scholarly journals Open Source 3D Printed Lung Tumor Movement Simulator for Radiotherapy Quality Assurance

Materials ◽  
2018 ◽  
Vol 11 (8) ◽  
pp. 1317 ◽  
Author(s):  
Darío Quiñones ◽  
David Soler-Egea ◽  
Víctor González-Pérez ◽  
Johanna Reibke ◽  
Elena Simarro-Mondejar ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Quality Assurance ◽  
Side Effects ◽  
Causes Of Death ◽  
Human Lung ◽  
Radiation Treatment ◽  
Lung Tumor ◽  
Moving Target ◽  
Treatment Plans ◽  
3D Printed

In OECD (Organization for Economic Co-operation and Development) countries, cancer is one of the main causes of death, lung cancer being one of the most aggressive. There are several techniques for the treatment of lung cancer, among which radiotherapy is one of the most effective and least invasive for the patient. However, it has associated difficulties due to the moving target tumor. It is possible to reduce the side effects of radiotherapy by effectively tracking a tumor and reducing target irradiation margins. This paper presents a custom electromechanical system that follows the movement of a lung tumor. For this purpose, a hysteresis loop of human lung movement during breathing was studied to obtain its characteristic movement equation. The system is controlled by an Arduino, steppers motors and a customized 3D printed mechanism to follow the characteristic human breathing, obtaining an accurate trajectory. The developed device helps the verification of individualized radiation treatment plans and permits the improvement of radiotherapy quality assurance procedures.

scholarly journals The Oncogenic Potential of a Mutant TP53 Gene Explored in Two Spontaneous Lung Cancer Mice Models

2020 ◽  
Author(s):  
Julian Ramelow ◽  
Christopher Brooks ◽  
Li GaO ◽  
Abeer A Almiman ◽  
Terence M Williams ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Mouse Models ◽  
Human Lung ◽  
Lung Tumor ◽  
Mutant Gene ◽  
Genetic Mutation ◽  
Tumor Formation ◽  
Human Lung Cancer ◽  
Oncogenic Potential ◽  
Age Related

Abstract BackgroundLung cancer is the number one cancer killer worldwide. A major impediment to progress in the lung cancer treatment field is the lack of realistic mouse models that replicate the complexity of human malignancy and immune contexture within the tumor microenvironment. Such models are urgently needed. Mutations of the tumor suppressor gene TP53 are among the most common alterations in human lung cancers.MethodsPreviously, we developed a line of lung cancer mouse model where mutant human TP53-273H is expressed in a lung specific manner in FVB/N background. To investigate whether the human TP53 mutant has a similar oncogenic potential when it is expressed in another strain of mouse, we crossed the FVB/N-SPC-TP53-273H mice to A/J strain and created A/J-SPC-TP53-273H transgenic mice. We then compared lung tumor formation between A/J-SPC-TP53-273H and FVB/N-SPC-TP53-273H.ResultsWe found the TP53-273H mutant gene has a similar oncogenic potential in lung tumor formation in both mice strains, although A/J strain mice have been found to be a highly susceptible strain in terms of carcinogen-induced lung cancer. Both transgenic lines survived more than 18 months and developed age related lung adenocarcinomas. With micro CT imaging, we found the FVB-SPC-TP53-273H mice survived more than 8 weeks after initial detection of lung cancer, providing a sufficient window for evaluating new anti-cancer agents.ConclusionsOncogenic potential of the most common genetic mutation, TP53-273H, in human lung cancer is unique when it is expressed in different strains of mice. Our mouse models are useful tools for testing novel immune check point inhibitors or other therapeutic strategies in treatment of lung cancer.

scholarly journals Morphological Changes in H1299 Human Lung Cancer Cells Following Millimeter-Wave Irradiation

2020 ◽  
Author(s):  
Konstantin Komoshvili ◽  
Tzippi Beker ◽  
Jacob Levitan ◽  
Asher Yahalom ◽  
Ayan Barbora ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Side Effects ◽  
Cancer Cells ◽  
Human Lung ◽  
Morphological Changes ◽  
Lung Cancer Cells ◽  
Human Lung Cancer ◽  
Physical Parameters ◽  
Dependent Manner ◽  
Human Lung Cancer Cells

Efficiently targeted cancer therapy without causing detrimental side effects is necessary for alleviating patient care and improving survival rates. This paper presents observations of morphological changes in H1299 human lung cancer cells following MMW irradiation (75 – 105 GHz) at a non-thermal power density of 0.2 mW/cm2, investigated over 14 days of subsequent physiological incubation following exposure. Microscopic analyses of physical parameters measured indicate MMW irradiation induces significant morphological changes characteristic of apoptosis and senescence. The Immediate short-term stress responses translate into long-term effects, retained over the duration of the experiment(s); reminiscent of the phenomenon of Accelerated Cellular Senescence (ACS) achieving terminal tumorigenic cell growth. Further, results were observed to be treatment-specific in energy (dose) dependent manner and were achieved without the use of chemotherapeutic agents, ionizing radiation or thermal ablation employed in conventional methods; thereby overcome associated side effects. Adaptation of the experimental parameters of this study in clinical oncology concomitant with current developmental trends of non-invasive medical endoscopy alleviates MMW therapy as an effective treatment procedure for human non-small cell lung cancer (NSLC)

scholarly journals Methyl DNA phosphate adduct formation in lung tumor tissue and adjacent normal tissue of lung cancer patients

2019 ◽  
Vol 40 (11) ◽  
pp. 1387-1394 ◽  
Author(s):  
Bin Ma ◽  
Peter W Villalta ◽  
J Bradley Hochalter ◽  
Irina Stepanov ◽  
Stephen S Hecht
Keyword(s):  
Lung Cancer ◽  
Dna Adducts ◽  
Human Lung ◽  
Lung Tumor ◽  
Normal Lung ◽  
Lung Cancer Patients ◽  
Normal Tissues ◽  
Phosphate Backbone ◽  
Limit Of Quantitation ◽  
Methylating Carcinogens

Abstract The formation of methyl DNA adducts is a critical step in carcinogenesis initiated by the exposure to methylating carcinogens. Methyl DNA phosphate adducts, formed by methylation of the oxygen atoms of the DNA phosphate backbone, have been detected in animals treated with methylating carcinogens. However, detection of these adducts in human tissues has not been reported. We developed an ultrasensitive liquid chromatography–nanoelectrospray ionization–high resolution tandem mass spectrometry method for detecting methyl DNA phosphate adducts. Using 50 μg of human lung DNA, a limit of quantitation of two adducts/1010 nucleobases was achieved. Twenty-two structurally unique methyl DNA phosphate adducts were detected in human lung DNA. The adduct levels were measured in both tumor and adjacent normal tissues from 30 patients with lung cancer, including 13 current smokers and 17 current non-smokers, as confirmed by measurements of urinary cotinine and 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol. Levels of total methyl DNA phosphate adducts in normal lung tissues were higher in smokers than non-smokers, with an average of 13 and 8 adducts/109 nucleobases, respectively. Methyl DNA phosphate adducts were also detected in lung tissues from untreated rats with steady-state levels of 5–7 adducts/109 nucleobases over a period of 70 weeks. This is the first study to report the detection of methyl DNA phosphate adducts in human lung tissues. The results provide new insights toward using these DNA adducts as potential biomarkers to study human exposure to environmental methylating carcinogens.

Optimizing radiation treatment plans for lung cancer using lung perfusion information

2002 ◽  
Vol 63 (2) ◽  
pp. 165-177 ◽  
Author(s):  
Yvette Seppenwoolde ◽  
Martijn Engelsman ◽  
Katrien De Jaeger ◽  
Sara H. Muller ◽  
Paul Baas ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Radiation Treatment ◽  
Lung Perfusion ◽  
Treatment Plans

scholarly journals Overexpression of CXCR7 accelerates tumor growth and metastasis of lung cancer cells

2020 ◽  
Vol 21 (1) ◽  
Author(s):  
Huan Liu ◽  
Qian Cheng ◽  
Dong-sheng Xu ◽  
Wen Wang ◽  
Zheng Fang ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Migration ◽  
Human Lung ◽  
Lung Tumor ◽  
Xenograft Model ◽  
Cell Polarization ◽  
Human Lung Cancer ◽  
Migration And Invasion ◽  
Mouse Xenograft ◽  
Mouse Xenograft Model

Abstract Background Under physiological conditions, CXCL12 modulates cell proliferation, survival, angiogenesis, and migration mainly through CXCR4. Interestingly, the newly discovered receptor CXCR7 for CXCL12 is highly expressed in many tumor cells as well as tumor-associated blood vessels, although the level of CXCR7 in normal cells is low. Recently, many studies have suggested that CXCR7 promotes cell growth and metastasis in more than 20 human malignancies, among which lung cancer is the leading cause of cancer-associated deaths worldwide. Thus, the mechanism of CXCR7 in the progression of lung cancer is urgently needed. Methods First, we explored CXCR4 and CXCR7 expression in human lung cancer specimens and cell lines by immunohistochemistry, western blot and flow cytometry. Then, we chose the human lung adenocarcinoma cell line A549 that stably overexpressed CXCR7 through the way of lentivirus-mediated transduction. Next, “wound healing” assay and transwell assay were applied to compare the cell migration and invasion ability, and stripe assay was used to evaluate the cell polarization. Last, our team established a mouse xenograft model of human lung cancer and monitored tumor proliferation and metastasis by firefly luciferase bioluminescence imaging in SCID/Beige mice. Results In clinical lung cancer samples, CXCR7 expression was almost not detected in normal tissue but upregulated in lung tumor tissue, whereas, CXCR4 was highly expressed in both normal and tumor tissues. Furthermore, overexpression of CXCR7 enhanced A549 cell migration and polarization in vitro. Besides, mouse xenograft model of human lung cancer showed that CXCR7 promoted primary lung tumor’s growth and metastasis to the second organ, such as liver or bone marrow in SCID/Beige mice in vivo. Conclusions This study describes the multiple functions of CXCR7 in lung cancer. Thus, these results suggest that CXCR7 may be a malignancy marker and may provide a novel target for anticancer therapy.

Metastatic lung cancer in patient with non-malignant neck pain: A case report

2017 ◽  
Vol 16 (1) ◽  
pp. 178
Author(s):  
W.Z. Pawlak ◽  
L. Svensson ◽  
P.F. Jensen
Keyword(s):  
Lung Cancer ◽  
Case Report ◽  
Side Effects ◽  
Neck Pain ◽  
Lung Tumor ◽  
Behavioral Therapy ◽  
Multidisciplinary Treatment ◽  
Cerebral Metastases ◽  
Experienced Fatigue ◽  
The Right

AbstractBackgroundSymptoms from disseminated cancer can develop very slowly. This could be very difficult to distinguish those symptoms from chronic disabilities and nuisances in patients with chronic non-malignant pain.ObjectiveIn this report, the case of a woman with both nonmalignant pain and cancer is presented.Case reportA 54 years old woman was referred by a general practitioner to Multidisciplinary Pain Center. The diagnosis was chronic non-malignant neck pain on the basis of degenerative columnar disease. The patient was also suffering from osteoporosis. During the first visit in the Center, the patient complained of shooting pains in the neck and had tingling sensations in the fingers – most of his right hand. Moreover, the patient experienced shooting pains in the hips, lower back and spine. The multidisciplinary treatment with medication, physical therapy, TENS and cognitive behavioral therapy was offered. Paracetamol together with gabapentin was used. The patient experienced relief of pain. The doses of gabapentin was escalated up to 2400 mg daily without significant side effects. Afterwards, the dose was gradually increased to 3600 mg daily and the patient experienced fatigue, mild headache and dizziness. These symptoms were initially interpreted as side effects of gabapentin. However, the tingling sensations in the fingers were almost disappeared. The doses of gabapentin was reduced, but without relief of symptoms. Within 2 weeks, the patient developed partial paresis of the right upper limb and aphasia. The patient was urgently referred to the neurologic inpatient clinic. CT- and MR-scans showed multiple cerebral metastases. Under the diagnostic workup the lung tumor was found. The biopsy showed pulmonary adenocarcinoma.ConclusionsThe symptoms of lung cancer with cerebral metastases can mimic side effects of gabapentin.

scholarly journals Overexpression of CXCR7 Accelerates Tumor Growth and Metastasis of Lung Cancer Cells

2020 ◽  
Author(s):  
Liu Huan ◽  
Cheng Qian ◽  
Xu Dong sheng ◽  
Wang Wen ◽  
Fang Zheng ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Migration ◽  
Human Lung ◽  
Lung Tumor ◽  
Xenograft Model ◽  
Cell Polarization ◽  
Human Lung Cancer ◽  
Migration And Invasion ◽  
Mouse Xenograft ◽  
Mouse Xenograft Model

Abstract Background: Under physiological conditions, CXCL12 modulates cell proliferation, survival, angiogenesis, and migration mainly through CXCR4. Interestingly, the newly discovered receptor CXCR7 for CXCL12 is highly expressed in many tumor cells as well as tumor-associated blood vessels, although the level of CXCR7 in normal cells is low. Recently, many studies have suggested that CXCR7 promotes cell growth and metastasis in more than 20 human malignancies, among which lung cancer is the leading cause of cancer-associated deaths worldwide. Thus, the mechanism of CXCR7 in the progression of lung cancer is urgently needed.Methods: First, we explored CXCR4 and CXCR7 expression in human lung cancer specimens and cell lines by immunohistochemistry, western blot and flow cytometry. Then, we chose the human lung adenocarcinoma cell line A549 that stably overexpressed CXCR7 through the way of lentivirus-mediated transduction. Next, “wound healing” assay and transwell assay were applied to compare the cell migration and invasion ability, and stripe assay was used to evaluate the cell polarization. Last, our team established a mouse xenograft model of human lung cancer and monitored tumor proliferation and metastasis by firefly luciferase bioluminescence imaging in SCID/Beige mice. Results: In clinical lung cancer samples, CXCR7 expression was almost not detected in normal tissue but upregulated in lung tumor tissue, whereas, CXCR4 was highly expressed in both normal and tumor tissues. Furthermore, overexpression of CXCR7 enhanced A549 cell migration and polarization in vitro. Besides, mouse xenograft model of human lung cancer showed that CXCR7 promoted primary lung tumor’s growth and metastasis to the second organ, such as liver or bone marrow in SCID/Beige mice in vivo.Conclusions: This study describes the multiple functions of CXCR7 in lung cancer. Thus, these results suggest that CXCR7 may be a malignancy marker and may provide a novel target for anticancer therapy.

scholarly journals Morphological Changes in H1299 Human Lung Cancer Cells Following Millimeter-Wave Irradiation

2020 ◽  
Author(s):  
Konstantin Komoshvili ◽  
Tzippi Becker ◽  
Jacob Levitan ◽  
Asher Yahalom ◽  
Ayan Barbora ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Side Effects ◽  
Cancer Cells ◽  
Human Lung ◽  
Morphological Changes ◽  
Lung Cancer Cells ◽  
Human Lung Cancer ◽  
Physical Parameters ◽  
Dependent Manner ◽  
Human Lung Cancer Cells

Efficiently targeted cancer therapy without causing detrimental side effects is necessary for alleviating patient care and improving survival rates. This paper presents observations of morphological changes in H1299 human lung cancer cells following W-band MMW irradiation (75 – 105 GHz) at a non-thermal power density of 0.2 mW/cm2, investigated over 14 days of subsequent physiological incubation following exposure. Microscopic analyses of physical parameters measured indicate MMW irradiation induces significant morphological changes characteristic of apoptosis and senescence. The Immediate short-term responses translate into long-term effects, retained over the duration of the experiment(s); reminiscent of the phenomenon of Accelerated Cellular Senescence (ACS) achieving terminal tumorigenic cell growth. Further, results were observed to be treatment-specific in energy (dose) dependent manner and were achieved without the use of chemotherapeutic agents, ionizing radiation or thermal ablation employed in conventional methods; thereby overcoming associated side effects. Adaptation of the experimental parameters of this study for clinical oncology concomitant with current developmental trends of non-invasive medical endoscopy alleviates MMW therapy as an effective treatment procedure for human non-small cell lung cancer (NSCLC).

scholarly journals Metatranscriptomic Analysis of Human Lung Metagenomes from Patients with Lung Cancer

Genes ◽  
2021 ◽  
Vol 12 (9) ◽  
pp. 1458
Author(s):  
Ya-Sian Chang ◽  
Ming-Hung Hsu ◽  
Siang-Jyun Tu ◽  
Ju-Chen Yen ◽  
Ya-Ting Lee ◽  
...  
Keyword(s):  
Lung Cancer ◽  
T Cells ◽  
Cancer Patients ◽  
Human Lung ◽  
Lung Tumor ◽  
Receptor Gene ◽  
Growth Factor Receptor ◽  
Good Prognosis ◽  
Human Lung Cancer ◽  
Immune Receptor

This study was designed to characterize the microbiomes of the lung tissues of lung cancer patients. RNA-sequencing was performed on lung tumor samples from 49 patients with lung cancer. Metatranscriptomics data were analyzed using SAMSA2 and Kraken2 software. 16S rRNA sequencing was also performed. The heterogeneous cellular landscape and immune repertoires of the lung samples were examined using xCell and TRUST4, respectively. We found that nine bacteria were significantly enriched in the lung tissues of cancer patients, and associated with reduced overall survival (OS). We also found that subjects with mutations in the epidermal growth factor receptor gene were less likely to experience the presence of Pseudomonas. aeruginosa. We found that the presence of CD8+ T-cells, CD4+ naive T-cells, dendritic cells, and CD4+ central memory T cells were associated with a good prognosis, while the presence of pro B-cells was associated with a poor prognosis. Furthermore, high clone numbers were associated with a high ImmuneScore for all immune receptor repertoires. Clone numbers and diversity were significantly higher in unpresented subjects compared to presented subjects. Our results provide insight into the microbiota of human lung cancer, and how its composition is linked to the tumor immune microenvironment, immune receptor repertoires, and OS.

scholarly journals The oncogenic potential of a mutant TP53 gene explored in two spontaneous lung cancer mice models

2020 ◽  
Author(s):  
Julian Ramelow ◽  
Christopher Brooks ◽  
Li GaO ◽  
Abeer A Almiman ◽  
Terence M Williams ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Mouse Models ◽  
Human Lung ◽  
Lung Tumor ◽  
Mutant Gene ◽  
Genetic Mutation ◽  
Tumor Formation ◽  
Human Lung Cancer ◽  
Oncogenic Potential ◽  
Age Related

Abstract Background: Lung cancer is the number one cancer killer worldwide. A major impediment to progress in the lung cancer treatment field is the lack of realistic mouse models that replicate the complexity of human malignancy and immune contexture within the tumor microenvironment. Such models are urgently needed. Mutations of the tumor suppressor gene TP53 are among the most common alterations in human lung cancers. Methods: Previously, we developed a line of lung cancer mouse model where mutant human TP53-273H is expressed in a lung specific manner in FVB/N background. To investigate whether the human TP53 mutant has a similar oncogenic potential when it is expressed in another strain of mouse, we crossed the FVB/N-SPC-TP53-273H mice to A/J strain and created A/J-SPC-TP53-273H transgenic mice. We then compared lung tumor formation between A/J-SPC-TP53-273H and FVB/N-SPC-TP53-273H. Results: We found the TP53-273H mutant gene has a similar oncogenic potential in lung tumor formation in both mice strains, although A/J strain mice have been found to be a highly susceptible strain in terms of carcinogen-induced lung cancer. Both transgenic lines survived more than 18 months and developed age related lung adenocarcinomas. With micro CT imaging, we found the FVB-SPC-TP53-273H mice survived more than 8 weeks after initial detection of lung cancer, providing a sufficient window for evaluating new anti-cancer agents. Conclusions: Oncogenic potential of the most common genetic mutation, TP53-273H, in human lung cancer is unique when it is expressed in different strains of mice. Our mouse models are useful tools for testing novel immune check point inhibitors or other therapeutic strategies in treatment of lung cancer.

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