Pulmonary metastasectomy in soft tissue sarcoma (STS) can lead to long-term survival. The aim of our study was to report on prognostic factors and the value of repeat resection in recurrent disease.
Seventy-eight pulmonary metastasectomies were performed on 42 STS patients from 1990 to 2005. Overall survival time and 3-year survival rate were evaluated. Subgroup analysis was performed on age, primary tumor stage, histological type and grade, occurrence and recurrence pattern, systemic treatment and number of resections.
The 3-year actuarial survival rate was 31%. Primary tumor grade and repeat resections were shown to be independent prognostic factors for survival.
Patients with repeat resections due to recurrent metastasis show a significantly better prognosis than those with only one resection. Thus, lacking randomised controlled data of the natural course of patients with unresected lung metastases to compare these results, metastasectomy in STS patients is also recommended in recurrent disease.
Bisphosphonate therapy has become a standard of care for patients with malignant bone disease. In addition, preclinical and preliminary clinical data suggest that bisphosphonates may prevent cancer-treatment-induced bone loss (CTIBL) and the development of malignant bone disease in patients with early-stage cancer. Patients who receive adjuvant hormonal therapy for breast cancer or androgen-deprivation therapy for prostate cancer are at an especially high risk for CTIBL because of reduced estrogenic signaling. Oral clodronate (Bonefos; Anthra Pharmaceuticals; Princeton, NJ), oral risedronate (Actonel; Proctor and Gamble Pharmaceuticals, Inc.; Cincinnati, OH), and i.v. zoledronic acid (Zometa; Novartis Pharmaceuticals Corp.; East Hanover, NJ) have all demonstrated promise in preventing CTIBL in patients receiving hormonal therapy for breast cancer. Zoledronic acid has demonstrated efficacy with the longest between-treatment interval (3-6 months) and is currently being investigated in the Zometa/Femara Adjuvant Synergy Trials (Z-FAST and ZO-FAST in the United States and Europe, respectively). In patients receiving androgen-deprivation therapy for prostate cancer, i.v. pamidronate (Aredia; Novartis Pharmaceuticals Corp.) and i.v. zoledronic acid both have demonstrated significant benefits over placebo, but only zoledronic acid produced significant increases in bone mineral density compared with baseline values. Additionally, bisphosphonates have demonstrated antitumor activities in preclinical models, and clinical trials with oral clodronate suggest that bisphosphonates might prevent or delay bone metastasis in patients with early-stage breast cancer. Clinical trials are investigating the effect of zoledronic acid on disease progression in patients with breast cancer, prostate cancer, and non-small cell lung cancer. The results of these clinical trials should further define the clinical benefit of bisphosphonates in the oncology setting.
The effect of pipe and cigar smoking on lung cancer risk is reviewed using data from an ongoing hospital-based, case-control study of smoking-related cancers. Data from 2,085 patients with histologically defined lung cancer and 3,948 matched controls interviewed between 1977 and 1984 were analyzed. Cigar and pipe smokers experienced much lower lung cancer risks than cigarette smokers. Risk, expressed as the odds ratio in current smokers of cigarettes only, was 16.0 times that of never smokers (95% confidence intervals, 12.2 to 20.9), 3.1 times that of cigars only (1.8 to 5.6), 1.9 times that of pipes only (0.8 to 4.3), and 2.5 times that of cigars and pipes (1.0 to 6.1). Risks were high in mixed smokers of cigars, pipes, or cigars and pipes, who also smoked cigarettes, odds ratio 10.5 (7.7 to 14.4). Among pipe and/or cigar smokers only, patients with lung cancer were more likely than controls to have been long-time smokers of 5 or more cigars or 5 or more pipefuls per day and to have inhaled. The odds ratio for those smoking 5 to 9 cigars or pipes per day was 3.2 and for those smoking 10 or more units 6.7. The odds ratio of those cigar or pipe smokers who inhaled was 12.3. The proportion of Kreyberg I cancers was higher in cigar and pipe smokers than in cigarette smokers.
Leptomeningeal carcinomatosis (LC) is a detrimental complication of patients with non-small-cell lung cancer (NSCLC). The effect of epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs) on the clinical outcome of these patients, particularly those with EGFR mutations, has not been studied yet.
We searched the database for lung cancer patients diagnosed from 2003 to 2010 in one Asian medical center. NSCLC patients who also had LC diagnosed by either cytology or brain neuroimaging studies were identified. The treatments and clinical outcomes were reviewed.
Of 5526 lung cancer patients, we identified 212 (3.8%) NSCLC patients with LC. Most patients (88.7%) had adenocarcinoma histology, and 129 (60.9%) patients had been treated with at least one regimen of EGFR TKI before the diagnosis of LC. One hundred and twenty-four (58.5%) patients were treated with EGFR TKI, and 128 (60.4%) patients were treated with whole-brain radiation therapy (WBRT) after the diagnosis of LC. The median overall survival was 4.5 months (95% confidence interval, 3.5-7.3). Multivariate analysis suggested that EGFR TKI therapy, WBRT, and cytotoxic chemotherapy were independent predictors for longer survival. Mutational status of EGFR was evaluated in 101 patients, and 75 mutations (74.3%) were detected. Among the 75 patients with EGFR mutations, EGFR TKI therapy and cytotoxic chemotherapy after diagnosis of LC remained the independent factors predictive of extended survival in the multivariate analysis.
Treatment of LC with EGFR TKI, cytotoxic chemotherapy, or WBRT in selected patients is associated with prolong survival period. These treatment options, especially EGFR TKIs, should be studied in patients with EGFR mutation-positive NSCLC and LC.
Lung cancer is the most common cause of cancer death with unchanged mortality for 50 years. Only localized nonsmall-cell lung cancer (NSCLC) is curable. In these patients it is essential to accurately predict survival to help identify those that will benefit from treatment and those at risk of relapse. Despite needing this clinical information, prospective data are lacking. We therefore prospectively identified prognostic factors in patients with potentially curable lung cancer. Over 2 years, 110 consecutive patients with confirmed localized NSCLC (stages 1-3A) were recruited from a single tertiary center. Prognostic factors investigated included age, gender, body mass index (BMI), performance status, comorbidity, disease stage, quality of life, and respiratory physiology. Patients were followed up for 3-5 years and mortality recorded. The data were analyzed using survival analysis methods. Twenty-eight patients died within 1 year, 15 patients died within 2 years, and 11 patients died within 3 years postsurgery. Kaplan-Meier survival estimates show a survival rate of 51% at 3 years. Factors significantly (p < 0.05) associated with poor overall survival were age at assessment, diabetes, serum albumin, peak VO(2) max, shuttle walk distance, and predicted postoperative transfer factor. In multiple-variable survival models, the strongest predictors of survival overall were diabetes and shuttle walk distance. The results show that potentially curable lung cancer patients should not be discriminated against with respect to weight and smoking history. Careful attention is required when managing patients with diabetes. Respiratory physiologic measurements were of limited value in predicting long-term survival after lung cancer surgery.
In order to analyse the possible mode and pathways of adrenal metastases from lung cancer, the frequency of adrenal metastases ipsilateral and contralateral to the site of the primary cancer was investigated based on autopsied lung cancer cases. In 405 of 1,607 such cases, adrenal metastases could be found: on both sides, 234; ipsilateral only, 105; contralateral only, 66 cases. In the early stages of tumor progression, a striking difference can be seen between the two sides. Ipsilateral metastases were of significantly higher incidence in early metastatic tumor stages, but later, in cases having six or more involved organs, the ipsilateral/contralateral quotient reaches 1. It is postulated that in the early stages adrenal metastases from lung cancer probably develop mainly by lymphogenous, but later mainly by hematogenous routes.
We have studied the effects of two human pancreatic cancer and two human small cell lung cancer cell lines on clotting and platelet aggregation. Both pancreatic lines markedly shortened recalcification times and induced platelet aggregation. The lung cancer lines produced little shortening of recalcification times and no platelet aggregation. The clotting and aggregation activities of the pancreatic lines were further characterized. Recalcification times following the addition of cancer cell line material to plasmas deficient in factors VII and X were markedly prolonged, suggesting that the activity is due to tissue factor. Hirudin, an inhibitor of thrombin from the saliva of leeches, and rabbit polyclonal immunoglobulin G anti-bovine brain tissue factor inhibited both procoagulant and aggregation activities. Apyrase (an enzyme degrading ADP), diisopropylfluorophosphate (a serine protease inhibitor) and L-trans-epoxysuccinylleucylamido(4-guanidino)butane (a cysteine protease inhibitor) failed to inhibit these activities. Increasing concentrations of heparin inhibited platelet aggregation. Subcellular fractionation studies showed these activities to be localized to the plasma membrane. The association between mucin and the acceleration of clotting has been well described. The absence of mucin in electron micrographs of these pancreatic whole cells, membrane fractions, and shed microvesicles, as well as the failure of chaotropic agents (i.e., agents stripping material extrinsic to the cell membrane such as mucin) to abrogate this activity support these activities being intrinsic to the plasma membrane. These data strongly suggest that these activities are due to tissue factor which appears to be released as microvesicles in vitro. The release of tissue factor via microvesicles in vivo is one possible mechanism for the coagulopathy sometimes seen in patients with pancreatic carcinoma.
The effects of lung cancer on the abilities of blood monocytes to produce interleukin-1 and to mediate antitumor activity were examined. The functional integrity of blood monocytes was determined by their capacity to respond in vitro to a variety of activating agents and become tumoricidal, as assessed by a radioactive release assay and ability to produce interleukin-1 in vitro. The results show that the presence of lung cancer significantly increased the number of harvested blood monocytes and that the spontaneous tumoricidal activity of these monocytes was slightly high as compared to monocytes obtained from healthy donors. The production of interleukin-1 by monocytes of healthy donors and lung cancer patients was similar. Blood monocytes obtained from lung cancer patients were less cytotoxic against allogeneic A375 melanoma cells as compared with those of healthy donors subsequent to incubation with a soluble muramyl dipeptide analog or lipopolysaccharide, but were as tumoricidal as those from healthy donors when activated with lipophilic muramyl tripeptide (MTP-PE) entrapped in multilamellar liposomes. The finding that monocytes of patients with lung cancer can respond to MTP-PE encapsulated in liposomes, recommends the use of these liposomes in therapy of human lung cancer.
Pdcd4 (programmed cell death 4) gene is tumor suppressor which expression is frequently down-regulated in tumors, which is considered as a diagnostic and prognostic marker as well as promising target for anti-cancer therapy. Pdcd4 protein is a target for post-translational regulation by phosphorylation marking Pdcd4 for degradation. We questioned if Pdcd4 mRNA decline in human lung tumors is accompanied by proportional depletion of Pdcd4 protein. We found that Pdcd4 protein-to-mRNA ratio varies greatly in human lung cancer cell lines. In squamous cell carcinoma samples where Pdcd4 mRNA suppression was found to be a typical event, Pdcd4 protein level frequently remained unchanged or even up-regulated. Our studies demonstrate that at least in squamous cell carcinoma, alterations in Pdcd4 mRNA and protein levels are not directly linked, and this fact should be taken into consideration when developing Pdcd4-based anti-cancer therapeutic approaches.
To assess the feasibility, reproducibility, and accuracy of volumetric lung image guidance using different thoracic landmarks for image registration.
In 30 lung patients, four independent observers conducted automated and manual image registrations on Day 1 cone-beam computed tomography data sets using the spine, carina, and tumor (720 image registrations). The image registration was timed, and the couch displacements were recorded. The intraclass correlation was used to assess reproducibility, and the Bland-Altman analysis was used to compare the automatic and manual matching methods. Tumor coverage (accuracy) was assessed through grading the tumor position after image matching against the internal target volume and planning target volume.
The image-guided process took an average of 1 min for all techniques, with the exception of manual tumor matching, which took 4 min. Reproducibility was greatest for automatic carina matching (intraclass correlation, 0.90-0.93) and lowest for manual tumor matching (intraclass correlation, 0.07-0.43) in the left-right, superoinferior, and anteroposterior directions, respectively. The Bland-Altman analysis showed no significant difference between the automatic and manual registration methods. The tumor was within the internal target volume 62% and 60% of the time and was outside the internal target volume, but within the planning target volume, 38% and 40% of the time after automatic spine and automatic carina matching, respectively.
For advanced lung cancer, the spine or carina can be used equally for cone-beam computed tomography image registration without compromising target coverage. The carina was more reproducible than the spine, but additional analysis is required to confirm its validation as a tumor surrogate. Soft-tissue registration is unsuitable at present, given the limitations in contrast resolution and the high interobserver variability.
Small cellular lung carcinoma (SCLC) cell lines are susceptible to lysis by NK cells. SCLC, normally negative for MHC class I Ag, were rendered positive for HLA-A and -B Ag by two methods: treatment with IFN-gamma or transfection with HLA class I genes. Exposure to IFN-gamma induced high levels of class I Ag and reduced susceptibility to NK-mediated lysis. However, transfection with either HLA-A2, HLA-B27, or HLA-B27 with beta 2m did not result in reduced susceptibility to NK cells. These transfectants expressed amounts of HLA class I Ag comparable to those in IFN-gamma-treated, untransfected cells. Transfection with the beta 2m gene or plasmid alone neither influenced levels of surface class I Ag nor resulted in reduced susceptibility to lysis by NK cells. Thus, the effects of IFN-gamma on NK susceptibility can be dissociated from the induction of class I Ag.
A right heart metastasis of a small-cell lung cancer was found on the whole-body F-fluoro-deoxy-glucose positron emission tomography/computed tomography (F-FDG-PET/CT) of a 69-year-old smoker investigated for a right pulmonary mass discovered on chest radiography after a fracture of the right humerus. The PET scan showed an increased FDG uptake by the mass in the right lung and an intense, atypical focal activity of the right ventricle strongly suggestive of a neoplastic process. CT-guided lung biopsy revealed a small-cell lung cancer and myocardial biopsy confirmed the presence of a cardiac metastasis. The patient was treated with six cycles of chemotherapy followed by radiation therapy, which included the heart lesion. At follow-up PET/CT 2 months after the end of treatment, the abnormal cardiac uptake had disappeared, whereas increased FDG uptake persisted in the pulmonary residual mass.
A Phase Ia clinical trial was undertaken to evaluate and compare murine monoclonal antibody KS1/4 and KS1/4-methotrexate immunoconjugate in patients with Stage IIIB or IV non-small cell carcinoma of the lung. Six patients received KS1/4 alone and five patients received KS1/4-methotrexate conjugate. The maximal total dose received per patient in both groups was 1661 mg. Mild to moderate side effects in both groups included fever, chills, anorexia, nausea, vomiting, diarrhea, anemia, and brief transaminasemia. One patient who received antibody alone had an apparent acute immune complex-mediated reaction. Ten of 11 patients had a human anti-mouse response. Posttreatment carcinoma biopsies revealed binding of monoclonal antibody KS1/4 and deposition of C3d and C4c complement fragments. Monoclonal antibody binding and complement deposition correlated with increasing doses of infused antibody. There was one possible clinical response.
Lymphokine-activated killer (LAK) cells are a heterogeneous population of immune effector cells that nonspecifically destroy neoplastic cells but not normal cells. Although parenteral treatment with interleukin-2 (IL-2) alone or a combination of IL-2 and LAK cells reduces tumor load and prolongs survival in mice with pulmonary, peritoneal, or hepatic metastases, the effect of these treatments on brain metastases has not been studied. To determine in an animal model if intracerebral metastases would be protected by the immunologically privileged status of the brain, intracardiac and intravenous injections of 10(5) KHT sarcoma cells were performed in C3H mice to create brain and lung metastases, respectively. The mice were treated with adoptive immunotherapy to determine if efficacy seen in an extracerebral site could be reproduced in the brain, and if histological examination of these brains would reveal a significant degree of lymphocyte infiltration and cytolytic activity. Animals were treated with either parenteral IL-2 (7500 U three times daily on Days 3 to 7 after tumor injection), or IL-2 plus LAK cells (7500 U IL-2 times daily on Days 3 to 7, and 10(8) LAK cells intravenously on Days 3 and 6 after tumor injection), or IL-2 excipient (three times daily on Days 3 to 7 after tumor injection). As compared to control animals, pulmonary metastases on Day 14 after tumor injection were reduced or eliminated in animals treated with either IL-2 or IL-2 plus LAK cells (p less than 0.01). In these same animals, there was no reduction in the number of intracerebral metastases and no evidence of lymphocytic infiltration or cytolytic activity in the brain. This is the first study that reveals an organ-specific resistance to the treatment of metastases with adoptive immunotherapy, and affirms the concern that due to inadequate trafficking of endogenous or exogenous-activated lymphocytes or due to inadequate activation of in situ brain lymphoid precursors, there is no rejection of tumors in the brain. This information suggests that brain metastases in patients with systemic malignancies will not respond to intravenous treatment with LAK cells and IL-2, and that alternative forms of treatment are needed. Furthermore, this modification of a previously existing model of murine brain metastasis provides a method for concurrently evaluating the effectiveness of treatments for intra- and extracranial cancers.
Pleuroperitoneal shunts were implanted in 17 patients with intractable pleural effusions, 15 of which were malignant and 2 benign. Complicating factors included 13 instances of severe trapped lung and 3 cases of synchronous ascites. There was one hospital death. Palliation of dyspnea at rest was achieved in all patients, although 3 required oxygen with exertion. Four shunts became occluded between 1 and 10 months after placement. Two of these were replaced. The remaining conduits continued to function to the present or until the patients' deaths between 1 and 28 months. Shunting allowed hospital discharge and provided symptomatic relief in a group of patients in whom other approaches had failed or were not applicable.
The possibility that corticosteroids influence lung maturation was suggested in 1968 by Buckingham et al. and supported by studies mounted in humans and in rabbits by Liggins and Howie and by a collaborative study from the N.I.H. To our knowledge no reverse process, i.e. the regulation of adrenal function by the lung, has been postulated. In attempting to isolate ACTH from fetal lung we found peptides which depressed corticosterone production. Eventually, we isolated a group of peptides from rabbit fetal lung which showed potent inhibition of corticosterone production in rat adrenal cell suspensions. Using high-resolution reverse-phase HPLC and high-sensitivity gas-phase sequencing techniques the primary structure of one of these peptides has been determined and it was called corticostatin. The adult rabbit lung contains a large quantity of a very similar peptide, which elutes close to corticostatin but whose amino acid composition differs by a single glycine and possibly a serine. This peptide is also potently corticostatic. We have isolated homologous human peptides but these show no apparent corticostatic activity in rat adrenal cell suspensions. They do, however, show interesting effects on in vitro growth of lung cell lines.
NAMI-A (imidazolium trans-imidazoledimethylsulfoxidetetrachlororuthenate, ImH[trans-RuCl4(DMSO)Im]) is a new ruthenium compound active against lung metastasis of solid metastasizing tumors. We have tested this compound in mice with Lewis lung carcinoma or MCa mammary carcinoma in order to compare the effects on primary tumor and lung metastases with possible alterations of cell cycle distribution of tumor cells. We have also investigated whether there were unequal tissue accumulations of the compound itself at different dose levels ranging from 17.5 to 70 mg/kg/day given for six consecutive days. NAMI-A caused a reduction of metastasis weight larger than that of metastasis number; we explain this finding as the capacity of NAMI-A to selectively interfere with the growth of metastases already settled in the lungs. However, this specificity is not simply related to a larger concentration of NAMI-A in the lungs than in other tissues. Following i.p. treatment, NAMI-A rapidly disappeared from the peritoneal cavity; its low blood concentration may be caused by rapid renal clearance. These data provide further evidence for a selective anti-metastasis effect of the ruthenium complex NAMI-A. The reduction of lung metastasis is followed by a significant prolongation of the host's life-time expectancy, indicating a therapeutic benefit of NAMI-A on lung metastases from solid tumors.
We report a very rare occurrence of a primary collision tumor in the lung consisting of squamous cell carcinoma and T-cell lymphoma. A squamous cell carcinoma was diagnosed histologically following a transbronchial lung biopsy in a 71-year-old woman, but the other component was diagnosed histologically and immunohistochemically only on examination of the resection specimen. The malignant lymphoma was stained by the monoclonal antibody UCHL-1 (anti-D45RO) against T-lymphocytes but was not stained by the L26 (anti-CD20) antibody against B-lymphocytes. Immunostaining for CD3 was positive, confirming a T-cell lineage. Despite systemic chemotherapy, the patient died 7 months after operation, from progression of the lymphoma. Our case, which illustrates interesting attributes of collision tumors, consisted of an ordinary squamous cell carcinoma and a rare T-cell lymphoma arising in the lung, with the latter part of the combination dictating subsequent treatment and outcome.
Shortly before his death in 1995, Kenneth B. Schwartz, a cancer patient at Massachusetts General Hospital (MGH), founded The Kenneth B. Schwartz Center at MGH (http://www.theschwarzcenter.org/rounds.asp). The Schwartz Center is a nonprofit organization dedicated to supporting and advancing compassionate health care delivery, which provides hope to the patient and support to caregivers, and encourages the healing process. The center sponsors the Schwartz Center Rounds, a monthly multidisciplinary forum where caregivers reflect on important psychosocial issues faced by patients, their families, and their caregivers, and gain insight and support from fellow staff members. Ageism is a pervasive problem throughout society. It is rooted in language, attitudes, beliefs, behaviors, and policies. Aging profoundly influences physiology, challenging the medical community to accommodate but not discriminate. The elderly are at an increased risk of disease and disability. Sixty percent of cancer occurs in people aged 65 and older, and the population is aging. The treatment of cancer in the elderly is complicated by comorbidities and other physiological factors, particularly renal, bone marrow, and metabolic reserve. Caregivers have to treat patients in a manner that optimizes treatment and avoids anticipated harm. However, the caregiver is often faced with situations where they must balance their personal beliefs, professional values, and knowledge of medicine with their patients' preferences and needs. Discussion in the Rounds focused on age bias, drug toxicity, life prolongation, and symptom relief, with the role of the caregiver, and the relationship to the patient, being pivotal.
Inactivation of tumor-infiltrating lymphocytes by immunomodulating cytokines shed by tumor cells into the tumor local microenvironment might be a potential escape strategy of various tumors from immune-immediate killing. Here, we provide an analysis of the cytokine profile at the tumor site in patients with non-small cell lung cancer (NSCLC).
Using in situ hybridization (ISH), we determined the mRNA expression in lymphocytes and tumor cells for IL-2, INF-gamma, IL-12 (p40), IL-18, IL-4, IL-10, TGF-beta1, IL-1, IL-3, IL-8, granulocyte-macrophage colony-stimulating factor (GM-CSF), TNF-alpha, and TGF-alpha in five fresh pleural effusion samples and 18 tumor tissue samples of patients with NSCLC.
In pleural effusion as well as in tumor tissue of NSCLC patients, the mRNA expression of IL-4, IL-10, TGF-alpha, and TGF-beta1 was significantly higher than that of IL-2, IL-12, IL-18 and INF-gamma. In contrast, the analysis of tuberculosis pleural effusion samples revealed lower mRNA levels for all cytokines and did not show any significant difference among them.
The predominant mRNA expression of type II and immunosuppressive cytokines in pleural effusion and tumor tissue of NSCLC patients mirrors an immunosuppressive state in the immunological microenvironment. The present study may, therefore, help to elucidate mechanisms of tumor escape and contribute to the development of an effective immunomodulatory treatment of NSCLC.
To evaluate the relation between occupational dust exposure and lung cancer in tin mines. This is an update of a previous study of miners with high exposure to dust at four tin mines in southern China.
A nested case-control study of 130 male lung cancer cases and 627 controls was initiated from a cohort study of 7855 subjects employed at least 1 year between 1972 and 1974 in four tin mines in China. Three of the tin mines were in Dachang and one was in Limu. Cumulative total exposure to dust and cumulative exposure to arsenic were calculated for each person based on industrial hygiene records. Measurements of arsenic, polycyclic aromatic hydrocarbons (PAHs), and radon in the work sites were also evaluated. Odds ratios (ORs), standard statistic analysis and logistic regression were used for analyses.
Increased risk of lung cancer was related to cumulative exposure to dust, duration of exposure, cumulative exposure to arsenic, and tobacco smoking. The risk ratios for low, medium, and high cumulative exposure to dust were 2.1 (95% confidence interval (95% CI) 1.1 to 3.8), 1.7 (95% CI 0.9 to 3.1), and 2.8 (95% CI 1.6 to 5.0) respectively after adjustment for smoking. The risk for lung cancer among workers with short, medium, and long exposure to dust were 1.9 (95% CI 1.0 to 3.5), 2.3 (95% CI 1.3 to 4.1), and 2.3 (95% CI 1.2 to 4.2) respectively after adjusting for smoking. Several sets of risk factors for lung cancer were compared, and the best predictive model included tobacco smoking (OR=1.6, 95% CI 1.1 to 2.4) and cumulative exposure to arsenic (ORs for different groups from low to high exposure were 2.1 (95% CI 1.1 to 3.9); 2.1 (95% CI 1.1 to 3.9); 1.8 (95% CI 1.0 to 3.6); and 3.6 (95% CI 1.8 5 to 7.3)). No excess of lung cancer was found among silicotic subjects in the Limu tin mine although there was a high prevalence of silicosis. Exposures to radon were low in the four tin mines and no carcinogenic PAHs were detected.
These findings provide little support for the hypothesis that respirable crystalline silica induces lung cancer. Ore dust in work sites acts as a carrier, the exposure to arsenic and tobacco smoking play a more important part in carcinogenesis of lung cancer in tin miners. Silicosis seems not to be related to the increased risk of lung cancer.
Correct staging of non small cell lung cancer (NSCLC) is vital for appropriate management. Initial staging is usually performed with computerised tomography (CT), but increasingly functional imaging using integrated positron emission tomography and CT (PET/CT) is being used to provide more accurate staging, guide biopsies, assess response to therapy and identify recurrent disease.
A 73-year-old male with stage IV lung adenocarcinoma presented with leg swelling and clubbing of the fingers on both hands upon physical examination, and bone scintigrams demonstrated marked accumulation of 99mTc-MDP in the long bones adjacent to the patellae. A diagnosis of hypertrophic pulmonary osteoarthropathy associated with primary lung cancer was made. Radiofrequency ablation (RFA) was utilized for cytoreduction, because the patient refused chemotherapy. One-month follow-up CT scans revealed low density of the ablated area associated with ablation necrosis. Cytoreduction by RFA rapidly alleviated the arthralgia and swelling, but not the clubbing of fingers. Follow-up bone scintigrams demonstrated a reduction in patellar uptake after RFA.
Because completion pneumonectomy is a procedure reputed to place patients at risk, we reviewed our results with the objective of identifying factors that influence complications and survival.
In a 25-year period, 80 completion pneumonectomies were performed after first operations for 17 cases of benign disease and 63 cases of lung cancer (89% stages I and II), with 7 of the latter patients receiving postoperative radiotherapy. Completion pneumonectomy was performed in 18 cases of benign disease and 62 cases of lung cancer: 28 second primary cancers, 26 recurrent cancers, 3 metastases, and 5 primary cancers in patients previously operated on for benign disease.
No intraoperative deaths occurred. Postoperative mortality rates were 5% for the entire series, 6.4% for patients operated on for cancer, and 0% for patients operated on for benign diseases. Patients previously irradiated and those operated on for infectious disease were at risk for postoperative empyema and fistula formation. In the cancer treatment group the actuarial 5-year survival was 36%, without significant difference between patients with recurrent and second primary lung cancers. The actuarial 5-year survivals were 51% for patients with stage I disease, 42% for patients with stage II disease, and 18% for patients with stage IIIA disease (P <.05).
Completion pneumonectomy can be performed with an acceptable operative mortality rate and offers a second chance for cure to patients with cancer. Patients previously irradiated and those requiring completion pneumonectomy for infectious benign disease are at risk for postoperative complications.