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A Case of Lung Adenocarcinoma Originating from an Old Posttraumatic Scar in a Young Patient

A Case of Lung Adenocarcinoma Originating from an Old Posttraumatic Scar in a Young Patient Hindawi Case Reports in Oncological Medicine Volume 2019, Article ID 8395389, 3 pages https://doi.org/10.1155/2019/8395389 Case Report A Case of Lung Adenocarcinoma Originating from an Old Posttraumatic Scar in a Young Patient 1 1 2 Fatima Ahmed, Hassaan Yasin , and Hesham E. Mohamed Department of Internal Medicine, Charleston Area Medical Center-West Virginia University, 3200 Maccorkle Avenue SE, Charleston, WV 25304, USA Department of Pulmonary Disease and Critical Care Medicine, Charleston Area Medical Center-West Virginia University, 3200 Maccorkle Avenue SE, Charleston, WV 25304, USA Correspondence should be addressed to Hassaan Yasin; hassaan_habib@hotmail.com Received 21 October 2018; Accepted 1 April 2019; Published 8 April 2019 Academic Editor: Raffaele Palmirotta Copyright © 2019 Fatima Ahmed et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. A relationship between lung scarring and cancer has been recognized for many decades but more evidence is needed to strengthen this association. A 34-year-old nonsmoker male with a history of left lower lobe lung scar secondary to a pulmonary contusion from a motor vehicle accident in 2012 was admitted with shortness of breath and cough. A computed tomography (CT) angiography of the chest demonstrated bilateral pulmonary emboli, left lower lobe mass, left lung septal thickening, and mediastinal lymphadenopathy. A CT-guided biopsy of the mass was performed, and pathology was consistent with lung adenocarcinoma. Staging work-up revealed a widely metastatic disease. The patient developed severe complications requiring hospitalization after the first cycle of chemotherapy and subsequently passed away. Lung scar carcinoma originates around peripheral scars resulting from a variety of infections, injuries, and lung diseases. It has poor prognosis because it metastasizes from relatively small lesions. Our case further endorses that lung scarring can potentially lead to the development of cancer. Furthermore, we want to highlight the need to conduct studies to determine if monitoring this patient population with periodic imaging can have a survival benefit. 1. Introduction 2. Case Presentation Lung cancer is the leading cause of cancer-related mortality A 34-year-old nonsmoker male patient presented to the worldwide. Although lung cancer is predominantly seen in emergency room with a one-week history of dyspnea, pleu- smokers, never-smokers (individuals who have smoked less ritic chest pain, and a nonproductive cough. His past medical than 100 cigarettes in their lifetime) account for 20% of cases history was significant for a motor vehicle accident five years globally [1]. Adenocarcinoma is the most common histologic earlier that had resulted in multiple left-sided rib fractures, type among both groups [2]. Although cigarette smoking is, pulmonary contusions, and a hemopneumothorax requiring by far, the biggest risk factor for developing lung cancer, tube thoracostomy (Figure 1); this left a residual nodular age, occupational exposures, environmental pollution, race, density in the left lower lobe (Figure 2). On physical exam, gender, and preexisting lung disease are all important he was afebrile, normotensive, tachycardic, hypoxic and in contributors [3]. There is an etiologic relationship between mild respiratory distress and had diminished breath sounds lung scarring and the development of pulmonary carcinoma bilaterally. [4]. In this article, we present a case of lung adenocarcinoma Laboratory work-up showed a white blood cell count of that originated from a posttraumatic scar. 20,500/mm . His electrocardiogram showed sinus tachycardia. 2 Case Reports in Oncological Medicine Figure 1: Computed tomography of the chest from January 2012 Figure 3: Computed tomography of the chest from June 2017 showing left-sided hemothorax and subcutaneous emphysema. showing a left lower lobe opacity with preseptal thickening and a small pleural effusion. treatment with carboplatin and paclitaxel was started. However, after the first cycle of chemotherapy, the patient became critically ill and was hospitalized. Subsequently, he developed features of disseminated intravascular coagulation and passed away shortly thereafter. 3. Discussion Lung scar carcinoma (LSC) was first described in 1939 by Friedrich as a form of lung cancer that originates from peripheral scars in the lung. These, in turn, may arise from infection, injury, intrinsic pulmonary disease, or recurrent episodes of tumor necrosis and healing [4]. The most com- mon etiologic factor for the development of LSC is scarring secondary to tuberculosis, but it is also known to occur in the setting of pneumonia, pulmonary abscess, bronchiectasis, and pulmonary infarction [5]. The pathogenesis involves Figure 2: Computed tomography of the chest from May 2012 showing a left lower lobe residual nodular density. production of acute-phase reactants during the inflammatory response, which leads to recruitment of leukocytes. These activated cells produce reactive oxygen species (ROS) that mediate mutagenic changes in deoxyribonucleic acid X-ray imaging of the chest revealed a left lung base opa- cification. Computed tomographic (CT) angiography of (DNA) and damage proteins involved in the maintenance the lung demonstrated bilateral pulmonary emboli, a of genomic stability [6, 7]. Chronic inflammation promotes 6 6×5 4 cm opacity in the left lower lobe with interlob- persistent DNA damage and eventual activation of onco- ular septal thickening, prominent interstitial infiltrates genes with subsequent neoplastic transformation. Inflamma- tory mediators such as tumor necrosis factor (TNF), within the left lung, and paratracheal lymphadenopathy (Figure 3). This opacity had enlarged significantly when transforming growth factor (TGF), and interleukins 1, 4, 6, compared to the one visualized at the same location in and 13 cause angiogenesis and fibrosis [6, 8] and are also 2012 (Figure 2). The patient was treated with IV heparin implicated in tumorigenesis. Notably, the Prostate, Lung, for pulmonary embolism. A CT-guided biopsy of the lung Colorectal, and Ovarian (PLCO) Cancer Screening Trial mass and endobronchial ultrasonographic sampling of the has demonstrated a two-fold increased risk of lung cancer mediastinal lymph nodes established the diagnosis of lung associated with the detection of pulmonary scarring on chest adenocarcinoma. Further imaging obtained to complete X-ray [9]. the staging work-up revealed widespread metastasis to LSC is most commonly subpleural adenocarcinoma with the bone. no evidence of bronchial origin and is characterized histolog- Immunohistochemical testing for programmed death- ically by contiguity with dense, hyalinized scar tissue that ligand 1 showed 50 percent expression. Molecular analysis itself does not comprise any tumor cells [4]. It is hypothe- did not show the presence of EGFR mutations and sized that impedance of lymphatic drainage by scar tissue ALK/ROS1 translocations. While these tests were pending, can lead to accumulation of malignant cells with subsequent Case Reports in Oncological Medicine 3 accelerated vascular and/or lymphatic spread of LSC, as was [4] R. K. Bobba, J. S. Holly, T. Loy, and M. C. Perry, “Scar carcinoma of the lung: a historical perspective,” Clinical Lung observed in our patient [10]. LSC therefore carries a dismal Cancer, vol. 12, no. 3, pp. 148–154, 2011. prognosis, with a five-year survival rate of only 5%, as [5] H. Yokoo and E. E. Suckow, “Peripheral lung cancers arising in opposed to 22% for non-LSC adenocarcinoma and 28% for scars,” Cancer, vol. 14, no. 6, pp. 1205–1215, 1961. non-LSC adenosquamous cell carcinoma [11]. It is, therefore, important to diagnose and treat this disease early. Because of [6] F. Balkwill and A. Mantovani, “Inflammation and cancer: back to Virchow?,” The Lancet, vol. 357, no. 9255, pp. 539– the physical overlap that exists between LSC and scar tissue 545, 2001. on CT imaging, the former is often misdiagnosed as an old fibrotic lesion in the absence of sequential imaging, [7] M. Jaiswal, N. F. LaRusso, L. J. Burgart, and G. J. Gores, “Inflammatory cytokines induce DNA damage and inhibit particularly in younger patients. However, radiographic DNA repair in cholangiocarcinoma cells by a nitric oxide- changes in scar tissue, such as expansion, vacuolation, ves- dependent mechanism,” Cancer Research, vol. 60, no. 1, sel convergence within the region of fibrosis, and emer- pp. 184–190, 2000. gence of well-defined surrounding ground-glass opacities [8] K. Dheda, H. Booth, J. F. Huggett, M. A. Johnson, A. Zumla, and spiculations, strongly support the presence of LSC. and G. A. W. Rook, “Lung remodeling in pulmonary tubercu- Vacuolation and ground-glass opacities are especially useful losis,” The Journal of Infectious Diseases, vol. 192, no. 7, in differentiating malignant from benign lesions. Ground- pp. 1201–1209, 2005. glass opacities surrounding areas of scar tissue are considered [9] Y.-Y. Yu, P. F. Pinsky, N. E. Caporaso et al., “Lung cancer risk to be reliable markers of early-stage LSC but tend to consol- following detection of pulmonary scarring by chest radiogra- idate over time and so run the risk of being missed if not phy in the Prostate, Lung, Colorectal, and Ovarian Cancer detected early enough [12]. Screening Trial,” Archives of Internal Medicine, vol. 168, no. 21, pp. 2326–2332, 2008. [10] R. Carroll, “The influence of lung scars on primary lung 4. Conclusion cancer,” The Journal of Pathology and Bacteriology, vol. 83, Our case serves to highlight the link between pulmonary no. 1, pp. 293–297, 1962. scarring and carcinogenesis, as well as to demonstrate the [11] L. J. Freant, W. L. Joseph, and P. C. Adkins, “Scar carcinoma of relentless course of lung scar carcinoma, which necessitates the lung. Fact or fantasy?,” The Annals of Thoracic Surgery, timely diagnosis. The USPSTF recommends annual screen- vol. 17, no. 6, pp. 531–537, 1974. ing for lung cancer with a low-dose CT scan of chest in adults [12] F. Gao, X. Ge, M. Li et al., “CT features of lung scar cancer,” aged 55 to 80 who have a 30 pack-year smoking history. Journal of Thoracic Disease, vol. 7, no. 3, pp. 273–280, 2015. However, no such recommendations exist for individuals with a known history of lung scarring. Our case reinforces the need for periodic CT imaging of the chest in this group of individuals who are at increased risk of this form of malig- nancy and underscores the need for evidence to determine the survival benefit of such a measure. Disclosure Hassaan Yasin’s present address is Marshall University, Joan C. Edwards School of Medicine, Edwards Comprehensive Cancer Center, 1400 Hal Greer Boulevard, Huntington, WV 25701, USA. Conflicts of Interest The authors declare that they have no conflicts of interest. References [1] D. M. Parkin, F. Bray, J. Ferlay, and P. Pisani, “Global cancer statistics, 2002,” CA: a Cancer Journal for Clinicians, vol. 55, no. 2, pp. 74–108, 2005. [2] S. Couraud, G. Zalcman, B. Milleron, F. Morin, and P. J. Souquet, “Lung cancer in never smokers – a review,” European Journal of Cancer, vol. 48, no. 9, pp. 1299–1311, 2012. [3] P. de Groot and R. F. Munden, “Lung cancer epidemiology, risk factors, and prevention,” Radiologic Clinics of North America, vol. 50, no. 5, pp. 863–876, 2012. MEDIATORS of INFLAMMATION The Scientific Gastroenterology Journal of World Journal Research and Practice Diabetes Research Disease Markers Hindawi Hindawi Publishing Corporation Hindawi Hindawi Hindawi Hindawi www.hindawi.com Volume 2018 http://www www.hindawi.com .hindawi.com V Volume 2018 olume 2013 www.hindawi.com Volume 2018 www.hindawi.com Volume 2018 www.hindawi.com Volume 2018 International Journal of Journal of Immunology Research Endocrinology Hindawi Hindawi www.hindawi.com Volume 2018 www.hindawi.com Volume 2018 Submit your manuscripts at www.hindawi.com BioMed PPAR Research Research International Hindawi Hindawi www.hindawi.com Volume 2018 www.hindawi.com Volume 2018 Journal of Obesity Evidence-Based Journal of Journal of Stem Cells Complementary and Ophthalmology International Alternative Medicine Oncology Hindawi Hindawi Hindawi Hindawi Hindawi www.hindawi.com Volume 2018 www.hindawi.com Volume 2018 www.hindawi.com Volume 2018 www.hindawi.com Volume 2018 www.hindawi.com Volume 2013 Parkinson’s Disease Computational and Behavioural Mathematical Methods AIDS Oxidative Medicine and in Medicine Neurology Research and Treatment Cellular Longevity Hindawi Hindawi Hindawi Hindawi Hindawi www.hindawi.com Volume 2018 www.hindawi.com Volume 2018 www.hindawi.com Volume 2018 www.hindawi.com Volume 2018 www.hindawi.com Volume 2018 http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Case Reports in Oncological Medicine Hindawi Publishing Corporation

A Case of Lung Adenocarcinoma Originating from an Old Posttraumatic Scar in a Young Patient

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Hindawi Publishing Corporation
Copyright
Copyright © 2019 Fatima Ahmed et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
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2090-6706
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2090-6714
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10.1155/2019/8395389
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Abstract

Hindawi Case Reports in Oncological Medicine Volume 2019, Article ID 8395389, 3 pages https://doi.org/10.1155/2019/8395389 Case Report A Case of Lung Adenocarcinoma Originating from an Old Posttraumatic Scar in a Young Patient 1 1 2 Fatima Ahmed, Hassaan Yasin , and Hesham E. Mohamed Department of Internal Medicine, Charleston Area Medical Center-West Virginia University, 3200 Maccorkle Avenue SE, Charleston, WV 25304, USA Department of Pulmonary Disease and Critical Care Medicine, Charleston Area Medical Center-West Virginia University, 3200 Maccorkle Avenue SE, Charleston, WV 25304, USA Correspondence should be addressed to Hassaan Yasin; hassaan_habib@hotmail.com Received 21 October 2018; Accepted 1 April 2019; Published 8 April 2019 Academic Editor: Raffaele Palmirotta Copyright © 2019 Fatima Ahmed et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. A relationship between lung scarring and cancer has been recognized for many decades but more evidence is needed to strengthen this association. A 34-year-old nonsmoker male with a history of left lower lobe lung scar secondary to a pulmonary contusion from a motor vehicle accident in 2012 was admitted with shortness of breath and cough. A computed tomography (CT) angiography of the chest demonstrated bilateral pulmonary emboli, left lower lobe mass, left lung septal thickening, and mediastinal lymphadenopathy. A CT-guided biopsy of the mass was performed, and pathology was consistent with lung adenocarcinoma. Staging work-up revealed a widely metastatic disease. The patient developed severe complications requiring hospitalization after the first cycle of chemotherapy and subsequently passed away. Lung scar carcinoma originates around peripheral scars resulting from a variety of infections, injuries, and lung diseases. It has poor prognosis because it metastasizes from relatively small lesions. Our case further endorses that lung scarring can potentially lead to the development of cancer. Furthermore, we want to highlight the need to conduct studies to determine if monitoring this patient population with periodic imaging can have a survival benefit. 1. Introduction 2. Case Presentation Lung cancer is the leading cause of cancer-related mortality A 34-year-old nonsmoker male patient presented to the worldwide. Although lung cancer is predominantly seen in emergency room with a one-week history of dyspnea, pleu- smokers, never-smokers (individuals who have smoked less ritic chest pain, and a nonproductive cough. His past medical than 100 cigarettes in their lifetime) account for 20% of cases history was significant for a motor vehicle accident five years globally [1]. Adenocarcinoma is the most common histologic earlier that had resulted in multiple left-sided rib fractures, type among both groups [2]. Although cigarette smoking is, pulmonary contusions, and a hemopneumothorax requiring by far, the biggest risk factor for developing lung cancer, tube thoracostomy (Figure 1); this left a residual nodular age, occupational exposures, environmental pollution, race, density in the left lower lobe (Figure 2). On physical exam, gender, and preexisting lung disease are all important he was afebrile, normotensive, tachycardic, hypoxic and in contributors [3]. There is an etiologic relationship between mild respiratory distress and had diminished breath sounds lung scarring and the development of pulmonary carcinoma bilaterally. [4]. In this article, we present a case of lung adenocarcinoma Laboratory work-up showed a white blood cell count of that originated from a posttraumatic scar. 20,500/mm . His electrocardiogram showed sinus tachycardia. 2 Case Reports in Oncological Medicine Figure 1: Computed tomography of the chest from January 2012 Figure 3: Computed tomography of the chest from June 2017 showing left-sided hemothorax and subcutaneous emphysema. showing a left lower lobe opacity with preseptal thickening and a small pleural effusion. treatment with carboplatin and paclitaxel was started. However, after the first cycle of chemotherapy, the patient became critically ill and was hospitalized. Subsequently, he developed features of disseminated intravascular coagulation and passed away shortly thereafter. 3. Discussion Lung scar carcinoma (LSC) was first described in 1939 by Friedrich as a form of lung cancer that originates from peripheral scars in the lung. These, in turn, may arise from infection, injury, intrinsic pulmonary disease, or recurrent episodes of tumor necrosis and healing [4]. The most com- mon etiologic factor for the development of LSC is scarring secondary to tuberculosis, but it is also known to occur in the setting of pneumonia, pulmonary abscess, bronchiectasis, and pulmonary infarction [5]. The pathogenesis involves Figure 2: Computed tomography of the chest from May 2012 showing a left lower lobe residual nodular density. production of acute-phase reactants during the inflammatory response, which leads to recruitment of leukocytes. These activated cells produce reactive oxygen species (ROS) that mediate mutagenic changes in deoxyribonucleic acid X-ray imaging of the chest revealed a left lung base opa- cification. Computed tomographic (CT) angiography of (DNA) and damage proteins involved in the maintenance the lung demonstrated bilateral pulmonary emboli, a of genomic stability [6, 7]. Chronic inflammation promotes 6 6×5 4 cm opacity in the left lower lobe with interlob- persistent DNA damage and eventual activation of onco- ular septal thickening, prominent interstitial infiltrates genes with subsequent neoplastic transformation. Inflamma- tory mediators such as tumor necrosis factor (TNF), within the left lung, and paratracheal lymphadenopathy (Figure 3). This opacity had enlarged significantly when transforming growth factor (TGF), and interleukins 1, 4, 6, compared to the one visualized at the same location in and 13 cause angiogenesis and fibrosis [6, 8] and are also 2012 (Figure 2). The patient was treated with IV heparin implicated in tumorigenesis. Notably, the Prostate, Lung, for pulmonary embolism. A CT-guided biopsy of the lung Colorectal, and Ovarian (PLCO) Cancer Screening Trial mass and endobronchial ultrasonographic sampling of the has demonstrated a two-fold increased risk of lung cancer mediastinal lymph nodes established the diagnosis of lung associated with the detection of pulmonary scarring on chest adenocarcinoma. Further imaging obtained to complete X-ray [9]. the staging work-up revealed widespread metastasis to LSC is most commonly subpleural adenocarcinoma with the bone. no evidence of bronchial origin and is characterized histolog- Immunohistochemical testing for programmed death- ically by contiguity with dense, hyalinized scar tissue that ligand 1 showed 50 percent expression. Molecular analysis itself does not comprise any tumor cells [4]. It is hypothe- did not show the presence of EGFR mutations and sized that impedance of lymphatic drainage by scar tissue ALK/ROS1 translocations. While these tests were pending, can lead to accumulation of malignant cells with subsequent Case Reports in Oncological Medicine 3 accelerated vascular and/or lymphatic spread of LSC, as was [4] R. K. Bobba, J. S. Holly, T. Loy, and M. C. Perry, “Scar carcinoma of the lung: a historical perspective,” Clinical Lung observed in our patient [10]. LSC therefore carries a dismal Cancer, vol. 12, no. 3, pp. 148–154, 2011. prognosis, with a five-year survival rate of only 5%, as [5] H. Yokoo and E. E. Suckow, “Peripheral lung cancers arising in opposed to 22% for non-LSC adenocarcinoma and 28% for scars,” Cancer, vol. 14, no. 6, pp. 1205–1215, 1961. non-LSC adenosquamous cell carcinoma [11]. It is, therefore, important to diagnose and treat this disease early. Because of [6] F. Balkwill and A. Mantovani, “Inflammation and cancer: back to Virchow?,” The Lancet, vol. 357, no. 9255, pp. 539– the physical overlap that exists between LSC and scar tissue 545, 2001. on CT imaging, the former is often misdiagnosed as an old fibrotic lesion in the absence of sequential imaging, [7] M. Jaiswal, N. F. LaRusso, L. J. Burgart, and G. J. Gores, “Inflammatory cytokines induce DNA damage and inhibit particularly in younger patients. However, radiographic DNA repair in cholangiocarcinoma cells by a nitric oxide- changes in scar tissue, such as expansion, vacuolation, ves- dependent mechanism,” Cancer Research, vol. 60, no. 1, sel convergence within the region of fibrosis, and emer- pp. 184–190, 2000. gence of well-defined surrounding ground-glass opacities [8] K. Dheda, H. Booth, J. F. Huggett, M. A. Johnson, A. Zumla, and spiculations, strongly support the presence of LSC. and G. A. W. Rook, “Lung remodeling in pulmonary tubercu- Vacuolation and ground-glass opacities are especially useful losis,” The Journal of Infectious Diseases, vol. 192, no. 7, in differentiating malignant from benign lesions. Ground- pp. 1201–1209, 2005. glass opacities surrounding areas of scar tissue are considered [9] Y.-Y. Yu, P. F. Pinsky, N. E. Caporaso et al., “Lung cancer risk to be reliable markers of early-stage LSC but tend to consol- following detection of pulmonary scarring by chest radiogra- idate over time and so run the risk of being missed if not phy in the Prostate, Lung, Colorectal, and Ovarian Cancer detected early enough [12]. Screening Trial,” Archives of Internal Medicine, vol. 168, no. 21, pp. 2326–2332, 2008. [10] R. Carroll, “The influence of lung scars on primary lung 4. Conclusion cancer,” The Journal of Pathology and Bacteriology, vol. 83, Our case serves to highlight the link between pulmonary no. 1, pp. 293–297, 1962. scarring and carcinogenesis, as well as to demonstrate the [11] L. J. Freant, W. L. Joseph, and P. C. Adkins, “Scar carcinoma of relentless course of lung scar carcinoma, which necessitates the lung. Fact or fantasy?,” The Annals of Thoracic Surgery, timely diagnosis. The USPSTF recommends annual screen- vol. 17, no. 6, pp. 531–537, 1974. ing for lung cancer with a low-dose CT scan of chest in adults [12] F. Gao, X. Ge, M. Li et al., “CT features of lung scar cancer,” aged 55 to 80 who have a 30 pack-year smoking history. Journal of Thoracic Disease, vol. 7, no. 3, pp. 273–280, 2015. However, no such recommendations exist for individuals with a known history of lung scarring. Our case reinforces the need for periodic CT imaging of the chest in this group of individuals who are at increased risk of this form of malig- nancy and underscores the need for evidence to determine the survival benefit of such a measure. Disclosure Hassaan Yasin’s present address is Marshall University, Joan C. Edwards School of Medicine, Edwards Comprehensive Cancer Center, 1400 Hal Greer Boulevard, Huntington, WV 25701, USA. Conflicts of Interest The authors declare that they have no conflicts of interest. References [1] D. M. Parkin, F. Bray, J. Ferlay, and P. Pisani, “Global cancer statistics, 2002,” CA: a Cancer Journal for Clinicians, vol. 55, no. 2, pp. 74–108, 2005. [2] S. Couraud, G. Zalcman, B. Milleron, F. Morin, and P. J. Souquet, “Lung cancer in never smokers – a review,” European Journal of Cancer, vol. 48, no. 9, pp. 1299–1311, 2012. [3] P. de Groot and R. F. Munden, “Lung cancer epidemiology, risk factors, and prevention,” Radiologic Clinics of North America, vol. 50, no. 5, pp. 863–876, 2012. MEDIATORS of INFLAMMATION The Scientific Gastroenterology Journal of World Journal Research and Practice Diabetes Research Disease Markers Hindawi Hindawi Publishing Corporation Hindawi Hindawi Hindawi Hindawi www.hindawi.com Volume 2018 http://www www.hindawi.com .hindawi.com V Volume 2018 olume 2013 www.hindawi.com Volume 2018 www.hindawi.com Volume 2018 www.hindawi.com Volume 2018 International Journal of Journal of Immunology Research Endocrinology Hindawi Hindawi www.hindawi.com Volume 2018 www.hindawi.com Volume 2018 Submit your manuscripts at www.hindawi.com BioMed PPAR Research Research International Hindawi Hindawi www.hindawi.com Volume 2018 www.hindawi.com Volume 2018 Journal of Obesity Evidence-Based Journal of Journal of Stem Cells Complementary and Ophthalmology International Alternative Medicine Oncology Hindawi Hindawi Hindawi Hindawi Hindawi www.hindawi.com Volume 2018 www.hindawi.com Volume 2018 www.hindawi.com Volume 2018 www.hindawi.com Volume 2018 www.hindawi.com Volume 2013 Parkinson’s Disease Computational and Behavioural Mathematical Methods AIDS Oxidative Medicine and in Medicine Neurology Research and Treatment Cellular Longevity Hindawi Hindawi Hindawi Hindawi Hindawi www.hindawi.com Volume 2018 www.hindawi.com Volume 2018 www.hindawi.com Volume 2018 www.hindawi.com Volume 2018 www.hindawi.com Volume 2018

Journal

Case Reports in Oncological MedicineHindawi Publishing Corporation

Published: Apr 8, 2019

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