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INTRODUCTION AND AIM: Despite the improvement in survival among patients with lung cancer as a result of the development of novel treatment options, acute respiratory failure (ARF), which may occur because of the disease itself, comorbidities or complications in treatment may be life threatening. The most commonly utilised treatment option in cancer patients with ARF is invasive mechanical ventilation (IMV). The prognosis of lung cancer patients admitted to the intensive care unit is poor. The use of non-invasive mechanical ventilation (NIMV) in the setting of ARF not only supports the respiratory muscles and facilitates alveolar ventilation and airway patency, but also reduces the risk of serious complications of IMV, such as ventilator-associated pneumonia. NIMV treatment in the event of respiratory failure has been associated with a high rate of mortality in recently diagnosed or progressive lung cancer with organ failure. However, studies in this regard are limited, and the role of NIMV has yet to be investigated in patients in hospital wards. Accordingly, the present study investigates retrospectively the success of NIMV among patients with lung cancer (including all stages and histopathological types) in a hospital ward setting and the influential factors. MATERIAL AND METHOD: The data of 42 patients with lung cancer and respiratory failure who were admitted to the palliative care service and received NIMV between 2014 and 2018 were reviewed retrospectively. Demographic features, comorbidities, respiratory failure types, rate of withdrawal from NIMV, frequencies of tracheostomy and intubation, bacteriologic examination of the airway samples, rate of discharge from hospital and any history of NIMV/USOT use at home were recorded. NIMV success was defined as the discharge of the patient from the hospital, with or without a respiratory support device. The primary end-point of the study was NIMV success, while the secondary end-point was NIMV success with respect to the underlying diagnosis and respiratory failure type. RESULTS: A total of 42 patients (38 males and 4 females) were included in the study, with a mean age of 67.4 ± 9.5 years. The rate of discharge from hospital was 71% across the entire study population, among which, 13 (31%) were discharged with USOT and 16 (38.1%) with NIMV. Among the 12 patients under palliative supportive treatment, 8 were discharged from the hospital. The success rates of NIMV in the respiratory failure aetiological subgroups were: 66% (12 patients) in the pneumonia subgroup and 71.4% (15 patients) in the COPD subgroup. The difference between these subgroups was not significant (P = .841). The success rate of NIMV in the hypercapnic and hypoxaemic respiratory failure subgroups was 72.7% (24 patients) and 66.6% (6 patients), respectively. There were no significant differences between the type of respiratory failure subgroups (P = .667). The success rate of NIMV was similar in patients with a positive airway sample microbiology (71.4%, n = 14) and those with no growth identified in the culture (70.3%, n = 28) (P = .834). CONCLUSION: In lung cancer patients with no contraindication, NIMV can be used to reduce or postpone the need for ICU admission, independent of disease stage, cellular type and underlying cause.
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Neoplasias Pulmonares , Ventilação não Invasiva , Insuficiência Respiratória , Idoso , Feminino , Humanos , Hipercapnia , Neoplasias Pulmonares/complicações , Neoplasias Pulmonares/terapia , Masculino , Pessoa de Meia-Idade , Respiração Artificial , Insuficiência Respiratória/etiologia , Insuficiência Respiratória/terapia , Estudos RetrospectivosRESUMO
Gangliosides are carbohydrate-containing sphingolipids that are widely expressed in normal tissues, making most subtypes unsuitable as targets for cancer therapy. However, the disialoganglioside GD2 subtype has limited expression in normal tissues but is overexpressed across a wide range of tumors. Disialoganglioside GD2 can be considered a tumor-associated antigen and well-suited as a target for cancer therapy. Disialoganglioside GD2 is implicated in tumor development and malignant phenotypes through enhanced cell proliferation, motility, migration, adhesion, and invasion, depending on the tumor type. This provides a rationale for targeting disialoganglioside GD2 in cancer therapy with the development of anti-GD2 monoclonal antibodies and other therapeutic approaches. Anti-GD2 monoclonal antibodies target GD2-expressing tumor cells, leading to phagocytosis and destruction by means of antibody-dependent cell-mediated cytotoxicity, lysis by complement-dependent cytotoxicity, and apoptosis and necrosis through direct induction of cell death. Anti-GD2 monoclonal antibodies may also prevent homing and adhesion of circulating malignant cells to the extracellular matrix. Disialoganglioside GD2 is highly expressed by almost all neuroblastomas, by most melanomas and retinoblastomas, and by many Ewing sarcomas and, to a more variable degree, by small cell lung cancer, gliomas, osteosarcomas, and soft tissue sarcomas. Successful treatment of disialoganglioside GD2-expressing tumors with anti-GD2 monoclonal antibodies is hindered by pharmacologic factors such as insufficient antibody affinity to mediate antibody-dependent cell-mediated cytotoxicity, inadequate penetration of antibody into the tumor microenvironment, and toxicity related to disialoganglioside GD2 expression by normal tissues such as peripheral sensory nerve fibers. Nonetheless, anti-GD2 monoclonal antibody dinutuximab (ch14.18) has been approved by the U.S. Food and Drug Administration and dinutuximab beta (ch14.18/CHO) has been approved by the European Medicines Agency for the treatment of high-risk neuroblastoma in pediatric patients. Clinical trials of anti-GD2 therapy are currently ongoing in patients with other types of disialoganglioside GD2-expressing tumors as well as neuroblastoma. In addition to anti-GD2 monoclonal antibodies, anti-GD2 therapeutic approaches include chimeric antigen receptor T-cell therapy, disialoganglioside GD2 vaccines, immunocytokines, immunotoxins, antibody-drug conjugates, radiolabeled antibodies, targeted nanoparticles, and T-cell engaging bispecific antibodies. Clinical trials should clarify further the potential of anti-GD2 therapy for disialoganglioside GD2-expressing malignant tumors.
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BACKGROUND: Even in oligometastatic stage 4 disease, survival rates are higher when curative approaches focus on both the primary tumour and metastasis. So, we aim to analyse our results of oligometastatic disease retrospectively. METHODS: In total, data on 52 non-small-cell lung cancer (NSCLC) patients with limited metastasis (one to three synchronous/metachronous) were retrospectively analysed. All treatment modalities associated with various treatment modalities [surgery, chemoradiotherapy (CRT), supportive care and palliative chemotherapy] were compared in terms of survival. Curative treatment consisted of surgery or CRT (concurrent or sequential). RESULTS: The median overall survival (OS) time was 35.2 ± 4.1 months. Surgery was superior to CRT in terms of OS (36.7 months vs 27.4 months, P > 0.05). Progression-free survival was 29.4 ± 3.9 months, and survival after first progression (SAFP) was 15.6 ± 2.8 months. Patients in whom a metastasectomy was performed had significantly higher rate of SAFP as compared with those who did not have a metastasectomy (20.07 ± 3.8 months vs 7.9 ± 1.7 months P = 0.046). According to pathological type, an adenocarcinoma was associated with better SAFP than a non-adenocarcinoma (23 ± 4.1 vs 6.4 ± 1.5, P = 0.002). The 1- and 2-years OS rates were 67% and 50.4%, respectively. Among the curative treatment group, the OS of patients younger than 65 years (n = 25) was 31 months, whereas that of patients older than 65 years (n = 13) was 22 months (P = 0.88). CONCLUSION: In well-selected NSCLC patients with limited metastasis, survival rates can reach up to 3 years, even in a geriatric population. Clinical N staging and co-morbidity are important prognostic factors.
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Carcinoma Pulmonar de Células não Pequenas/secundário , Quimiorradioterapia/métodos , Neoplasias Pulmonares/patologia , Cuidados Paliativos/métodos , Adenocarcinoma/mortalidade , Adenocarcinoma/patologia , Adulto , Idoso , Carcinoma Pulmonar de Células não Pequenas/tratamento farmacológico , Carcinoma Pulmonar de Células não Pequenas/radioterapia , Carcinoma Pulmonar de Células não Pequenas/cirurgia , Estudos de Casos e Controles , Comorbidade , Intervalo Livre de Doença , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Estadiamento de Neoplasias/métodos , Prognóstico , Intervalo Livre de Progressão , Estudos Retrospectivos , Taxa de Sobrevida , Resultado do Tratamento , Turquia/epidemiologiaRESUMO
OBJECTIVES: Consolidation/tumour (C/T) ratio means the maximum diameter of the consolidation is divided by the maximum diameter of the tumour and it is predictive for pathologic subtypes and prognosis after resection of the tumour. The purpose of this study is to clarify impact of C/T ratio along with maximum standardized uptake value (SUV) in pathological stage I lung adenocarcinoma. METHODS: Only patients with pathological stage I lung adenocarcinoma diagnosed by resection were included. Prognostic impact of C/T ratio and SUVmax were analysed by using regression analyses. RESULTS: Totally 156 patients (121 males, 35 females) were evaluated retrospectively. Overall survival (OS) and progression free survival (PFS) were higher in patients with C/T ratio ≥0.5 (OS: 46.3 ± 23.7 vs 30.4 ± 14.6, P = 0.002 and PFS: 43.0 ± 25.4 vs 27.8 ± 15.8, P = 0.005). But PFS and OS curves did not reveal any significant differences with Kaplan-Meier method (P = 0.45 and P = 0.055 respectively). Resection type (limited vs anatomic) and C/T ratio were predictors for OS in multivariate analyses (resection type: HR: 2.21 (1.01-4.83), P = 0.045 and C/T ratio: HR: 0.44 (0.20-0.98), P = 0.045). For PFS, resection type and SUVmax had prognostic significance (resection type: HR: 3.56 (1.64-7.74), P = 0.001 and SUVmax: HR: 1.31 (0.82-2.99), P = .002). CONCLUSION: In pathological stage 1 lung adenocarcinomas, SUVmax and surgery type are important predictors for recurrence rates. For early stage, adenocarcinoma patients with high SUVmax value, tumour size ≥3 cm and high grade subtype, C/T ratio should not be considered significant alone on survival and recurrence.
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Adenocarcinoma de Pulmão/diagnóstico , Neoplasias Pulmonares/diagnóstico , Estadiamento de Neoplasias/métodos , Pneumonectomia , Adenocarcinoma de Pulmão/cirurgia , Feminino , Seguimentos , Humanos , Neoplasias Pulmonares/cirurgia , Masculino , Pessoa de Meia-Idade , Tomografia por Emissão de Pósitrons/métodos , Período Pré-Operatório , Prognóstico , Estudos Retrospectivos , Tomografia Computadorizada por Raios X/métodosRESUMO
INTRODUCTION: Lung cancer is the leading cause of cancer-related death worldwide. It is usually diagnosed at advanced stage for which platinum-based chemotherapy had been the standard approach, although with limited clinical benefits. Discovery of oncogenic EGFR mutations in lung cancer have shifted the treatment paradigm with molecularly targeted therapies. AREAS COVERED: EGFR tyrosine kinase inhibitors (TKIs) have become the first-line choice in patients with advanced NSCLC harboring EGFR activating mutations. However, resistance to targeted therapy develops inevitably during the course of treatment. Multiple mechanisms of acquired resistance have been discovered, most commonly the secondary mutation of T790M in exon 20. The second- and third-generation EGFR TKIs are holding promise to overcome T790M-associated acquired resistance and currently being tested in clinical trials. In this article, we focus on the emerging approaches to overcome the different mechanisms of resistance to targeted therapies in patients with EGFR-mutant advanced NSCLC. EXPERT OPINION: It is essential to uncover the complex mechanisms underlying the progression of lung cancer after upfront EGFR TKIs. Next generation, in particular, the third generations of EGFR TKIs have been developed against acquired T790M mutation with promising clinical activity and better toxicity profile. Combination of targeted therapies has also been explored. Further studies are needed to detect the real-time changes of the resistance mechanisms and to develop new therapeutic strategies for lung cancer patients with EGFR mutations.