the morphological diagnosis. All
patients underwent initial surgery with or without optimal debulking.
All of them received a platinum-based systemic chemotherapy.
Intraperitoneal treatment with cisplatin and hyperthermia was performed
in two cases. Four patients are dead (3 PSC, 1 PMM), two are alive (one
in partial remission (1 PSC) and one is having treatment (1 PMM)), one
is in complete remission (1 PMM) and one is lost to follow up (1 MMP).
PSC and PMM are difficult to distinguish since they share the embryonic
cOElomic epithelium as a common origin. The clinical presentations are
similar and usually include the detection of a pelvic mass and/or
diffuse peritoneal carcinomatosis with or without malignant ascites.
Therefore, the accuracy and reliability of the initial histological
examination is of crucial importance. Further attempts will be required
to better identify the most active therapeutic post-surgical
combinations, especially for PMM.
11
UI - 11676187
AU - Barbieri PG; Lombardi S; Candela A; Pezzotti C; Binda I
TI -
[Incidence of malignant mesothelioma (1980-1999) and asbestos exposure
in 190 cases diagnosed among residents of the province of Brescia]
SO - Med Lav 2001 Jul-Aug;92(4):249-62
AD - Servizio Prevenzione e Sicurezza degli Ambienti di Lavoro, Azienda
Sanitaria Locale Provincia di Brescia. clarar@tin.it
Several cases of malignant mesothelioma (MM) previously unknown to the
Occupational Health and Safety Service were recognised in the Province
of Brescia after an active surveillance program carried out during the
first nineteen years of operation; a large proportion of the cases
involved workers occupationally exposed to asbestos. A local
Mesothelioma Register was subsequently set up in 1993 and by the end of
1999, 190 MM cases had been collected. The annual incidence ratio
(standardized on the Italian population, census 1981, x100,000
person-years) was calculated in the 1980-1999 period and showed an
increasing trend for location in the pleura in both sexes; in the
1996-1999 period the incidence ratio was 2.95 for males and 1.35 for
females. In the same period, this trend was not observed for peritoneal
location, with an incidence ratio of 0.17 and 0.37 for males and females
respectively. 161 pleural MM (84.7%) and 28 peritoneal MM (14.7%) are
described; histopathologic diagnosis was performed in 161 cases (84.7%).
Anamneses were collected for 88% of the cases but with direct
information from patients only in 65% of these in the recent period.
Only 7 cases of asbestosis were diagnosed in the MM cases, whereas 31
cases of pleural abnormalities were observed but only 17 of these were
observed in workers occupationally exposed to asbestos. Occupational
asbestos exposure was evaluated as certain, probable or possible in 45%
of total cases and in 54% of recently (1996-1999) observed cases, which
were ten times more frequent in males. Exposure occurred in sectors
works where asbestos was not used as raw material, such as construction,
iron and steel and metal working. MM's from environmental and
non-occupational exposure to asbestos were very few, 1.5% and 0.5%
respectively. In 65 MM's asbestos exposure was unknown (34.2%); 50% of
these concerned females; for whom the industry and jobs are discussed.
The distribution of histologic types of MM was similar in asbestos
exposed and non exposed cases. No association between peritoneal
mesotheliomas and heavy exposure to asbestos was observed. Ten cases of
MM were diagnosed in subjects under 45 years old (5.2%) with only one
case occupationally exposed. 2 cases were exposed to radiation therapy
(1%) and 2 cases to thoracic trauma (1%). Although in Italy MM has been
included in the list of compensatable occupational diseases by law since
1994, a large number of cases occupationally exposed to asbestos are
still not recognised by the National Insurance Institute (INAIL). A
number of problems limiting work of the Mesothelioma Register and its
usefulness are discussed. The Lombardy Mesothelioma Register set up in
past.
12
UI - 12064559
AU - Kitamura F; Araki S; Suzuki Y; Yokoyama K; Tanigawa T; Iwasaki R
TI -
Assessment of the mutations of p53 suppressor gene and Ha- and Ki-ras
oncogenes in malignant mesothelioma in relation to asbestos exposure: a
study of 12 American patients.
SO - Ind Health 2002 Apr;40(2):175-81
AD - Department of Public Health and Occupational Medicine, Graduate School
of Medicine, The University of Tokyo, Japan.
In our previous study, we found no genetic alteration in exons 1 and 2
of Ha- and Ki-ras oncogenes nor in exons 5 to 9 of the p53 suppressor
gene in seven Japanese malignant mesothelioma patients exposed to
asbestos. To examine further whether malignant mesothelioma due to
asbestos has genetic alterations in the p53 suppressor gene and in Ha-
and Ki-ras oncogenes, we analyzed point mutations of these genes in
paraffin embedded operative open biopsied samples of the primary tumor
of malignant mesothelioma in twelve American patients. The genetic
analysis was conducted by the PCR-SSCP (polymerase chain reaction
single-strand conformation polymorphism) method in all patients and by
sequencing analysis of DNA bases in the two patients with suspected gene
mutation. The analysis of the p53 suppressor gene showed an amino acid
converting mutation of exon 7 in one patient and a polymorphism of exon
6 in another patient; the former patient was a heavy smoker with a
biphasic cell type. No genetic alteration was found in exons 1 and 2 of
Ha- and Ki-ras oncogenes in any of the patients. The results suggest
that the effects of asbestos on the p53 suppressor gene and Ha- and
Ki-ras oncogenes in malignant mesothelioma are negligible. Further
studies are needed to examine whether the observed mutation of the p53
suppressor gene is due to the combined effects of asbestos and smoking
or to other unknown factors.
13
UI - 12046609
AU - Friedman MT; Gentile P; Tarectecan A; Fuchs A
TI -
Malignant mesothelioma: immunohistochemistry and DNA ploidy analysis as
methods to differentiate mesothelioma from benign reactive mesothelial
cell proliferation and adenocarcinoma in pleural and peritoneal
effusions.
SO - Arch Pathol Lab Med 1996 Oct;120(10):959-66
AD - Long Island Jewish Medical Center, Department of Pathology, Albert
Einstein College of Medicine, New Hyde Park, NY 11040, USA.
OBJECTIVE: To determine whether malignant mesotheliomas can be
differentiated from adenocarcinomas and benign reactive mesothelial
cells in pleural and peritoneal fluids using immunohistochemical
analysis in conjunction with DNA ploidy analysis. DESIGN: Sixteen cases
of malignant mesothelioma, including epithelial, sarcomatous, and
biphasic types, were collected. DNA analysis using flow cytometry and/or
image analysis was performed on paraffin-embedded tissue from 15 of the
mesothelioma cases, as well as on cytospin cell preparations from
samples of pleural and peritoneal fluids from cases with either
cytologically proven adenocarcinoma (seven cases) or benign reactive
mesothelial cells (seven cases). Immunohistochemical studies were done
in 15 mesotheliomas, 5 adenocarcinomas, and 4 benign reactive
mesothelial cell effusions. RESULTS: All malignant mesotheliomas tested
(100%) stained positively for prekeratin, whereas stains for
carcinoembryonic antigen, B72.3, Leu-M1, and Ber-EP4 were negative.
Stains vimentin, epithelial membrane antigen, and CA125 were positive in
75%, 75%, and 25% of cases tested, respectively. Benign reactive
mesothelial cell cases stained similarly. Adenocarcinomas were more
likely to react positively with B72.3, Ber-EP4, and carcinoembryonic
antigen, and negatively with vimentin. DNA analysis showed that all
benign cases were diploid, while all adenocarcinomas were nondiploid.
Fifty-three percent of the malignant mesotheliomas were nondiploid.
Sensitivity for detection of nondiploidy was greater for image analysis
than for flow cytometry (100% vs 75%). CONCLUSIONS: B72.3, Ber-EP4,
carcinoembryonic antigen, and vimentin are useful immunohistochemical
markers in differentiating malignant mesotheliomas from adenocarcinomas,
whereas immunohistochemistry does not reliably distinguish malignant
from benign hyperplastic mesothelial cells. The addition of DNA ploidy
studies is useful for differentiating the latter two groups.
14
UI - 11937311
AU - van Meerbeeck JP; Baas P; Debruyne C; Smit EF; van Klaveren RJ;
TI -
Galdermans D; Lentz MA; Manegold C; Giaccone G; EORTC Lung Cancer Group
A phase II EORTC study of temozolomide in patients with malignant
pleural mesothelioma.
SO - Eur J Cancer 2002 Apr;38(6):779-83
AD - Erasmus MC-Department of Pulmonology, PO Box 5201, NL-3008 AE,
Rotterdam, The Netherlands. vanmeerbeeck@svlo.azr.nl
The aim of this study was to investigate the anti-tumour activity of
temozolomide in patients with malignant pleural mesothelioma. 27
chemotherapy-naive patients with histologically-proven malignant
mesothelioma were treated with temozolomide 200 mg/m2/day, given orally
on days 1-5 of each 28-day cycle. Therapy continued up to 10 cycles
unless disease progression or excessive toxicity mandated
discontinuation. Toxicity, symptom improvement and pain intensity were
regularly assessed. With a median relative dose intensity of 97%,
toxicity was moderate with grade 3 or more nausea, vomiting,
thrombocytopenia, leucocytopenia, neutropenia, febrile leucocytopenia,
arthralgia, infection and fever with infection occurring in 13, 13, 10,
3, 7 and 3% of patients for the remaining events, respectively. Overall,
1 objective response was observed (response rate 4%, 95% Confidence
Interval (CI): 0.1-19). Median survival was 8.2 months. Symptom
assessment showed no improvement and an increase of pain was observed
during the study. Thus, oral temozolomide is an inactive agent in
malignant mesothelioma.
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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