Journal Thoracic Oncology

Abstracts Journal of Thoracic Oncology • Volume 12 Issue S1 January 2017
patient is now alive healthily in his 8th year postoperatively, Conclusion:
Giant SFTP is rare, easily to be misdiagnosed to malignant mesothelioma,
losing opportunity of being cured. Biopsy is the key point to make a right
diagnosis. Giant SFTP, benign or malignant, usually is operable; complete en
bloc resection of the whole tumor and enough resection of originated visceral
pleura and lung tissue is the key point to avoid recurrence, to cure SFTP. (This
study was partly supported by Science Foundation of Shenyang City, China,
No. F16-206-9-05).
Keywords: SOLITARY FIBROUS TUMOR OF THE PLEURA, traditional standard
posterolateral thoracotomy, Mesothelioma, biopsy
POSTER SESSION 2 – P2.04: MESOTHELIOMA/THYMIC MALIGNANCIES/ESOPHAGEAL
CANCER/OTHER THORACIC MALIGNANCIES
ESOPHAGEAL CANCER AND OTHER MALIGNANCIES –
TUESDAY, DECEMBER 6, 2016
P2.04-051 PALLIATIVE TREATMENT OF DYSPHAGIA SYNDROME IN
PATIENTS WITH GASTROESOPHAGEAL CANCER
Anatoliy Kasatov 1 , Irina Schetkina 2 , Iuliia Trefilova 3
1 Hospital Surgery Department, Perm State Medical University Named After
Acad. E.A. Vagner” Ministry of Healthcare of Russia, Perm/Russian Federation,
2 Toracic Surgery, Ministry of Healthcare of Perm Region State Budget Health Care
Establishment“Ordena “Znak Pocheta” Perm Regional Clinical Hospital”, Perm/
Russian Federation, 3 Hospital Surgery Department, “Perm State Medical University
Named After Acad. E.A. Vagner” Ministry of Healthcare of Russia, Perm/Russian
Federation
Background: Cancer of esophagus and cardia takes the 7th place in the
structure of oncological diseases in Russia and the 3rd place among tumors
of gastrointestinal tract. Despite the development of modern methods of
diagnosis, esophageal cancer is often detected only when a clear obstruction
of the esophagus happens, in stages IIIB and IV. Distant metastasis and
the advance of cancer at the moment of diagnoses make it impossible to
provide definitive therapy. In this case, therapy which is aimed to reduce the
esophagus obstruction becomes particularly relevant. The surgical approach
also remains relevant, either the open surgery specifically gastrostomy
including endoscopic one or endoprosthesis of esophagus with intraluminal
stenting is preferable. Methods: In total 167 patients with dysphagia
complaints of different severity were hospitalized to the department
of Thoracic Surgery of Perm Regional Clinical Hospital during the period
of 2013-2015. In 57.9% cases (96 patients) the esophageal squamous cell
cancer was the reason of dysphagia, and in 42.1% cases (71 patients) it was
adenocarcinoma of cardia with junction to lower third of esophagus. The
patient’s mean age was 62.8 years. Results: Aphagia was revealed in 18.5%
cases and 78.2% of patients could only drink. All patients reported a decrease
in body weight due to malnutrition.Stages IIIB and IV cancer were diagnosed
in 118 (70.7%). Endoscopic gullet bougienage with intraluminal self-expanding
stenting was performed in 122 patients. Four patients with IIB and IIIA stages
of esophagus cancer had the stents because of the severe comorbidity that
disables definitive surgical treatment. In 28 patients (22.9%) the migration
of the stent was diagnosed, in 10 of them (8.1%) the re-stenting was required
later; in the remaining 18 patients the correction during the first day after
stenting was enough. All patients declared a decrease in dysphagia starting
from the 2nd day after stenting. The absence of dysphagia at time of hospital
discharge was reveled in 82.9% cases. Mean life span of patients after
stenting was 9.58 months.Only in 1 case (0.8%) the cardia cancer bleeding was
diagnosed 3 days after stenting and one patient (0.8%) with the bougienage
of tumor and stenting had complication in form of esophageal perforation.
The mean duration of hospitalization was 7.6 days. Conclusion: Therefore,
esophageal endoprosthesis is a highly effective, minimally invasive treatment
for dysphagia in incurable oncologic patients with dysphagia that makes
self-enteral feeding capable, provides adequate nutritional support, and
significantly improves the quality of life.
Keywords: dysphagia, esophageal endoprosthesis, esophageal cancer,
palliative treatment
POSTER SESSION 2 – P2.04: MESOTHELIOMA/THYMIC MALIGNANCIES/ESOPHAGEAL
CANCER/OTHER THORACIC MALIGNANCIES
ESOPHAGEAL CANCER AND OTHER MALIGNANCIES –
TUESDAY, DECEMBER 6, 2016
P2.04-052 PROMOTER HYPERMETHYLATION OF DNA MISMATCH
REPAIR GENE HMLH1 OF LUNG CANCER IN CHROMATE-EXPOSED
WORKERS
Mitsuhiro Tsuboi 1 , Kazuya Kondo 2 , Koichiro Kajiura 3 , Hiromitsu Takizawa 3 ,
Toru Sawada 4 , Naoya Kawakita 4 , Hiroaki Toba 4 , Yukikiyo Kawakami 4 ,
Mitsuteru Yoshida 1 , Akira Tangoku 4
1 Department of Thoraci,endocrine Surgery and Oncology, Institute of Biomedical
Sciences, Tokushima University Graduate School, Tokushima City/Japan,
2 Department of Oncological Medical Services, Institute of Biomedical Sciences,
Tokushima University Graduate School, Tokushima City/Japan, 3 Department
of Thoracic, Endocrine Surgery and Oncology, Institute of Biomedical Sciences,
Tokushima University Graduate School, Tokushima City/Japan, 4 Department of
Thoracic and Endocrine Surgery and Oncology, Institute of Health Biosciences, the
University of Tokushima Graduate School, Tokushima/Japan
Background: Although it is known that chromium is an important inhaled
carcinogen for lung cancer, there are few reports about genetic effects of
chromium in oncogenic process. Our previous studies revealed that chromate
lung cancer frequently had microsatellite instability (MSI), and that MSI was
associated with the loss of expression of MLH1, which is one of the essential
DNA mismatch repair proteins. Inactivation of MLH1 due to promoter
methylation causes high level of microsatellite instability in hereditary
nonpolyposis colorectal cancer (HNPCC). Therefore, we hypothesized
that loss of expression of MLH1 in chromate lung cancer is caused by MLH1
promoter methylation similar to HNPCC. In the present study, we analyze
DNA methylation of MLH1 promoter regions in chromate and non-chromate
lung cancers and clarify whether methylation of MLH1 has the influence on
MLH1 protein expression and MSI. Methods: Thirty-three tumor samples
from chromate workers with lung cancer and thirteen tumor samples from
lung cancer patients without chromate exposure (non-chromate group)
were obtained. DNA was extracted from chromate and non-chromate lung
cancer and bisulfite pyrosequencing was used to examine DNA methylation
levels of MLH1 promoter regions. MSI, MLH1 protein expression of these
tumor samples have been investigated in our previous studies. Results: High
methylation levels of MLH1 promoter regions were found in 42.4% (7/33)
of chromate lung cancers and 15.4% (2/13) of non-chromate lung cancers.
Methylation rates of MLH1 promoter region and the grade of MSI were related
to positive correlation in chromate lung cancers. Immunohistochemistry for
MLH1 was performed in 24 chromate lung cancer, High methylation of MLH1
was found in 27.3% (3/11) of tumors with repression of MLH1 protein and
4.3% (1/13) of tumors with normal expression of MLH1 protein. Conclusion:
According to the present data, DNA methylation of MLH1 promoter regions
might contribute to loss of expression of MLH1 protein and MSI. We speculate
that in addition to genetic changes, epigenetic events have emerged in
chromium carcinogenesis.
Keywords: microsatellite instability, MLH1, promoter methylation, chromium
POSTER SESSION 2 – P2.04: MESOTHELIOMA/THYMIC MALIGNANCIES/ESOPHAGEAL
CANCER/OTHER THORACIC MALIGNANCIES
ESOPHAGEAL CANCER AND OTHER MALIGNANCIES –
TUESDAY, DECEMBER 6, 2016
P2.04-053 SURGERY OF MULTIPLE LUNG METASTASES IN PATIENTS
WITH SARCOMAS AND EPITHELIAL TUMORS
Evgeny Smolenov 1 , Yury Ragulin 1 , Vladimir Usachev 1 , Aleksey Starodubtcev 2 ,
Aleksander Popov 3 , Aleksander Kurilchik 2 , Ivan Zaborskiy 3
1 Thoracic Department, Medical Radiological Research Center, Obninsk/Russian
Federation, 2 Radiology Department, Medical Radiological Research Center,
Obninsk/Russian Federation, 3 Urology Department, Medical Radiological Research
Center, Obninsk/Russian Federation
Background: Pulmonary metastases are the most common recurrences
of bone or soft tissue sarcomas and epithelial tumors. A role of surgical
treatment in management of multiple lung metastases has not been
well-established. We aimed to assess the rates of early post-operational
complications and survival outcomes after pulmonary resection for multiple
metastases. Methods: A series of patients who underwent pulmonary
resections for multiple metastases (≥4) between January 2004 and December
2015 in Medical Radiological Research Center (Obninsk, Russia) were
retrospectively evaluated. Perioperative clinical and histopathological data
and long-time survival were analyzed. Results: Forty seven patients who
received surgical treatment for multiple lung metastases were included in
the analysis (24 males). Mean age was 44 years (range 18-70). Twenty nine
patients had primary diagnosis of bone or soft tissue sarcoma and 18 patients
had epithelial tumors. All subjects received radical surgical treatment of
primary cancer in combination with radiation therapy (in 25 subjects) or
chemotherapy (in 35 subjects). The mean time to detection of lung metastasis
was 15 months. Bilateral lung involvement was identified in 32 patients.
Eighty four operations were performed (76 atypical resections, 6 lobectomy,
1 segmentectomy and 1 pneumonectomy). In average, 6 lesions were removed
(range 4-103). Nd:YAG laser (length of wave 1318nm) used in 44 operations and
electrocautery in 32 cases. In case of bilateral lesions surgical interventions
were performed 4-6 weeks apart. In 4 patients metastatic process was
not confirmed (tuberculosis, fibrosis and necrosis). Early postoperative
complications were observed in 7 subjects (5 cases of pneumothorax,
durable lymphorrhea and phlebothrombosis. The rate of postoperative
complications were similar when laser (3/44) or electrocautery (4/32) were
used. There was no mortality within 30 days post operation. Mean survival
Copyright © 2016 by the International Association for the Study of Lung Cancer
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