Profiling non-small cell lung cancer reveals that PD-L1 is associated with wild type EGFR and vascular invasion, and immunohistochemistry quantification of PD-L1 correlates weakly with RT-qPCR.

Most lung cancer patients are diagnosed at an advanced stage, limiting their treatment options with very low response rate. Lung cancer is the most common cause of cancer death worldwide. Therapies that target driver gene mutations (e.

Molecular profiling of non-small cell lung cancer.

Lung cancer is generally treated with conventional therapies, including chemotherapy and radiation. These methods, however, are not specific to cancer cells and instead attack every cell present, including normal cells. Personalized therapies provide more efficient treatment options as they target the individual's genetic makeup.

Crizotinib inhibition of positive tumours in advanced non-small-cell lung cancer: a Canadian perspective.

The ros1 kinase is an oncogenic driver in non-small-cell lung cancer (nsclc). Fusion events involving the gene are found in 1%-2% of nsclc patients and lead to deregulation of a tyrosine kinase-mediated multi-use intracellular signalling pathway, which then promotes the growth, proliferation, and progression of tumour cells. fusion is a distinct molecular subtype of nsclc, found independently of other recognized driver mutations, and it is predominantly identified in younger patients (<50 years of age), women, never-smokers, and patients with adenocarcinoma histology.

Canadian perspectives: update on inhibition of -positive tumours in advanced non-small-cell lung cancer.

Background: Inhibition of the anaplastic lymphoma kinase (alk) oncogenic driver in advanced non-small-cell lung carcinoma (nsclc) improves survival. In 2015, Canadian thoracic oncology specialists published a consensus guideline about the identification and treatment of positive patients, recommending use of the alk inhibitor crizotinib in the first line. New scientific literature warrants a consensus update.

Canadian consensus: inhibition of ALK-positive tumours in advanced non-small-cell lung cancer.

Anaplastic lymphoma kinase (alk) is an oncogenic driver in non-small-cell lung cancer (nsclc). Chromosomal rearrangements involving the ALK gene occur in up to 4% of nonsquamous nsclc patients and lead to constitutive activation of the alk signalling pathway. ALK-positive nsclc is found in relatively young patients, with a median age of 50 years.

Prevention of alopecia in medical and interventional chemotherapy patients.

Background: Chemotherapy-induced alopecia is one of the most distressing side effects of cancer treatment. Although there have been a number of investigated strategies to reduce this, there is no standard of care for treatment.

Objective: This review aims to summarize the relevant evidence for the treatments available for chemotherapy-induced alopecia.

A personalized approach to treatment: use of EGFR tyrosine kinase inhibitors for the treatment of non-small-cell lung cancer in Canada.

Lung cancer is one of the most commonly diagnosed malignancies and the leading cause of cancer-related mortality in Canada. The heterogeneity of nsclc and the importance of linking new targeted agents to the appropriate disease subtype require an individualized approach to treatment. In patients with EGFR (epidermal growth factor receptor gene) mutations, EGFR tyrosine kinase inhibitors (TKIs) provide a highly effective treatment option, with improved toxicity compared with standard chemotherapy.

Brief report: a phase II study of sunitinib in malignant pleural mesothelioma. the NCIC Clinical Trials Group.

Introduction: Malignant pleural mesothelioma (MPM) is an aggressive malignancy that most often presents at an advanced, incurable stage. After the failure of standard first-line cisplatin/antifolate chemotherapy, there is no accepted treatment. The vascular endothelial growth factor pathway may be a relevant therapeutic target in MPM.

The role of the epidermal growth factor receptor tyrosine kinase inhibitors as therapy for advanced, metastatic, and recurrent non-small-cell lung cancer: a Canadian national consensus statement.

Purpose: To provide consensus recommendations on the use of epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIS) in patients with advanced or meta-static non-small-cell lung cancer (NSCLC).

Methods: Using a systematic literature search, phase II trials, randomized phase III trials, and meta-analyses were identified for inclusion.

Results: A total of forty-six trials were included.

Adjuvant chemotherapy uptake in non-small cell lung cancer.

Introduction: Adjuvant chemotherapy in non-small cell lung cancer (NSCLC) has become a new standard of care. This study examines the uptake patterns for adjuvant chemotherapy outside of clinical trials.

Methods: A retrospective study of all patients diagnosed with NSCLC in the year 2005 who underwent curative-intent surgery in Nova Scotia, Canada was conducted.

Waiting times in early-stage non-small cell lung cancer (NSCLC).

Introduction: Wait times in cancer care continue to be an important clinical, social, and political issue. This study examines wait times along the care path from suspicious imaging study (Detection) to adjuvant chemotherapy initiation (Chemotherapy) for patients with early-stage non-small cell lung cancer (NSCLC) who undergo surgical resection.

Methods: A retrospective chart review of patients diagnosed in 2005 with NSCLC who underwent curative-intent surgery in Nova Scotia, Canada was conducted to abstract dates of care events (Detection, Surgery Consultation, Surgery, Medical Oncology [MO] Referral, MO Consultation and Chemotherapy) and patient characteristics.

Analysis of diethyltoluamide (DEET) following intentional oral ingestion of Muscol.

N,N-Diethyl-m-toluamide (DEET) is an effective component of several insect repellent products. A 19-year-old woman was admitted to the emergency department following ingestion of 15-25 mL 95% diethyltoluamide (Muscol). Serum and urine toxicology screening tests were negative except for detection of DEET.

Tumour necrosis factor-alpha but not interleukin-1 induces polymorphonuclear leucocyte migration through fibroblast layers by a fibroblast-dependent mechanism.

Interleukin-1 (IL-1) and tumour necrosis factor-alpha (TNF-alpha) both induce polymorphonuclear leucocyte (PMNL) infiltration into tissues and they have a synergistic action in this respect. We and others have observed that IL-1 alpha and TNF-alpha induce 51Cr-labelled PMNL migration across monolayers of umbilical vein endothelium via an endothelial cell-dependent mechanism. Here we investigated the interaction of PMNL with fibroblasts, since PMNL probably encounter such cells in many tissues once they traverse the vascular wall.

Rabbit alveolar macrophages stimulated with endotoxin and lung fragments from endotoxemic rabbits produce a leukocyte infiltration-inducing factor that lacks IL-1, TNF alpha, or chemotactic activity.

We reported previously that rabbit pleural and peritoneal macrophages (Møs) and human Mø stimulated with endotoxin (LPS) release a protein factor of 45 to 60 kd that induces local polymorphonuclear leukocyte (PMNL) infiltration upon intradermal injection in rabbits. In the case of the human Mø product, it was shown to be distinct from interleukin-1 (IL-1), tumor necrosis factors (TNF alpha), granulocyte macrophage colony stimulating factor (GMCSF), IL-6, and lower molecular weight PMNL chemotactic factors. Here, we examined resident rabbit alveolar Møs to determine if they produce a similar factor following in vitro or in vivo exposure to LPS.

Interleukin-1 and tumour necrosis factor alpha induced polymorphonuclear leukocyte-endothelial cell adhesion and transendothelial migration in vitro: the effect of apical versus basal monolayer stimulation.

The cytokines interleukin-1 (IL-1) and tumour necrosis factor alpha (TNF alpha) enhance polymorphonuclear leukocyte (PMNL) adhesion to vascular endothelium by an endothelial cell dependent mechanism in vitro and induce PMNL infiltration in vivo In this study, we employed human umbilical vein endothelium (HUVE) cultured on microporous membrane filters to form a monolayer, a system in which PMNL adherence and PMNL transendothelial migration could be measured using 51Cr-labelled human PMNL. In this system, it was found that PMNL adhesion and migration were dependent on prior treatment of the HUVE monolayer with IL-1 or TNF alpha for at least 2 h and that cytokine could be removed prior to the addition of PMNL without any effect on the response. PMNL adherence to the HUVE was maximal by 30 min and was followed by progressive migration of PMNL across the monolayer and the membrane filter into the lower chamber.