Background: Lung cancer stem cells (CSCs) share many characteristics with normal stem cells, such as self-renewal and multipotentiality. High expression of aldehyde dehydrogenase (ALDH) has been detected in many tumors, particularly in the CSC compartment, and it plays an important role in tumor proliferation, metastasis, and drug resistance. CD44 is commonly used as a cell surface marker of cancer stem-like cells in epithelial tumors. The aim of this study was to isolate and analyze cancer stem-like cells from surgically removed specimens to compare lung adenocarcinoma (ADENO) and squamous (SQUAMO) cell carcinoma. Methods: The ALDEFLUOR assay was used to identify and sort ALDH high and ALDH low human lung cancer cells following tissue digestion. Fluorescence-activated cell sorting analysis for CD44 was performed with tumor cells. Quantitative real-time PCR was performed to assess the expression of SOX2 and NANOG as stemness markers. ALDH1A1 expression was additionally determined by immunohistochemistry. Anchorage-independent ALDH high cell growth was also evaluated. ALDH high ADENO and SQUAMO cells were cultured to analyze spheroid formation. Results: All specimens contained 0.5-12.5% ALDH high cells with 3.8-18.9% CD44-positive cells. SOX2 and NANOG relative expression in ALDH high compared to ALDH low cells in ADENO and SQUAMO was analyzed and compared between the histotypes. Immunohistochemistry confirmed the presence of ALDH1A1 in the sections. SOX2 and NANOG were expressed at higher levels in the ALDH high subpopulation than in the ALDH low subpopulation only in ADENO cells, and the opposite result was seen in SQUAMO cells. In vitro functional assays demonstrated that ALDH high cells exhibited migration capacity with distinct behaviors between ALDH high spheres in ADENO vs. SQUAMO samples.
Emerging evidence suggests that a small subpopulation of cancer stem cells (CSCs) is responsible for initiation, progression, and metastasis cascade in tumors. CSCs share characteristics with normal stem cells, i.e., self-renewal and differentiation potential, suggesting that they can drive cancer progression. Consequently, targeting CSCs to prevent tumor growth or regrowth might offer a chance to lead the fight against cancer. CSCs create their niche, a specific area within tissue with a unique microenvironment that sustains their vital functions. Interactions between CSCs and their niches play a critical role in regulating CSCs’ self-renewal and tumorigenesis. Differences observed in the frequency of CSCs, due to the phenotypic plasticity of many cancer cells, remain a challenge in cancer therapeutics, since CSCs can modulate their transcriptional activities into a more stem-like state to protect themselves from destruction. This plasticity represents an essential step for future therapeutic approaches. Regarding self-renewal, CSCs are modulated by the same molecular pathways found in normal stem cells, such as Wnt/β-catenin signaling, Notch signaling, and Hedgehog signaling. Another key characteristic of CSCs is their resistance to standard chemotherapy and radiotherapy treatments, due to their capacity to rest in a quiescent state. This review will analyze the primary mechanisms involved in CSC tumorigenesis, with particular attention to the roles of CSCs in tumor progression in benign and malignant diseases; and will examine future perspectives on the identification of new markers to better control tumorigenesis, as well as dissecting the metastasis process.
Such findings show that pulmonary resection for bronchogenic cancer is feasible and justified in patients more than 70 years old, even if a higher incidence of cardiovascular complications may occur: a careful preoperative selection ought to be performed and lobectomy should be preferred.
Cancer stem cells (CSCs) have been considered the key drivers of cancer initiation and progression due to their unlimited self-renewal capacity and their ability to induce tumor formation. Macrophages, particularly tumor-associated macrophages (TAMs), establish a tumor microenvironment to protect and induce CSCs development and dissemination. Many studies in the past decade have been performed to understand the molecular mediators of CSCs and TAMs, and several studies have elucidated the complex crosstalk that occurs between these two cell types. The aim of this review is to define the complex crosstalk between these two cell types and to highlight potential future anti-cancer strategies.
Background: Elastofibroma dorsi (ED) is a benign soft-tissue tumor of the chest wall located near the tip of the scapula. Clinical presentation includes swelling, pain and impairment of shoulder movements.The present literature relies only on few small case series. The aim of this study was to analyze the surgical management of ED, focusing on the debated topics regarding preoperative evaluation, operative technique, post-operative outcome and follow-up. Methods:We conducted a single-center retrospective cohort analysis of patients operated for ED between 2003 and 2018. Diagnostic techniques were ultrasonography (US), computed tomography (CT-scan) and magnetic resonance imaging (MRI). CT-scan represented our preferred imaging study for preoperative assessment. Surgery was proposed for symptomatic and/or large lesions. Marginal excision through a musclesparing approach was performed. An open-door follow-up policy was adopted. All clinical, radiological, perioperative and pathological variables were matched in a univariate analysis. A multivariate analysis was performed to investigate risk factors for postoperative complications. Correlations analysis between radiological and pathological measurements of elastofibroma was conducted.Results: Seventy elastofibromas were excised in 59 patients. Mean age was 59 years and female prevalence was 59%. All elastofibromas were completely resected with no recurrence. Postoperative complications rate was 17%. Complications were mild in most cases. At the univariate analysis, patients with body mass index (BMI) >25 had a longer operative time (P=0.048), patients on antiplatelet medications experienced a prolonged drainage time (P=0.006) and a higher rate of complications (P=0.038); the occurrence of complications resulted in prolonged drainage time (P=0.047) and length of stay (P=0.023). A BMI ≤25 was the only independent risk factor for postoperative morbidity (OR 8.71, P=0.024). CT-scan showed the highest correlation with pathological size (r=0.819), US the lowest (r=0.421).Conclusions: Marginal resection through a muscle-sparing approach is safe and effective for the treatment of ED. CT-scan can be adequate for preoperative assessment. Giving the benign nature of the lesion and the absence of recurrence after complete resection, an open-door follow-up may be appropriate.
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