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Introduction: The head and neck are frequent sites for the development of cutaneous cancer and squamous cell carcinoma of the skin (SCC), one of the more frequent malignant non-melanoma skin neoplasms in Chile (436 per 100,000 inhabitants). Between 5-10% skin SCC progresses aggressively generating metastasis to parotid and cervical lymph nodes. Case Report: A 82 years old male, presents painful increased volume lesion in the mandibular area. He has a history of chronic arterial hypertension, acute renal failure, SCC of the scalp, extra-pulmonary tuberculosis, chronic sun exposure and smoking. Extraoral examination showed a 4 cm lesion in the posterior third of the mandibular branch, with undefined edges, a firm consistency and painful on palpation. Intraorally, erythematous mucosa is observed, as well as lack of lubrication, tenderness and cortical bone expansion. Incisional biopsy is performed, imaging and histological exams are requested. The results indicate the presence of SCC, and therefore referral to secondary care. Many risk factors are associated with SCC development, with ultraviolet radiation the most relevant in this case, favoring its appearance on the scalp. The probability of metastasis is low, but when it happens, the majority of cases that started in the scalp, disseminate to the parotid and cervical region. Conclusion: The SCC has a good prognosis. However, there are antecedents, such as size and location, that must alert the professional to perform the monitoring, early screening, control of metastatic nodes in maxillofacial area.
Introducción: La cabeza y el cuello son sitios frecuentes de desarrollo de cáncer cutáneo y el carcinoma epidermoide de piel (CEC) es una de las neoplasias malignas sin melanoma más frecuentes en Chile (436 por 100.000 habitantes). Entre el 5% y el 10% del CCE cutáneo progresa de forma agresiva y genera metástasis en los ganglios linfáticos parótidos y cervicales. Reporte de Caso: Varón de 82 años, presenta lesión dolorosa de aumento de volumen en zona mandibular. Tiene antecedentes de hipertensión arterial crónica, insuficiencia renal aguda, CCE del cuero cabelludo, tuberculosis extrapulmonar, exposición crónica al sol y tabaquismo. El examen extraoral mostró una lesión de 4 cm en el tercio posterior de la rama mandibular, con bordes indefinidos, consistencia firme y dolorosa a la palpación. Intraoralmente se observa mucosa eritematosa, así como falta de lubricación, dolor a la palpación y expansión del hueso cortical. Se realiza biopsia incisional, se solicitan exámenes de imagen e histológicos. Los resultados indican la presencia de CCE y, por tanto, derivación a atención secundaria. Son muchos los factores de riesgo asociados al desarrollo de CEC, siendo la radiación ultravioleta la más relevante en este caso, favoreciendo su aparición en el cuero cabelludo. La probabilidad de metástasis es baja, pero cuando ocurre, la mayoría de los casos que comenzaron en el cuero cabelludo se diseminan a la región parotídea y cervical. Conclusión: El SCC tiene un buen pronóstico. Sin embargo, existen antecedentes, como tamaño y ubicación, que deben alertar al profesional para realizar el seguimiento, cribado precoz, control de ganglios metastásicos en zona maxilofacial.
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Humans , Male , Aged, 80 and over , Scalp/pathology , Skin Neoplasms/diagnosis , Parotid Neoplasms/secondary , Carcinoma, Squamous Cell/secondary , Head and Neck Neoplasms/diagnosis , Mouth Neoplasms , Parotid Neoplasms/diagnosis , Carcinoma, Squamous Cell/diagnosis , Tomography, X-Ray Computed , Neoplasm MetastasisABSTRACT
Pancreatic cancer is one of the common malignancies in digestive system. The etiology of pancreatic cancer is not clear at present. Besides the correlation with smoking, alcohol, diabetes and chronic pancreatitis, the inordinate gut microbiota is also an importantly risk factor for pancreatic cancer in recent researches. Meanwhile, the gut microbiota is likely a new direction for the diagnosis and treatment of pancreatic cancer. Therefore, this review summarize the correlation between gut microbiota and pancreatic cancer, as well as the research progress of gut microbiota in the incidence, diagnosis and treatment of pancreatic cancer.
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Vascular endothelial growth factor receptors (VEGFRs) consist of three receptor tyrosine kinase (RTK) superfamily members and two non-RTK superfamily members and bind to the ligand in a non-one-to-one way. VEGFRs mediate various signaling pathways such as Raf1→MAP2K1/2→ERK1/2 through cell surface receptor internalization and thus promote the proliferation of hepatocellular carcinoma cells, angiogenesis, and lymphangiogenesis. VEGFRs can be highly expressed in local cancerous lesions of liver cancer patients, which is a key factor mediating malignant proliferation, invasion, and metastasis of hepatocellular carcinoma, and the expression of VEGFRs is negatively correlated with progression-free survival. Matrix metalloproteinase-9 and heat shock protein 90β can upregulate VEGFRs to promote the proliferation and metastasis of hepatoma cells, while miR-203a, miR-378a, and miR-199a-3p can downregulate VEGFR expression and inhibit hepatoma cell infiltration. Targeted drug therapy based on VEGFR can induce the apoptosis of hepatoma cells, block tumor angiogenesis, and delay disease progression.
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Gastric cancer is one of the malignant tumors with high morbidity and high mortality in China.Research has shown that viral infection is closely related to the occurrence of gastric cancer.EpsteinBarr virus-associated gastric cancer characterized by EB virus infection has been classified as a subtype of gastric cancer,whose epidemiology,pathogenesis,clinical and histopathologic features have been studied in detail.At the same time,oncolytic viruses reveal the inhibitory effect of the virus on tumors,and their ability to target and kill tumor cells is used in the treatment of some advanced cancers.This article will review the research advances about relevance to gastric cancer of several viruses that have been reported and the latest progress in anticancer mechanisms and combined therapies for oncolytic viruses.
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Se expone el caso de un neonato, a quien durante el examen físico se le palpa una masa en el hipocondrio izquierdo. Le realizan ecografía abdominal con hallazgo de una masa de probable origen suprarrenal; la resonancia magnética (RM) muestra una masa dependiente del mesenterio. En cirugía se observa importante adhesión a los órganos vecinos, se le realiza biopsia con resultado de tumor miofibroblástico. Este tumor hace parte del grupo heterogéneo de lesiones formadoras de masa llamado pseudotumor inflamatorio, el cual se define como una neoplasia fibroblástica/ miofibroblástica, con potencial biológico intermedio, de mayor ocurrencia en niños. Dada la baja frecuencia de aparición en edad neonatal, se realiza una revisión de la literatura acerca de su etiología, diagnóstico y tratamiento.
We present the case of a neonate, who upon physical examination a mass is palpated in the left hypochondrium, Abdominal ultrasound is performed with finding of a mass of probable adrenal origin; magnetic resonance imaging (MRI) shows a mass dependent on the mesentery. In surgery, important adhesion to neighboring organs is observed; biopsy is performed with the result of myofibroblastic tumor. This tumor is part of the heterogeneous group of mass-forming lesions called inflammatory pseudotumor, which is defined as a fibroblastic/myofibroblastic neoplasm, with intermediate biological potential, of greater occurrence in children. Given the low frequency of appearance in neonatal age, a review of the literature about its aetiology, diagnosis and treatment is carried out.
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Humans , Myofibroblasts , Infant, Newborn , Abdominal Injuries , Neoplastic ProcessesABSTRACT
TP53-induced glycolysis and apoptosis regulator (TIGAR ) is a p53- inducible target gene. TIGAR -encoding protein can inhibit glycolysis through reducing the intracellular level of fructose-2,6-bisphosphate which is the strongest activator of 6-phosphofructokinase 1 (PFK1), because PRK1 is a key enzyme in glycolytic pathway of tumor cells. TIGAR can promote glucose metabolism more to the pentose phosphate pathway (PPP), increase the productions of nicotinamide adenine dinucleotide phosphate (NADPH) and glutathione (GSH), and reduce the level of intracellular reactive oxygen species (ROS). Therefore, TIGAR is an important factor to maintain the homeostasis status of redox, and to regulate apoptosis of tumor cells. Recent studies showed that TIGAR plays an important role in tumorigenesis, progression and metastasis process. Moreover, the interference of TIGAR gene expression can enhance the radiosensitivity and chemosensitivity of many kinds of tumor cells, suggesting that TIGAR may become a potential target for the treatment of tumor. This article reviews the latest advances in the role of TIGAR in tumorigenesis, progression, metastasis and its targeted therapy.
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Estrogen receptor-alpha 36 (ER-α36), which is a new type of ER with a relative molecular weight of 3.57×104, has been demonstrated to have many important physiological functions in different tissues and organs in recent years. Many studies have shown that the occurrence and development of cancer are closely related to the expression level of ER-α36, which suggests that ER-α36 may serve as a potential therapeutic target in the treatment of some cancers. This paper reviews the advances in research on the correlation between ER-α36 and some cancers such as breast cancer, gastric cancer, liver cancer, and so on.
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Objective: To investigate the effect of Lianhua Shenjia Formula (this formula is extracted from the effective components of four traditional Chinese medicines: phillygenin, trichosanthin, codonopsis pilosulaglycoprotein and triterpenes compound of Cortex Periplocae) on β-catenin protein expression during the process of esophageal precancerous changes in C57BL/6 mice induced by 4-nitro quinoline1-oxide (4NQO), and to explore the possible mechanism of this formula inhibiting precancerous changes in esophagus. Methods: The expressions of β-catenin protein in different-stage esophageal precancerous lesion tissues in mice induced by 4NQO and before and after Lianhua Shenjia Formula treatment were detected by immunohistochemistry. Results: The abnormal expression rate of β-catenin protein in esophageal squamous cells was increased over time in 4NQO control group, and this rate reached 62.5% (10/16) in the 24th week, which was significantly higher than that in the normal control group (P < 0.01). The abnormal expression rates of β-catenin protein in Lianhua Shenjia Formula treatment group and all-trans retinoic acid (ATRA) treatment group were both decreased as compared with that of 4NQO control group (P < 0.01); however, there was no significant difference between Lianhua Shenjia Formula treatment group and ATRA treatment group. Conclusion: The Lianhua Shenjia Formula can inhibit the accumulation of β-catenin protein, and this may be one of the mechanisms of Lianhua Shenjia Formula inhibiting the development and progression of esophageal carcinoma.
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HIV /AIDS related lymphoma (ARL)are a group of heterogeneity of neoplasms,and they have poor prognosis.The factors of pathogenesis elucidated in recent years include immune injury caused by HIV,EB virus infection and genetic changes.There are four pathological types of ARL,including diffuse large B cell lymphoma,Burkitt lymphoma,plasmablastic lymphoma and primary effusion lymphoma.Morphological characteristics,immunophenotype markers and clinical data should be combined to make diagnosis and differen-tial diagnosis,which will facilitate timely treatment and improve prognosis.
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Peroxisome proliferator activated receptor-γ (PPARγ) is a member of the nuclear receptor superfamily of ligand-activated transcription factors that plays a critical role in regulating glucose and lipid homeostasis,and in the processes of tumor cell proliferation,differentiation,apoptosis,invasion and distant metastasis.Studies demonstrate that PPARγexpression is detected in human lung cancer tissues and numerous lung cancer cell lines.Activation of PPARγthrough its ligands impedes significantly a variety of tumor progression,including lung cancer.However,systemic activation of PPARγhas been reported to be protumorigenic in some in vitro systems and in vivo models.
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Majority of experimental and clinical studies have shown a pro-tumoral function of tumor-associated macrophages (TAMs) which occupy a large part in matrix cells. TAMs promote tumor cell invasion and migration, and their number is related to malignant degree and poor prognosis. Macrophages plasticity makes it possible to change the tumor microenvironment and remodel tumor immune in cancer immunotherapy. Increasing researches have revealed the TAMs' effect on tumor microenvironment and put forward tumor immune treatments aiming at TAMs. Here this review presents the recent research of TAMs in remodeling tumor immune microenvironment and immune targeted therapies, such as the origin of TAMs, the immunosuppression effect of TAMs on tumor microenvironment, tumor extracellular matrix remodeling, and promotion of angiogenesis and lymphangiogenesis Copyright © 2013 by TUMOR.
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Objective: To investigate the proliferation, adhesion, migration, invasion, and contraction capacities of carcinoma-associated fibroblasts (CAFs) in human breast cancer microenvironment. Methods: The protein expressions of fibronectin (FN), alpha-smooth-muscle actin (α-SMA) and fibroblast activation protein (FAP) were detected by Western blotting, so as to distinguish CAFs cells from normal fibroblasts (NFs). The proliferation of CAFs and NFs was detected by Roche xCellingence system, cell counting, and cell counting kit-8 (CCK-8) assay. The adhesion, migration, invasion and contraction capacities of CAFs were evaluated by the cell adhesion experiment, Roche xCellingence system, Transwell invasion assay and collagen gel contraction assay, respectively. Results: The primary CAFs and NFs cells which were isolated from human breast cancer grew in good condition with active proliferation. The linear types and trends of their growth curves were accorded with the cell growth characteristics. While compared with NFs, CAFs had a robust proliferation capacity, and the obviously stronger abilities of adhesion, migration, invasion, and contraction. Conclusion: There are prodigious differences of proliferation and migration between CAFs and NFs cells in human breast cancer microenvironment. CAFs have the stronger abilities of proliferation, adhesion, migration, invasion, and contraction than NFs. Copyright © 2013 by TUMOR.
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Aldo-keto reductase reductase (AKR) superfamily is NADPH-dependent oxidoreductase.As a rate-limiting enzyme in polyols metabolic pathway,the activation or inactivation of AKR involves in neoplastic process of lung cancer with the metabolism of environment toxic.AKR is related to drug resistance of chemotherapy,which will be the prognostic factor of lung cancer.
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Objective To investigate the role of UDP-glucuronosyltransferase 1A (UGT1A),nuclear factor erythroid-2-related factor 2 (Nrf2) and kelch-like ECH-associated protein 1 ( Keapl ) in the tumorigenesis of colonic carcinoma.Methods The expressions of UGT1 A,Nrf2 and Keapl were detected in normal colonic mucosa(24 cases),adenoma tissue (30 cases) and adenocarcinoma tissue (77 cases) by immunohistochemistry,and the relationship between their expressions and the clinical pathological characteristics was analyzed.Results The positive rates of UGT1 A in normal colonic mucosa,adenoma and adenocarcinoma tissue were 83.3％ ( 20/24),80.0％ ( 24/30 ) and 53.2％ ( 41/77 ),respectively.The positive rate of UGT1A in adenocarcinoma was lower than those in colonic mucosa and adenoma ( all P ＜0.05 ).On the contrary,the positive rates of Nrf2 in adenoma [70.0％ (21/30) ] and adenocarcinoma tissue [ 87.0％ (67/77) ] were higher than that in normal colonic tissue [ 41.7％ (10/24),all P =0.000 ].The positive rates of Keapl in normal colonic mucosa,adenoma and adenocarcinoma tissue were 54.2％ ( 13/24),70.0％ (21/30) and 61.0％ (47/77),respectively ( normal colonic tissue vs adenocarcinoma tissue,P =0.040 ; adenoma vs adenocarcinoma,P =0.002 ).There was no correlation between the expression of UGT1 A,Nrf2 and the clinicopathologic features of colon carcinoma,while the differences of Keapl positive rates in the various degrees of tumor differentiation [ moderately-well differentiated vs poorly differentiated:70.0％ (35/50) vs 44.4％ (12/27) ] and invasion [T1-T2 vs T3-T4:78.8％ (26/33) vs 47.7％ (21/44) ]were statistically significant (all P ＜ 0.05 ).Conclusion The decreased expression of UGT1A and the dysregulation of Nrf2/Keapl system may play a role in colonic tumorigenesis.
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The expression of transforming growth factor(TGF)-β supeffamily co-receptor (Tβ3R) Ⅲ is often lost in many kinds of cancers.Tβ3RⅢ plays a role of negative regulation in tumorigenesis.T3RⅢ could regulate the cellular invasion,migration,proliferation and apoptosis by multiple mechanisms,such as mediating the TGF-β signaling pathway,impacting the mitogen-activated protein kinase(MAPK),nuclear factor-kappa B (NF-κB) and Cdc42 and producing soluble TβR(sTβR) Ⅲ.Defining the mechanisms of absence and physiological functions of TβR Ⅲ in cancers has great significant for the diagnosis,treatment and prognosis of cancer.
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Multinolular and intrahepatic recurrent HCC can originate from intrahepatic metastasis and multiple origins, and their colnal origin is closely related to the clinical diagnosis and treatment. To designate suitable therapeutic strategies according to their colnal origin is a new challenge needs to be tackled urgently. This paper reviews recent progress in the clinicopathological features, molecular diagnosis and clinical outcomes of multiple origin HCC.
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Toll-like receptor (TLR) plays a crucial role in innate immune response and the subsequent induction of adaptive immunity. TLR is expressed on immune cells as well as epithelial cells and tumor cells. When endogenous and exogenous ligands bind with TLR, TLR signaling pathways are activated and a large number of inflammatory cytokines are released, creating an inflammatory microenvironment and leading to tumor formation, invasion and metastasis.
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Studies indicate that miRNAs correlate closely with tumorigenesis and tumor biological be-haviors, and play a significant role as a kind of regnlating factor in tumorigenesis, tumor cells proliferation, dif-ferentiation, apoptosis, invasion and metastasis, as well as in drug resistance of tumors. Further study of the targets and mechanisms of miRNA may be helpful to recognize the characterization of tumor biology and etiolo-gy, and bring new strategies for tumor therapy.
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Malignant transformation of a neurilemmoma is an exceedingly rare event. We describe a case of intrathoracic ancient neurilemmoma undergoing a malignant change in a 39-yr-old man. The patient presented with right flank and chest pain for several months. Plain radiography and CT scan of the chest showed a soft tissue mass lesion at the extrapleural space with erosion of surrounding ribs at the right basal lung area. The excised mass was encapsulated and measured 4.5 x 3.5 x 2.3 cm. The cut surface showed grayish-white and glistening with a focal cystic change and hemorrhage. Necrosis was not seen. Histologically, the tumor showed the features of classic neurilemmoma composed of the Antoni type A and B areas with perivascular hyalinization. In addition, obviously histo-logically malignant foci manifested by presence of markedly increased cellularity with fascicular arrangement, active mitotic activity, hyperchromasia, and gradual loss of original neurilemmomatous feature were noted.
Subject(s)
Adult , Humans , Male , Cell Transformation, Neoplastic , Diagnosis, Differential , Neurilemmoma/complications , Neurilemmoma/pathology , Neurofibromatosis 1/complications , Neurofibromatosis 1/pathology , Thoracic Neoplasms/etiology , Thoracic Neoplasms/pathology , Biomarkers, TumorABSTRACT
Objective To investigate the biological effects of human gastric carcinoma cell line SGC-7901 transinfected by antisence vascular endothelial growth factor-C (anti VEGF-C) gene on the tumorigenicity and vascular generation,and explore the role of VEGF-C gene in metastasis and vascular generation of gastric cancer.MethodsThirty nude mice were randomly divided into three groups (10 each):transgenic anti VEGF-C group,transgenic pure liposome group and non-transgenic group.0.2ml (1?107/ml) of SGC-7901 suspension,either transinfected by anti VEGF-C gene,or by pure liposome,or transinfected nil,was respectively subcutaneously injected into the three groups of mice,once every 2 days for 3 consecutive days.After injection,the size and growth velocity of the neoplasm were measured.The microlymphatic vessel density (MLVD) and microvessel density (MVD) of tumor were also determined.ResultsThe neoplasm grew more slowly and was smaller in the mice of transgenic anti VEGF-C group than in non-transgenic ones.At the end of the 1st,2nd and 3rd week,the MLVD in the mice of transgenic anti VEGF-C group was 4.0?2.2,6.0?3.1 and 9.0?2.7/high field (/HF),respectively.In the transgenic pure liposome group,the MLVD was 6.0?8.7,9.0?3.5 and 18.0?7.2/HF,respectively.In the non-transgenic group,the MLVD was 7.0?4.9,9.0?6.4 and 19.0?6.5/HF,respectively.The MVD in the transgenic anti VEGF-C group was 3.0?2.4,5.0?2.1 and 8.0?1.7/HF,respectively.In the transgenic pure liposome group was 4.0?1.8,6.0?2.7 and 10.0?1.3/HF,respectively,and in non-transgenic group was 4.0?1.5,6.0?1.3 and 9.0?1.2/HF,respectively.There existed significant difference in lymphangiogenesis of the tumor (P0.05).ConclusionsThe anti VEGF-C gene may suppress the tumorigenicity and lymphangiogenesis of human SGC-7901 gastric carcinoma cells,but have little effect on angiogenesis of the tumor.VEGF-C might participate in the lymphangiogenesis of gastric tumor.