[Differential diagnosis of lung cancer and tumor metastases to the lungs, bening lung tumor, pleural tumors, and encysted pleurisy].
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Diagnosis, Differential↗
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[Lung neoplasms. Observations on cases of emergency lung surgery and heart-lung function].
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Electrocardiography↗
Experimental studies of inhibitory factors to lung cancer: inhibitory effect of homologous lung tissue-adjuvant on metastatic lung tumors of mice.
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Animals↗
Bridge to lung transplantation with the novel pumpless interventional lung assist device NovaLung.
BACKGROUND: Worsening of lung failure in patients awaiting a lung transplantation might lead to ventilation-refractory hypercapnia and respiratory acidosis. Most transplant centers consider pretransplantation extracorporeal membrane oxygenation as a contraindication for lung transplantation because of the poor outcome. We have, for the first time, applied the novel pumpless interventional lung assist NovaLung for bridge to lung transplantation in patients with severe ventilation-refractory hypercapnia. We report on our initial experience. METHODS: Between March 2003 and March 2005, 176 lung transplantations were performed, of which 60% were high-urgency lung transplantations. Twelve of the high-urgency recipients had severe ventilation-refractory hypercapnia and respiratory acidosis. These patients were connected to the novel pumpless interventional lung assist NovaLung for bridge to lung transplantation. RESULTS: The length of interventional lung assist NovaLung support was 15 +/- 8 days (4-32 days). PaO2, pH, and PaCO2 levels in arterial blood prior to interventional lung assist NovaLung implantation were 71 +/- 27 mm Hg, 7.121 +/- 0.1, and 128 +/- 42 mm Hg, respectively. Six hours after interventional lung assist NovaLung implantation, PaO2, pH, and PaCO2 levels had changed to 83 +/- 17 mm Hg (ns), 7.344 +/- 0.1 (P < .05), and 52 +/- 5 mm Hg (P < .05), respectively. Four patients died of multiorgan failure, 2 patients before and 2 after lung transplantation. Thus, 10 out of 12 patients were successfully bridged to lung transplantation, and 8 are still alive (1-year survival, 80%). CONCLUSIONS: This report suggests that interventional lung assist NovaLung implantation is an effective bridge to lung transplantation strategy in patients with ventilation-refractory hypercapnia.
Acidosis, Respiratory↗
Evidence for cytotoxic T lymphocyte response against human lung cancer: reconstitution of antigenic epitope with peptide eluted from lung adenocarcinoma MHC class I.
BACKGROUND: Cancer-associated, major histocompatibility complex (MHC)-restricted peptide antigens have been elucidated in human melanomas and ovarian, breast, and renal carcinomas; but relatively little is known about lung cancer antigens. METHODS: To work toward delineation of lung cancer-associated antigens, we developed tumor infiltrating lymphocytes (TILs), peripheral blood mononuclear cell-derived cytolytic T cell lines (CTL), autologous lung cancer cell lines, and normal lung cell lines from 17 patients undergoing lung cancer resections. The TILs and CTL lines were subsequently evaluated for markers of activation and specific lysis of autologous or allogeneic lung cancer cell lines or both. RESULTS: Freshly isolated TILs contained a more activated T cell population compared with the patients' peripheral blood T cells as evidenced by an increased expression of HLA-DR, CD25, and CD45RO. TILs isolated from 15 patients lysed allogeneic lung cancer lines. TILs lysed autologous lung cancer but not autologous normal lung or Epstein-Barr virus transformed B cell lines (B-LCL) in 4 of 8 cases tested, suggesting tumor specificity. A CTL line (RHPBL57.1) was generated from peripheral blood mononuclear cells of an HLA-A24(+) patient by stimulation against an established HLA-A24(+) allogeneic lung cancer cell line. RHPBL57.1 lysed the lung cancer cell line in an HLA-A24-restricted manner. Moreover, RHPBL57.1 specifically lysed autologous B-LCL pulsed with peptides, eluted from MHC class I and isolated from the HLA-A24(+) lung cancer cell line. CONCLUSIONS: TILs isolated from patients with lung cancer are predominantly an activated population of T cells with evidence of tumor and MHC class I-restricted lysis. Furthermore, we provide evidence for a lung cancer-associated, MHC class I-bound peptide antigen(s) that reconstitutes the epitope recognized by a lung cancer specific CD8(+) T cell line derived from a patient with lung cancer.
Adenocarcinoma↗
Amiodarone causes acute oxidant lung injury in ventilated and perfused rabbit lungs.
Amiodarone (ADR), a new antiarrhythmic drug for life-threatening cardiac arrhythmias, causes pneumonitis or lung fibrosis in a sizeable minority of patients. The cause of lung damage is not known. We have shown that infusion of 10 mg amiodarone into the inflow circuit of ventilated and perfused rabbit lungs causes immediate increase in pulmonary artery pressure (mean +/- SEM) (from 13.6 +/- 1.2 to 40.6 +/- 9.5 mm Hg, p less than 0.01) and pulmonary edema with marked increase in the pulmonary generation of thromboxane and leukotrienes C4 and/or D4. Albumin (2 g%) in the perfusate prevents any increase in lung perfusion pressure or edema formation. When lung perfusion pressure increase is blocked with the combined cyclooxygenase and lipoxygenase inhibitor enolicam sodium (CG5391B, 35 microM in perfusate), significant lung edema still occurs after amiodarone, indicating that amiodarone causes increased alveolar-capillary membrane permeability. Addition of catalase (100 U/ml) or superoxide dismutase and catalase (100 U/ml each) to perfusate fails to protect from amiodarone lung injury. Immediate infusion of amiodarone (10 mg) into lungs ventilated with room air (ADR + RA) causes an increase in lung weight gain from baseline (delta W) of 5.7 +/- 1.5 g/min. Compared with ADR + RA, ventilation of lungs with 4% O2 (delta W = 0.7 +/- 0.3 g/min, p less than 0.05), pretreatment of rabbits for 3 days with butylated hydroxyanisole (BHA, 100 mg/kg/day i.p., delta W = 0.05 +/- 0.02 g/min, p less than 0.01), pretreatment of rabbits for 3 days with vitamin E (Vit E, 300 U/day orally, delta W = 0.6 +/- 0.2 g/min, p less than 0.05), or addition of N-acetylcysteine to the lung perfusate (NAC, 5 mM, delta W = 0.1 +/- 0.08 g/min, p less than 0.01) all protect from lung edema formation after amiodarone. Amiodarone (100 mg) also caused a marked increase in luminol-enhanced lung chemiluminescence, lung production of superoxide anion (O2-), and tissue levels of lung glutathione disulfide. These results suggest that amiodarone causes lung injury by an oxidant mechanism.
Amiodarone↗
The cat lung strip as an in vitro preparation of peripheral airways: a comparison of beta-adrenoceptor agonists, autacoids and anaphylactic challenge on the lung strip and trachea.
1 A new in vitro preparation, the isolated lung strip of the cat, is described for investigating the direct effect of drugs on the smooth muscle of the peripheral airways of the lung. The preparation comprises a thin strip of lung parenchyma which can be mounted in a conventional organ bath for isometric tension recording. Its pharmacological responses have been characterized and compared with the isolated tracheal preparation of the cat. 2 The lung strip exhibited an intrinsic tone which was relaxed by catecholamines, aminophylline and flufenamate. It was contracted strongly by histamine, prostaglandin F2alpha, acetylcholine, compound 48/80, potassium depolarizing solution and alternating current field stimulation. In contrast, the cat trachea was unresponsive to histamine and prostaglandin F2alpha and did not exhibit an intrinsic tone. 3 (-)-Isoprenaline and (-)-adrenaline were much more potent in relaxing the lung strip than the trachea. The potency order of relaxation responses to isoprenaline, adrenaline and (+/-)-noradrenaline in the lung strip was isoprenaline greater than adrenaline greater than noradrenaline but in the trachea was isoprenaline greater than noradrenaline greater than or equal to adrenaline. 4 beta2-Adrenoceptor selective agonists salbutamol and terbutaline were more potent in the lung strip than the trachea, suggesting beta2-adrenoceptors predominated in the lung strip. Propranolol was equipotent in inhibiting isoprenaline relexations of the lung strip and trachea, whereas practolol was much less effective in inhibiting lung strip than trachea, further supporting a predominance of beta2-adrenoceptors in lung strip and beta1-adrenoceptors in trachea. 5 Strong Schultz-Dale type contractions were elicited in both lung strips and trachea by Ascaris lumbricoides antigen in actively sensitized cats. The initial phase of the contractile response of the lung strip following challenge was shown to be due to histamine release and was absent in the trachea. The delayed phase of the contraction which took several minutes to develop in both the mepyramine-treated lung strip and trachea was not due to prostaglandins E1, F2alpha or bradykinin, the probable mediator being slow reacting substance of anaphylaxis (SRS-A). 6 It is concluded that the isolated lung strip of the cat is useful as an in vitro model for investigating the effect of drugs on the smooth muscle of the peripheral airways of the lungs.
Adrenergic beta-Agonists↗
Distribution and quantitation of lung parenchymal contractile tissue in ovine lentivirus-induced lymphoid interstitial pneumonia. Do tissue forces limit lung distensibility?
BACKGROUND: Lymphoid interstitial pneumonia (LIP) is frequently identified in sheep infected with the ovine lentivirus, maedi-visna virus (MVV). Functional consequences of this condition include a reduction in lung distensibility that cannot be explained by the density of surface forces within the lung parenchyma. A potential source of tissue forces to account for this functional deficit is the substantial parenchymal smooth muscle hyperplasia that is a feature of the lung pathology. This investigation examines the relationship between lung distensibility and the quantity and distribution of smooth muscle hyperplasia in MVV-induced LIP. EXPERIMENTAL DESIGN: Immunohistochemical localization of alpha-smooth muscle actin (ASMA) was used to identify parenchymal contractile tissue. The distribution and morphometric quantitation of ASMA in lung parenchyma was determined in normal sheep lungs and in lungs from sheep seropositive for MVV. The relationship between the volume density of ASMA in lung parenchyma (Vv'ASMA') and static lung compliance (Cst) and lung distensibility (K) was examined. RESULTS: In normal lungs, ASMA was expressed by typical smooth muscle cells surrounding airways and blood vessels, by cells at the alveolar septal tips protruding into the alveolar ducts, and, rarely, by individual cells within septa. In MVV-seropositive sheep with minimal histopathology, increased ASMA expression occurred in association with early interstitial infiltrates and was located both at septal tips and within septa. With more severe pathology, ASMA-expressing cells became organized into bundles within obviously thickened septa and septal tips. In maedi, Vv'ASMA' is negatively correlated with K and Cst (rs = -0.614; p < 0.005; and rs = -0.504; p < 0.025, respectively). However, partial correlation coefficients indicate that Vv'ASMA' and lung parenchymal tissue density (Vvt) are strongly interdependent. CONCLUSIONS: ASMA expression in normal sheep lung parenchyma follows a similar pattern of distribution to that described for human lungs. The quantity of ASMA in lung parenchyma in LIP associated with MVV infection is negatively correlated with lung distensibility; however, whether this is a causal association remains undetermined.
Actins↗
Compensatory growth of porcine right lungs after chronic rejection of transplanted left lungs.
Neonatal lung hypoplasia is frequently a fatal condition often associated with congenital diaphragmatic hernia. Unilateral lung transplantation rarely has been performed for this indication, although it is a potential solution. It is not known whether the transplant needs to function permanently or to act as a bridge until the native lung develops. It is also not known whether the native lung will grow in the face of an immunosuppressed state and chronic rejection of the transplanted lung. We therefore developed a porcine model of left lung rejection to study this. Infant swine underwent left lung transplantation. Chronic rejection occurred in all, resulting in nonfunction of the transplanted lung. The right lungs of these animals were compared with the right lungs of size-matched and age-matched control animals not given immunosuppressive treatment and not undergoing transplantation. There were no differences in terms of the functional residual capacity, airway compliance, and airway resistance among the groups. There was a significant increase in the pulmonary vascular resistance in the animals with transplanted lungs. There was also a significant increase in the lung weight in these animals. Unilateral pneumonectomies were done in 4 infant pigs to serve as controls. Three of the 4 did not survive the operation because of acute pulmonary failure. In conclusion, the study group exhibited evidence of compensatory growth that was not seen in the control animals, as shown by the increase in lung weight. This suggests that contralateral lung growth occurs in a growing animal, despite the effects of immunosuppression therapy and chronic rejection of the transplanted lung.
Animals↗
Increased soluble E-Selectin is associated with lung inflammation, and lung injury in hyperoxia-exposed rats.
The pulmonary damage caused by prolonged exposure to high oxygen concentrations is accompanied by lung inflammation, which may contribute to the expression of hyperoxic lung injury. In turn, adhesion molecules are crucial for initiating inflammatory responses. The goal of the present study was to investigate the association of contents of soluble adhesion molecules in plasma or alveolar fluids of hyperoxic rats with lung expression of adhesion molecules, lung inflammation and lung injury. We exposed adult Sprague-Dawley rats to > 95% oxygen for up to 60 h and measured the contents of intercellular adhesion molecule-I (ICAM-I) and E-Selectin in plasma and lung tissue expression of the same molecules, and we assessed lung myeloperoxidase (MPO) activties and lung water contents as indices of lung inflammation and injury, respectively. We also assessed ICAM-I content in lavage samples, because ICAM-I may be shed from the alveolar epithelium. Lung water was elevated at 60 h of hyperoxia-exposure, and this effect was preceded by increases in lung MPO activities. Lung ICAM-I expression was more than doubled at 48 h, although soluble ICAM-I contents were not elevated in plasma or lavage. Soluble E-Selectin was increased by more than 50% at 24 h of hyperoxia-exposure, while lung expressions of E-Selectin were not increased until 48 h. The sequence of the events observed in the present studies suggests that E-Selectin contributes to lung inflammation in hyperoxia and the acceleration of lung injury immediately following the inflammatory response suggests a pivotal role for inflammation in this injury.
Analysis of Variance↗
Impact of interstitial lung disease on surgical morbidity and mortality for lung cancer: analyses of short-term and long-term outcomes.
BACKGROUND: This study investigated postoperative morbidity, mortality, and the long-term survival for patients with lung cancer who have interstitial lung diseases. METHODS: A retrospective chart review of 931 patients with lung cancer who underwent pulmonary resection at Chiba University Hospital between 1990 and 2000 was undertaken. Interstitial lung disease was defined by medical history, physical examination, and abnormalities compatible with bilateral lung fibrosis on chest computed tomography or high-resolution computed tomography (36 patients: 3.9%, interstitial lung diseases group). The remaining 895 patients (96.1%) were categorized as non-interstitial lung disease group. RESULTS: The incidence of postoperative pneumonia and acute or exacerbation of interstitial pneumonia was higher in the interstitial lung disease group (all P <.05). Thirty-day mortality was statistically equivalent between the interstitial lung disease and the non-interstitial lung disease groups (P =.30). The 5-year overall survivals were 62.5% (non-interstitial lung disease) and 35.6% (interstitial lung disease). Respiratory failure was the second main cause of death after the recurrence of primary cancer in the interstitial lung disease group. The risk factors for long-term mortality were interstitial lung diseases, advanced pathologic stage, male sex, high age, and positive smoking history (all P <.05). CONCLUSIONS: Interstitial lung disease was a risk factor for developing postoperative morbidity and mortality and poor long-term survival due to the occurrence of respiratory failure.
Age Factors↗
Differential lung ventilation after single-lung transplantation for emphysema.
OBJECTIVE: To review outcome and cardiovascular and respiratory function after initiation of differential lung ventilation for acute severe native lung hyperinflation in patients who have had a single-lung transplant for end-stage emphysema. DESIGN: Retrospective review. SETTING: Cardiothoracic tertiary referral center. PARTICIPANTS: Thirteen patients who had differential lung ventilation for acute severe native lung hyperinflation, of a total of 132 patients who had a single-lung transplant for end-stage emphysema between 1988 and the end of 2000. INTERVENTIONS: None. measurements and main results: Thirteen patients had differential lung ventilation for acute severe native lung hyperinflation; 7 survived to 1 year after transplant. There was a highly significant (p = 0.0006) improvement in mean PaO(2) from 8.23 (95% confidence interval [CI], 6.15 to 10.3) to 16.6 (95% CI, 12.84 to 20.45) 1 hour after start of differential lung ventilation. The average ratio of estimated dynamic compliance in the native lung compared with the transplanted (donor) lung was 2.69 (95% CI, 1.75 to 3.62). CONCLUSION: In addition to previous case reports, this series shows that differential lung ventilation is an appropriate treatment for acute severe native lung hyperinflation. A difference in estimated effective dynamic compliance of > or = 2.69 between native and transplanted lung may require differential lung ventilation.
Adult↗
Second lung cancers in patients after treatment for an initial lung cancer.
BACKGROUND: Prospectively and retrospectively identified patient cohorts that were successfully treated for primary lung cancer have been followed to document the rate of development of and the effectiveness of treatment of second lung cancers. This review was performed to assess rates of second lung cancer development, factors associated with the development of these cancers, and the success of their treatment. METHODS: The MEDLINE database was searched to identify articles published in English concerning lung cancers, second primary cancers, treatment of these cancers, and patient survival. RESULTS: The risk of developing a second lung cancer in patients who survived resection of a non-small-cell lung cancer is approximately 1%-2% per patient per year. Approximately one half of the patients who develop second non-small-cell lung cancers can have these tumors resected. The median survival from diagnosis of a second lung cancer in these patients is between 1 and 2 years, with a 5-year survival of approximately 20% (range, 4%-32%). The average risk of developing a second lung cancer in patients who survived small-cell lung cancer is approximately 6% per patient per year. For patients who survived small-cell cancer, the risk increases from approximately 2% to greater than 10% per patient per year 10 years after initial treatment. Only 7% (range, 6%-12%) of patients treated for small-cell lung cancer survive 2 years or more. Survivors who continue to smoke cigarettes have an increased risk of developing a second lung cancer. CONCLUSIONS: In patients surviving an initial lung cancer, the cumulative risk for the development of a second primary lung cancer makes this cancer a common cause of death. The high risk of developing a second lung cancer makes patients with these cancers an important population for study of surveillance strategies and chemoprevention agents.
Carcinoma, Non-Small-Cell Lung↗
Lung transplantation for advanced bronchioloalveolar carcinoma confined to the lungs.
BACKGROUND: Bronchioloalveolar carcinoma (BAC) is a well-differentiated lung adenocarcinoma that has a tendency to spread chiefly within the confines of the lung by aerogenous and lymphatic routes and may therefore be amenable to local therapy. However, a high rate of local recurrence after lung transplantation was recently reported. We describe two patients with unresectable and recurrent extensive BAC limited to the lung parenchyma who underwent lung transplantation with curative intent. METHODS: Patients were chosen to receive lung transplants for BAC if they met the following criteria: (1) recurrent or unresectable BAC limited to the lung parenchyma without nodal involvement and (2) suitable candidate for lung transplantation. RESULTS: The first patient relapsed in the lungs at 9 months after transplantation. The pattern of disease suggested contamination of the new lungs at the time of implantation. Repeat lung transplantation was performed, with cardiopulmonary bypass and irrigation of the remaining upper airway. This patient has had no evidence of local or systemic tumor recurrence at more than 4 years since the second transplantation. The second patient underwent transplantation using the modified technique and expired 16 months after transplantation of other causes. An autopsy showed no evidence of recurrent BAC in the lungs or of metastatic lesions at any site. CONCLUSIONS: Lung transplantation may be an option for unresectable or recurrent BAC confined to the lungs. Isolation of the diseased lungs and the use of cardiopulmonary bypass during surgery may be important in this disease and should be studied further.
Adenocarcinoma, Bronchiolo-Alveolar↗
Expression of tumor necrosis factor receptors in human lung cancer cells and normal lung tissues.
The purpose of this study was to investigate the expression of tumor necrosis factor (TNF) receptors for the control of the biologic action of TNF-alpha in lung cancer cells and normal lung tissues. Lung cancer specimens and normal lung tissues were freshly obtained in pairs from 15 patients who underwent surgery for lung cancer. Thirteen lung cancer specimens expressed the 55 kDa TNF receptor messenger RNA (mRNA), whereas only six lung cancer specimens expressed the 75 kDa TNF receptor mRNA by Northern blot analysis. The 55 kDa and 75 kDa TNF receptors mRNA were detected in all and 11 normal lung tissues, respectively. All four lung carcinoma cell lines examined expressed the 55 kDa TNF receptor mRNA, but only RERF-LC-MS (MS) expressed both the 55 kDa and 75 kDa TNF receptors mRNA. Immunohistochemical examination revealed that lung cancer cells expressed the 55 kDa TNF receptor, but not the 75 kDa TNF receptor at the protein level. In normal lung tissues, the 55 kDa TNF receptor was detected in alveolar macrophages, bronchioles, and some small vessels. The 75 kDa TNF receptor was detected in alveolar macrophages. All four lung carcinoma cell lines examined exhibited the only 55 kDa TNF receptor. TNF-mediated tumor cell lysis was observed in all lung carcinoma cell lines that exhibited the 55 kDa TNF receptor except A549, which is a TNF-insensitive cell line. In surface binding assays, specific surface binding of TNF-alpha to TNF-insensitive cell line A549 was observed to be about half that of TNF-sensitive cell lines. We demonstrated the expression of two distinct TNF receptors in human lung cancer and normal lung tissue.(ABSTRACT TRUNCATED AT 250 WORDS)
Humans↗
Lung function decline in cystic fibrosis patients and timing for lung transplantation referral.
STUDY OBJECTIVES: To determine risk factors associated with an accelerated decline in lung function in cystic fibrosis (CF), and whether longitudinal changes in FEV(1) would be a better predictor of the need for referral for lung transplantation than any single value for FEV(1.) DESIGN: The rate of decline in pulmonary function was determined by standard linear regression from each patient's calendar year's best percentage of predicted FEV(1) (%FEV(1)) over at least 4 years, and patients were classified into three cohorts based on their rate of decline. Differences between groups in age, weight-for-age z score, gender, genotype, pancreatic status, diabetes, and the presence of various lung microbial isolates were analyzed. A subset of 30 patients referred for lung transplantation were further analyzed, and a prediction model for lung transplantation referral was created using the patient's rate of decline in lung function, the mean waiting time for donor organs, and the average level of lung function of patients prior to lung transplantation. PATIENTS: One hundred fifty-three patients with CF followed up at the Washington University Adult Cystic Fibrosis Center. RESULTS: Younger age, malnutrition, and concurrent infection with both Pseudomonas aeruginosa and Staphylococcus aureus were significant (p < 0.05) risk factors for rapidly declining lung function. Among patients with rapidly declining lung function, referral for lung transplantation would have occurred 8.4 months earlier than actual referral age (p < 0.05) if the prediction model had been used, possibly resulting in additional patient salvage in several cases. CONCLUSIONS: Rate of decline in lung function should be routinely evaluated in patients with CF, and a prediction model utilizing the rate of decline in %FEV(1), and the median regional waiting period for donor lungs for patients with CF may assist in the timing of referral for lung transplantation and more rapidly declining lung function.
Adult↗
Acute lung injury in lung allografts.
BACKGROUND: Acute alveolar injury is a pathologic description of a nonspecific response of the lung to an acute injury. It has been our experience that acute alveolar injury may be seen in transbronchial biopsy and open lung biopsy specimens from patients who have successfully undergone lung transplantation. Because no studies of the clinical significance of acute alveolar injury in lung transplant recipients are available in the literature, we reviewed the impact of this pathologic finding in patients who underwent transplantation in the Toronto Lung Transplant Program. METHODS: From November 1983 through December 1992, we retrospectively reviewed all transbronchial biopsies and open lung biopsies performed in lung transplant recipients. RESULTS: Of the 137 transplantations performed (53 single and 84 double) acute alveolar injury was observed in 21 single (34 of 173 transbronchial biopsy and 3 of 11 open lung biopsy) lung biopsy) and 22 double (38 of 415 transbronchial biopsy and 3 of 11 open lung biopsy) lung transplantations. We sought to explain this finding on the basis of the concurrent clinical scenario. Acute alveolar injury occurred most commonly in association with infection (52%) followed by postoperative period (19%) and acute (16%) rejection. Acute alveolar injury occurred as an isolated finding in 7% of patients. It occurred within the first 4 months after transplantation in 80% of cases. In 10 of 21 single lung transplantations and 12 of 22 double lung transplantations, acute alveolar injury was seen at least twice. However, no difference was found in mortality between such patients (6 of 10 single and 6 of 12 double lung transplantations) and patients with only one episode of acute alveolar injury. CONCLUSION: Acute alveolar injury is a relatively common finding in histologic specimens from patients with lung transplantation and is most commonly associated with infection.
Biopsy↗
Abnormal FHIT transcripts found in both lung cancer and normal lung tissue.
Occurrence of abnormal transcripts of the FHIT (fragile histidine triad) gene has been reported in various types of cancer. On the other hand, aberrant transcripts are sometimes found in non-neoplastic tissues, so the relationship between the presence of abnormal transcripts of the FHIT gene and cancer pathogenesis is controversial. We investigated alterations in the FHIT locus, detected by nested reverse transcription-polymerase chain reaction and/or allelic status, in 88 primary lung cancers and normal lung tissues, and 22 normal lung tissues with metastatic lung cancer as a control. The frequencies of abnormal transcripts were 59% in lung cancer, 35% in paired normal lung, and 64% in normal control lung; the difference in frequencies between lung cancer and paired normal lung was significant, while that between lung cancer and normal control lung was not. Sequence analysis revealed that there were no cancer-specific abnormal transcripts entirely missing two or more exons, nor were the abnormal transcripts of lung cancer identical with those of paired normal lung in the same individual. Furthermore, we found no correlation between loss of heterozygosity in the FHIT locus and occurrence of abnormal FHIT transcripts. These results suggest that the presence of abnormal FHIT transcripts, in terms of their frequency and variety, is not cancer-specific in lung carcinogenesis, and the abnormality may be mainly due to abnormal splicing and processing of the transcripts. To estimate the precise function of the FHIT gene, further study of the FHIT protein in lung carcinogenesis is needed.
Acid Anhydride Hydrolases↗