Cytological characteristics of pulmonary pleomorphic and giant cell carcinomas.

OBJECTIVE: To establish cytological features of pulmonary pleomorphic carcinoma (PC) or giant cell carcinoma (GC), we evaluated the cytological characteristics of these tumors using a multidisciplinary approach. STUDY DESIGN: Samples from 13 surgically resected and histologically confirmed PC or GC patients were collected from our institutes. Eight cases without prior chemotherapy before surgery were selected, and cytological features were analyzed. RESULTS: The background contained numerous lymphocytes and neutrophils. The tumor cells were arranged in flat loose clusters, but some were in fascicles. The shape of the tumor cell was spindle or pleomorphic, and the sizes of the tumor cells varied by more than 5-fold. The tumor cells had an abundant, thick and well-demarcated cytoplasm. The location of the nucleus was centrifugal, and the nucleus was oval or irregularly shaped. Multinucleated giant cells were frequently observed. The size of the nucleus was more than 5 times that of normal lymphocytes, and its size also varied by more than 5-fold. The nuclear membrane was thin, and nuclear chromatin was coarsely granular, while the nucleolus was single and round. CONCLUSION: PC or GC has characteristic cytological features, however, spindle cells tended to be hardly observed in cytological specimens in some cases.

New method for separation of subpopulations from a heterogeneous colon cancer cell line.

BACKGROUND: To understand the heterogeneity of human colon cancers, a new method to separate cancer subpopulations was developed. MATERIALS AND METHODS: Cells from a human colon cancer cell line, DLD-1, were seeded on an 8 microm pore membrane. After six hours, the cells which remained beneath the membrane as well as the cells which dropped onto the 24-well plate were collected. To clarify the differences between the two subpopulations, transepithelial electrical resistance (TEER) and immunocytochemistry were evaluated. RESULTS: Two subpopulations, clones D and A, were separated from DLD-1 with the newly developed method. Both subpopulations showed quite different TEER values and different arrangements of cell-cell contact. In addition, the distinct subcellular localizations of claudin family proteins and zonula occludens-1 (ZO-1) were identified. CONCLUSION: A new separation method to isolate colon cancer subpopulations was established in which the intercellular junctions differed. This method can be considered as a helpful tool in the investigation of colon cancer heterogeneity.

Decrease of telomeres and increase of interstitial telomeric sites in chromosomes of short-term cultured gastric carcinoma cells detected by fluorescence in situ hybridization.

BACKGROUND: Deletion or shortening of chromosomal telomeres is associated with cellular aging and carcinogenesis. Telomeric sites are interstitially located in chromosomes. To clarify the frequency of telomerase abnormalities in cancer and their relationship with any characteristics of gastric carcinomas, telomeric aberrations in eleven cultured specimens of human gastric cancer were investigated by cytogenetic analysis. MATERIALS AND METHODS: Chromosomal metaphase specimens, obtained by primary culture of cells from surgical specimens of eleven gastric cancer patients, were examined by fluorescent in situ hybridization (FISH) using all telomeric and chromosome 17 specific-telomeric DNA probes. The number of telomeric signals and interstitial telomeric signals (ITS) were counted. DNA ploidy was examined by flow cytometry. RESULTS: The mean telomere signal per nucleus (MTS) observed in peripheral blood lymphocytes (PBLs) of normal volunteers (n=10) was 71.3+/-3.9%. The MTS in the carcinoma cells (46.9+/-2.6%) was significantly lower than in PBLs (p<0.01). Although ITS were not observed in PBLs, the mean rate of ITS was 41.2+/-22.0%, and the mean rate of ITS per chromosome was 2.1+/-2.1% in the cancer specimens. In DNA aneuploid carcinoma cells, the MTS was significantly lower, the mean rate of ITS tended to be higher (p=0.072), and the mean rate of ITS per chromosome was significantly higher (p<0.05), than in DNA diploid lymphocytes. Histologically, the mean rate of ITS per chromosome in carcinomas with venous infiltrations was significantly greater than in those without (p<0.05). CONCLUSION: Deletion and interstitial translocation of telomeric loci of chromosomes were frequent alterations in gastric carcinoma cells and increased numbers of interstitial telomeric signals were associated with venous invasion.

Video-assisted thoracic surgery lobectomy reduces the morbidity after surgery for stage I non-small cell lung cancer.

OBJECTIVE: We conducted this study to evaluate the surgical invasiveness and the safety of video-assisted thoracic surgery lobectomy for stage I lung cancer. METHODS: Video-assisted thoracic surgery lobectomies were performed on 43 patients with clinical stage IA non-small cell lung cancer. We compared the surgical invasiveness parameters with 42 patients who underwent lobectomy by conventional thoracotomy. RESULTS: Intraoperative blood loss was significantly less than that in the conventional thoracotomy group (151+/-149 vs. 362+/-321 g, p<0.01). Chest tube duration (3.0+/-2.1 vs. 3.9+/-1.9 days) was significantly shorter than those in the conventional thoracotomy group (p<0.05). The visual analog scale which was evaluated as postoperative pain level on postoperative day 7, maximum white blood count and C-reactive protein level were significantly lower than those in the conventional thoracotomy group (p<0.05). The morbidity rate was significantly lower than that in the conventional thoracotomy group (25.6% vs. 47.6%, p<0.05). Sputum retention and arrhythmia were significantly less frequent than in the conventional thoracotomy group (p<0.05). We experienced no operative deaths in both groups. CONCLUSION: We conclude that video-assisted thoracic surgery lobectomy for stage I non-small cell lung cancer patients is a less invasive and safer procedure with a lower morbidity rate compared with lobectomy by thoracotomy.

Cytological characteristics of pulmonary large cell neuroendocrine carcinoma.

To establish cytological features of pulmonary large cell neuroendocrine carcinoma (LCNEC), we evaluated the cytological characteristics of LCNEC. Samples from 25 histologically confirmed LCNECs (14 touch imprint (TI) and 11 curettage) were analyzed. The findings were compared with those for seven small cell lung carcinomas. Cytological findings of TIs were as follows: Tumor cells were medium- to large-sized, round or polygonal, and nuclear polymorphism was observed. Some of the tumor cells had clearly identified cytoplasms, but naked nuclei were frequently observed. Nuclei were round, oval, or polygonal, and possessed thin and smooth nuclear membranes. The nuclear chromatin pattern was finely or coarsely granular. One or two nucleoli were observed in the nuclei, but were inconspicuous in some cases. Tumor cells appeared in clusters, and rosette formation was observed, but single cells were frequently observed also. Necrotic background and nuclear streaking were frequently observed. In brush or curettage specimens, the number of cells observed on a glass was small, but the findings were almost the same as those for the TI samples. TI samples have characteristic features, such as a neuroendocrine morphologic pattern, large cell size, abundant cytoplasm, finely or coarsely granular chromatin of the nucleus, and prominent nucleoli, and the diagnosis of LCNEC is possible. In brush or curettage specimen, the LCNEC diagnosis may be possible if a sufficient number of tumor cells are obtained.

Polymorphism in the thymidylate synthase promoter enhancer region is not an efficacious marker for tumor sensitivity to 5-fluorouracil-based oral adjuvant chemotherapy in colorectal cancer.

Thymidylate synthase (TS) is the target enzyme of 5-fluoropyrimidines. The TS gene promoter enhancer region (TSER) possesses tandem, repeated, regulatory sequences that are polymorphic in humans. This polymorphism has been reported to influence TS expression in vitro and in vivo. In this study, we assessed whether or not the TSER genotype is an efficacious marker for tumor sensitivity to 5-fluorouracil (5-FU)-based oral adjuvant chemotherapy for colorectal cancer. One hundred and thirty-five Japanese patients who received curative resection and 5-FU-based oral adjuvant chemotherapy were studied. TSER genotypes of the tumors were analyzed by PCR. The numbers of repeated sequences of representative bands were determined by direct sequence. The genotypes of two-/two-repeats (TSER 2/2), two-/three-repeats (TSER 2/3), three-/three-repeats (TSER 3/3), and three-/five-repeats (TSER 3/5) were found in 11 (8.1%), 32 (23.7%), 85 (63.0%), and 7 (5.2%) tumors, respectively. Patients were classified into two groups: TSER 2/2 or 2/3 group; and the TSER 3/3 group. The relationship between the TSER genotype group and disease-free intervals was analyzed by univariate and multivariate analyses. Five-year disease-free survivals of the TSER 2/2 or 2/3 group and the TSER 3/3 group were 77% and 75%, respectively (P = 0.89). Multivariate analysis revealed that stage was the only independent prognostic factor and that the TSER genotype did not have a prognostic significance (hazard ratio for TSER 3/3, 0.91; P = 0.84). In conclusion, TSER genotype is not an efficacious marker for tumor sensitivity to 5-FU-based oral adjuvant chemotherapy for Japanese colorectal cancer patients after curative resection.

Tumor dihydropyrimidine dehydrogenase in stage II and III colorectal cancer: low level expression is a beneficial marker in oral-adjuvant chemotherapy, but is also a predictor for poor prognosis in patients treated with curative surgery alone.

The aim of this study was to evaluate the prognostic significance of tumor dihydropyrimidine dehydroganase (DPD) in curatively resected colorectal cancer patients who received or did not receive oral 5-FU based-adjuvant chemotherapy. Among 182 patients with stage II-III colorectal cancers, 89 patients (adjuvant chemotherapy group) received oral 5-FU based-adjuvant chemotherapy, and 93 patients (surgery alone group) did not receive 5-FU. DPD expressions in the tumors and in the normal colonic mucosa were measured by enzyme-linked immunosorbent assays. The mean DPD expression of the tumors was significantly lower than that of the normal mucosa (54.4 +/- 40.4 versus 72.3 +/- 23.3 Unit/mg protein, P < 0.01). For survival analyses, we designated the cut-off value of tumor DPD as its median value (46.3). In the adjuvant chemotherapy group, high tumor DPD levels were associated with poor survival (HR, 5.24; P = 0.03). In the surgery alone group, high tumor DPD levels were associated with better survival (HR, 0.32; P = 0.02). In conclusion, tumor DPD level is an efficacious marker in oral 5-FU based-adjuvant chemotherapy for colorectal cancer; however, low tumor DPD predicts reduced survival in patients treated with curative surgery alone.

Comparative genomic hybridization analysis detected frequent overrepresentation of chromosome 3q in squamous cell carcinoma of the lung.

The aim of this study was to provide cytogenetic data about squamous cell carcinomas of the lung and to evaluate their characteristic alterations and histogenetic relations. We analyzed 41 squamous cell lung carcinomas by comparative genomic hybridization (CGH) technique. CGH was performed using directly fluorochrome-conjugated DNA. Chromosomal regions where the mean ratio fell below 0.75 were therefore considered to reflect DNA copy number loss (underrepresentation), whereas regions where the mean ratio exceeded 1.25 were considered gains (overrepresentations) in the tumor genome. Overrepresentations were considered to be high-level amplification when the fluorescence ratio exceeded 1.5. Chromosomal imbalances were observed in every case. Copy number gains frequently were detected at 3q, 5p, 8q, 12p, and Xq. Losses were found at 16p, 4q, 5q, 3p, 17p, and 16q. DNA amplifications were observed at 12 regions: 3q26.1-27, 8q13-23.1, 12p12.3-pter, 12q15, 2p14-16, 4q28-31.2, 5p13.1-pter, 6q21-22.3, 7p11.2-13, 13q21.2-32, 18p11.2-pter, and 20p11.2-pter. Gains on 3q were frequently detected not only in the more than 3 cm group (79%) but also in the 3 cm or less group (77%). The mean frequency of gained or lost chromosomal regions was 7.2+/-4.7 in the 3 cm or less group (n=13) and 10.2+/-6.3 in the more than 3 cm group (n=28) (P=0.4503). The mean frequency of gained or lost chromosomal regions was significantly higher in the carcinoma with lymph node metastasis group (12.5+/-7.6 regions) (n=12) than in the carcinoma without lymph node metastasis group (7.9+/-4.6) (n=29) (P=0.0251). In conclusion, an increased copy number at 3q may contribute to the development of squamous cell carcinoma of the lung.

Tumor dihydropyrimidine dehydrogenase expression is a useful marker in adjuvant therapy with oral fluoropyrimidines after curative resection of colorectal cancer.

PURPOSE: Dihydropyrimidine dehydrogenase (DPD) is the rate-limiting enzyme of 5-fluoropyrimidine (5-FU) catabolism. We examined whether tumor DPD expression is an effective marker in adjuvant therapy with oral fluoropyrimidines after curative resection of colorectal cancer. METHODS: We studied 89 patients with stage II-III colorectal cancers who had undergone curative resections and received oral 5-FU-based adjuvant chemotherapy. The levels of DPD expression in tumor and normal colonic mucosa were measured by an enzyme-linked immunosorbent assay. In 53 tumor samples, DPD enzymatic activity was also analyzed in order to evaluate the relationship between DPD expression and enzymatic activity. RESULTS: DPD expression significantly correlated with DPD enzymatic activity in these 53 tumors ( r=0.56; P<0.001). DPD expression in the tumors was significantly lower than in normal mucosa (47.1+/-30.8 and 56.4+/-18.5 U/mg protein, respectively; P<0.05). We designated the cut-off value of tumor DPD as its median value (46.0 U/mg protein). Patients with low DPD expression had longer disease-free intervals than those with high DPD expression according to univariate analysis ( P=0.026). In a multivariate analysis, low DPD expression was significantly and independently associated with better survival. CONCLUSIONS: Tumor DPD expression is a useful marker for use with adjuvant chemotherapy with oral fluoropyrimidines after curative resection of colorectal cancer.

Genetic analysis of radiation-associated rectal cancer.

Genetic aberrations in radiation-associated colorectal cancer have not been studied in detail. We analyzed genetic aberrations in five rectal cancers that developed long after radiotherapy had been performed for cervical cancer. Microsatellite instability (MSI) in tumors was examined at five loci: D2S123, D3S966, TP53, DCC, and BAT26. Mutation of simple repeat sequences within the hMSH3, BAX, and transforming growth factor Beta type II receptor ( TGFBetaRII) genes was examined by polymerase chain reaction and single-strand conformation polymorphism (PCR-SSCP). Mutation of p53 exons 5-8 was examined by PCR-SSP and direct sequencing. Mutations of the K- ras gene were analyzed by two-step PCR. No MSI was found in tumor specimens at any of the loci examined, and no mutations in the target genes were observed. K- ras mutation was detected in two carcinomas, but not in their irradiated normal mucosa, while p53 mutation was observed in another two carcinomas, but not in their irradiated normal mucosa. Our results suggest that the radiation-associated rectal carcinomas examined in this study did not develop through the mutator phenotype pathway; rather, tumorigenesis was probably mediated through the multistep carcinogenesis pathway.

Bcl-2 protein expression correlates with better prognosis in patients with advanced non-small cell lung cancer.

BACKGROUND: Regulation of apoptosis is an important mechanism during the development of tumors including non-small cell lung cancer (NSCLC). The aim of this study was to assess the relationship between p53 and bcl-2 expression and various clinicopathological features and survival in patients with NSCLC. MATERIALS AND METHODS: Histological specimens obtained from 120 patients with stage I-III NSCLC were examined immunohistochemically for p53 and bcl-2. RESULTS: Positive immunostaining for p53 was observed in 50 and for bcl-2 in 35 patients. Tumors with lymph node metastasis were significantly more likely to be bcl-2-positive. However, there was no correlation between p53 immunostaining and clinicopathological parameters. Cox proportional hazard multiple regression analyses identified gender, N status and bcl-2 expression as independent prognostic factors. When advanced stage tumors or tumors with lymph node metastasis were analyzed, a more favorable survival was noted in patients with bcl-2-positive tumors than those with bcl-2-negative tumors. CONCLUSION: Bcl-2 protein expression correlates with better prognosis in patients with advanced NSCLC.

Frequent gains of 20q and losses of 18q are associated with lymph node metastasis in intestinal-type gastric cancer.

BACKGROUND: The genetic aberrations associated with development and progression of gastric carcinomas (GCs) are poorly understood. The aim of this study was to identify chromosomal aberrations associated with the development and/or progression of intestinal-type GC. MATERIALS AND METHODS: Comparative genomic hybridization (CGH) analysis was applied to 36 intestinal-type GCs. We compared chromosomal aberrations detected by CGH analysis with clinicopathological parameters. RESULTS: Frequent gains of DNA copy number were found on 8q, 13q, 20q, 3q, 6q and losses were found on 17p, 18q in intestinal-type GCs. No significant differences were observed in the chromosomal aberrations between tumor stage, tumor location, peritoneal dissemination, liver metastasis or other distant metastasis. However, the frequencies of 20q12-13 gain and 18q21-22 loss were significantly higher in tumors with lymph node metastasis than in those without metastasis. CONCLUSION: Gains of 20q and losses of 18q may contribute to lymph node metastasis and the malignant phenotype in intestinal-type GCs.

Numerical aberrations of chromosome 17 and the p53 locus in small hepatocellular carcinomas.

To investigate numerical aberrations of chromosome 17 and the p53 locus in early stages of hepatocellular carcinoma (HCC), 12 fresh-frozen specimens of small HCCs (less than 30 mm in size) were examined by dual-color fluorescence in situ hybridization. We used a chromosome 17 alpha-satellite DNA probe and a p53 locus-specific DNA probe. We also performed immunohistochemical analysis for p53 protein in the same cases. Gain of chromosome 17 was the most frequently observed anomaly, present in 58% of cases, and deletion of the p53 locus was observed in 50% of cases. The combination of chromosome 17 gain and p53 locus deletion was observed in 33.3% of cases. However, overexpression of p53 protein was not observed in any specimens. Our results suggest that gain of chromosome 17 and deletion of the p53 locus could represent early genetic events, prior to overexpression of p53 protein due to mutation, in early stage HCC.

Chromosome 8 numerical aberrations in stage II invasive ductal carcinoma: correlation with patient outcome and poor prognosis.

Aberrations in chromosome 8 are common in breast cancer. However, the relationship between numerical aberrations of chromosome 8 and clinical behavior (especially prognosis) in breast cancer is not well understood. In this study, a total of 40 specimens of stage II invasive ductal carcinomas (IDCs) was analyzed by fluorescence in situ hybridization (FISH) with a chromosome 8 centromere-specific probe and DNA flow cytometry (stage IIA: 20 cases; stage IIB: 20 cases). All cases were followed for at least 5.7 yr (mean: 7.5 yr; median: 7.7 yr) after surgery or until death. Single (loss), double, and triple or more signals (gain) of chromosome 8 were found in 7.6 +/- 3.5% (range: 2-16%; median: 7%), 53.7 +/- 13.2% (range: 25-81%, median: 53%), and 38.7 +/- 13.2% (range: 17-65%, median: 38%), respectively, of tumors. The frequencies of chromosome 8 gain and disomy correlated with patient outcome (respectively p < 0.05 and p < 0.01). When median ratios of chromosome 8 loss, disomy, and gain were used as the cutoff values, the survival curves revealed that patients in the low-frequency group survived significantly longer than those in the high-frequency group for chromosome 8 gain (p < 0.05), and patients in the high-frequency group survived significantly longer than those in the low-frequency group for chromosome 8 disomy (p < 0.05). Poor prognosis was not associated with age, tumor size, lymph node metastasis, histologic type, TNM stage, estrogen-receptor status, progesterone- receptor status, or DNA ploidy. Our results suggest that the frequencies of chromosome 8 gain and disomy is a potentially useful parameter for predicting prognosis of stage II IDCs.

Clinical significance of nm23 expression and chromosome 17 numerical aberrations in primary gastric cancer.

The metastasis suppressor gene nm23 located on chromosome 17 might be one of the targets in deletions of chromosome 17. In this study, we analyzed the expression of nm23 and chromosome 17 aberrations in gastric cancer and assessed their clinicopathological and prognostic significance. In 103 gastric cancer patients, we examined nm23 expression by immunohistochemistry and detected chromosome 17 aberrations by fluorescence in situ hybridization. There was a significant difference in the expression of nm23 among differentiated histologic types (well > moderately > poorly) (p < 0.01). Negative expression of nm23 correlated with depth of invasion (p < 0.01), lymph node metastasis (p < 0.05), lymphatic invasion (p < 0.05), venous invasion (p < 0.05), poor prognosis (p < 0.05), and chromosome 17 loss (p < 0.05). Chromosome 17 aberrations broadly correlated with clinicopathological variables and were associated with poor prognosis (p < 0.05). Univariate analyses identified nm23 (p < 0.05), chromosome 17 aberrations (p < 0.05), tumor size (p < 0.01), depth of invasion (p < 0.0001), lymph node metastasis (P < 0.001), hepatic metastasis (p < 0.01), peritoneal dissemination (p < 0.01), and lymphatic invasion (p < 0.01) as significant prognostic factors. Multivariate analysis showed that expression of nm23 and chromosome 17 aberrations were not independent prognostic indicators. Our results indicate that negative expression of nm23 and chromosome 17 numerical aberrations correlate with tumor progression and poor prognosis but are not independent prognostic indicators.

Development of a novel cell-based assay to evaluate the malignant potential of cancer in vitro.

BACKGROUND: Metastasis is a leading cause of cancer death. To evaluate the complex metastatic process in vitro, an attempt was made to develop a cell-based assay (Can kit) that could evaluate the late stages of metastasis. MATERIALS AND METHODS: Two membrane chambers were set up of which the upper membrane chamber with 8 mum pores was covered with normal cell layers. Cancer cells were introduced to the upper chamber and after passing through the normal cell layers dropped through onto the lower chamber membrane where cancer colonies formed and were evaluated based on the reduction of transepithelial electrical resistance (TEER) with a Madin-Darby canine kidney (MDCK) cell monolayer. RESULTS: When two pairs of cancer cell lines, with different metastatic potentials in vivo, were applied to the Can kit assay, differences in potentials between the two cell lines in vitro were demonstrated. The reduction in the TEER was correlated with the total area of the cancer colonies and the production of matrix metalloproteinases (MMPs). CONCLUSION: A cell-based assay able to evaluate the malignant potential of cancer in vitro was developed and is considered to be useful for research and the clinical examination of cancer metastatic potential.

Surgical treatment for lung cancer in octogenarians.

PURPOSE: We conducted this study in order to determine how we should perform the surgical treatment for clinical stage I non-small cell lung cancer (NSCLC) in octogenarians. METHODS: Thirty-three octogenarians with clinical stage I NSCLC participated in this study. They were retrospectively divided into two groups: one group of 11 patients who underwent a lymph node dissection (ND group), and one group of 22 patients who did not undergo this procedure (ND0 group). We analyzed the surgical invasiveness, morbidity, mortality, and survival in both groups. RESULTS: The morbidity rate in the ND group (45%) was higher than that in the ND0 group (23%); however, the difference was no statistically significant (P = 0.1805). There was no significant difference in the overall survival rates of the two groups (P = 0.1647), and the median survival time of the ND0 group (76 months) was slightly longer than that of the ND group (26 months). There was no significant difference in local recurrence rate between the two groups (9.1% vs 4.5%, P = 0.6059). CONCLUSION: We thus conclude that a limited operation without lymph node dissection might be the best surgical treatment for carefully selected octogenarians with clinical stage I NSCLC.

Pulmonary tractotomy for a patient with traumatic penetrating lung injury: report of a case.

We report a case of traumatic hemopneumothorax caused by penetrating lung injury in a 26-year-old man. The patient underwent emergency thoractomy, which revealed hemorrhage in the lingular segment of the left lung. We found the bleeding point and controlled the hemorrhage using pulmonary tractotomy by inserting a linear stapler into the stab wound in the pulmonary parenchyma. The original technique of pulmonary tractotomy was performed for complete through-and-through injury by dividing the bridge of lung tissue between the aortic clamps. We were able to apply this procedure safely to stop bleeding from a stab wound that did not go through the lung. Thus, pulmonary tractotomy is an effective damage-control operation for the lung with obvious advantages over major lung resection.

Postoperative complications of pulmonary resection after platinum-based induction chemotherapy for primary lung cancer.

PURPOSE: We investigated the postoperative complications that developed in patients who underwent surgery after induction chemotherapy (IC) for primary lung cancer. METHODS: Twenty-seven patients underwent surgery after receiving IC; for advanced non-small cell lung cancer in 16, and for small cell lung cancer in 11. All patients were given the platinum-based chemotherapy regimen. RESULTS: Lobectomies were performed for 18 patients, bilobectomies for 4, pneumonectomies for 2, and partial resections or segmentectomies for 3. There were two postoperative deaths; one caused by adult respiratory distress syndrome (ARDS) and one caused by respiratory failure, resulting in a mortality rate of 7.4%. The postoperative complications included sputum retention in six patients, ARDS in two, anastomotic dehiscence after bronchoplasty in one, and pneumonia in one, resulting in 44.4% morbidity. The morbidity of patients who had received IC (IC group) was higher than that of a comparative group of 560 who underwent lung resection without IC during the same period (non-IC group), but the difference was not significant (44.4% vs 22.6%; P = 0.16). Both ARDS and bronchial insufficiency occurred more frequently in the IC group than in the non-IC group, but the differences were not significant ( P = 0.25). CONCLUSIONS: These findings indicate the feasibility of treating primary lung cancer with IC followed by surgery as long as a cautious operative procedure is used and careful postoperative management is given, paying particular attention to the risk of ARDS and bronchial complications.

Detection of p53 gene mutations by nonisotopic RNase cleavage assay as a predictor of poor prognosis in colorectal cancers.

The present study was undertaken to evaluate p53 gene mutation as a prognostic factor in patients with colorectal cancer. Nonisotopic RNase cleavage assay (NIRCA), recently used for detecting gene mutations, was employed to detect p53 gene mutations in this study. In 15 samples of colorectal tumors, NIRCA was confirmed to be simple, accurate, and thus useful for clinical use, compared with polymerase chain reaction single-strand conformational polymorphism (PCR-SSCP). In another group of 79 cases of colorectal cancer analyzed for p53 gene mutation by using NIRCA, mutations were detected in 58 of 79 (73.4%) cases. Multivariate Cox proportional-hazards analysis showed that p53 gene mutation was a significant prognostic factor in patients with colorectal cancer. Our results showed that NIRCA is a simple and sensitive method, and thus useful for genetic screening of colorectal cancer. Furthermore, our results showed that p53 gene mutation is an independent predictor of poor prognosis in colorectal cancers.