Journal articles on the topic 'Cancer cell metastasis'
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Park, Hyung Kyu, Joungho Han, Ghee Young Kwon, Min-Kyung Yeo, and Go Eun Bae. "Patterns of Extrathoracic Metastasis in Lung Cancer Patients." Current Oncology 29, no. 11 (November 16, 2022): 8794–801. http://dx.doi.org/10.3390/curroncol29110691.
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Metastasis is a major cause of death in lung cancer patients. Therefore, a deeper understanding of the metastatic mechanisms is important for developing better management strategies for lung cancer patients. This study evaluated the patterns of extrathoracic metastases in lung cancer. We retrieved data for 25,103 lung cancer patients from an institutional database and then evaluated the impacts of clinicopathologic factors on metastasis patterns. We found that 36.5% of patients had extrathoracic metastasis. Younger patients had a significantly higher extrathoracic metastasis rate in most histologic subtypes. Metastases to the bone (58.3%), central nervous system (CNS) (44.3%), liver (26.6%) and adrenal gland (18.3%) accounted for 85.5% of all extrathoracic metastases. Patients with nonmucinous adenocarcinoma had significantly higher bone metastasis rate. Patients with small cell carcinoma and large cell neuroendocrine carcinoma (LCNEC) had significantly higher liver metastasis rates. Further, patients with LCNEC also had a significantly lower bone metastasis rate, and patients with squamous cell carcinoma had a significantly lower CNS metastasis rate. Patients with multiple cancers had similar patterns of metastasis compared to patients with only lung cancer. In conclusion, different histologic subtypes of lung cancer have different metastatic patterns. Our study might help clinicians decide on follow-up strategies.
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Voss, Gjendine, Benedikta S. Haflidadóttir, Helena Järemo, Margareta Persson, Tina Catela Ivkovic, Pernilla Wikström, and Yvonne Ceder. "Regulation of cell–cell adhesion in prostate cancer cells by microRNA-96 through upregulation of E-Cadherin and EpCAM." Carcinogenesis 41, no. 7 (November 18, 2019): 865–74. http://dx.doi.org/10.1093/carcin/bgz191.
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Abstract Prostate cancer is one of the most common cancers in men, yet the biology behind lethal disease progression and bone metastasis is poorly understood. In this study, we found elevated levels of microRNA-96 (miR-96) in prostate cancer bone metastasis samples. To determine the molecular mechanisms by which miR-96 deregulation contributes to metastatic progression, we performed an Argonaute2-immunoprecipitation assay, in which mRNAs associated with cell–cell interaction were enriched. The expression of two cell adhesion molecules, E-Cadherin and EpCAM, was upregulated by miR-96, and potential targets sites were identified in the coding sequences of their mRNAs. We further showed that miR-96 enhanced cell–cell adhesion between prostate cancer cells as well as their ability to bind to osteoblasts. Our findings suggest that increased levels of miR-96 give prostate cancer cells an advantage at forming metastases in the bone microenvironment due to increased cell–cell interaction. We propose that miR-96 promotes bone metastasis in prostate cancer patients by facilitating the outgrowth of macroscopic tumours in the bone.
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Alkhayat, Hana, and Chih-ho Hong. "Cutaneous Metastases from Non-Small Cell Lung Cancer." Journal of Cutaneous Medicine and Surgery 10, no. 6 (November 2006): 304–7. http://dx.doi.org/10.2310/7750.2006.00061.
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Background: Cutaneous metastases are an uncommon phenomenon that occurs in a few patients with metastatic disease. Early recognition of a cutaneous metastasis is important as it may be the presenting sign of an underlying malignancy. These metastases usually indicate advanced disease and carry a poor prognosis. Objectives: We present two cases with cutaneous metastasis from primary non-small cell lung cancer. We seek to familiarize dermatologists with the unusual presentations of cutaneous metastases. Conclusion: In our two cases, the diagnosis of the metastatic cutaneous lesion ultimately led to the correct diagnosis of an underlying malignancy.
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Su, ChunXia, Juan Zhou, Xiangling Chu, and Jing Zhao. "Genetic mutations associated with lung cancer metastasis to the brain." Journal of Global Oncology 5, suppl (October 7, 2019): 41. http://dx.doi.org/10.1200/jgo.2019.5.suppl.41.
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41 Background: Lung cancer is the most common cause of mortality in both men and women, accounting for one-quarter of all cancer deaths. Most lung cancer-associated deaths result from metastasis, especially brain metastasis. Metastasis associated mutations are important biomarkers for metastasis prediction and outcome improvement. The current study aimed to reveal the molecular mechanisms and the genetic alterations involved in metastasis from lung tumors to the brain. Methods: We carried out whole exome sequencing (WES) of the primary tumors and the corresponding brain metastases from 15 patients with metastatic non-small-cell lung carcinoma. Results: We identified novel lung cancer metastases associated genes (CHEK2P2, BAGE2, AHNAK2) and epigenetic factors (miR-4436A, miR-6077). Lung-brain metastasis samples have more similar Ti/Tv(transition/transversion) profile with brain cancer. Focal adhesion, PI3K-Akt signaling pathway, MAPK signaling pathway are some of the most important tumor onset and metastasis pathways. Alternative splicing, Methylation and EGF-like domain are important metabolic abnormal for the lung-metastasis cancers. Conclusions: We conducted a pairwise lung-brain metastasis based WES and identified some novel metastasis related mutations which provided potential biomarkers for prognosis and targeted therapeutics.
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Kiberstis, P. A. "Engineering cancer cell metastasis." Science 347, no. 6221 (January 29, 2015): 516. http://dx.doi.org/10.1126/science.347.6221.516-c.
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Hassan, B. B., S. M. Elshafae, W. Supsavhad, J. K. Simmons, W. P. Dirksen, S. M. Sokkar, and T. J. Rosol. "Feline Mammary Cancer." Veterinary Pathology 54, no. 1 (July 11, 2016): 32–43. http://dx.doi.org/10.1177/0300985816650243.
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Feline mammary carcinoma (FMC) is similar to human breast cancer in the late age of onset, incidence, histopathologic features, biological behavior, and pattern of metastasis. Therefore, FMC has been proposed as a relevant model for aggressive human breast cancer. The goals of this study were to develop a nude mouse model of FMC tumor growth and metastasis and to measure the expression of genes responsible for lymphangiogenesis, angiogenesis, tumor progression, and lymph node metastasis in FMC tissues and cell lines. Two primary FMC tissues were injected subcutaneously, and 6 FMC cell lines were injected into 3 sites (subcutaneous, intratibial, and intracardiac) in nude mice. Tumors and metastases were monitored using bioluminescent imaging and characterized by gross necropsy, radiology, and histopathology. Molecular characterization of invasion and metastasis genes in FMC was conducted using quantitative real-time reverse transcription polymerase chain reaction in 6 primary FMC tissues, 2 subcutaneous FMC xenografts, and 6 FMC cell lines. The histologic appearance of the subcutaneous xenografts resembled the primary tumors. No metastasis was evident following subcutaneous injection of tumor tissues and cell lines, whereas lung, brain, liver, kidney, eye, and bone metastases were confirmed following intratibial and intracardiac injection of FMC cell lines. Finally, 15 genes were differentially expressed in the FMC tissues and cell lines. The highly expressed genes in all samples were PDGFA, PDGFB, PDGFC, FGF2, EGFR, ERBB2, ERBB3, VEGFD, VEGFR3, and MYOF. Three genes ( PDGFD, ANGPT2, and VEGFC) were confirmed to be of stromal origin. This investigation demonstrated the usefulness of nude mouse models of experimental FMC and identified molecular targets of FMC progression and metastasis.
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Hoang, Tien Manh, and Thi Thanh Nguyen. "Comparative analysis of overall survival in non-small cell lung cancer patients with and without different organ metastases." Ministry of Science and Technology, Vietnam 64, no. 3 (March 15, 2022): 33–38. http://dx.doi.org/10.31276/vjste.64(1).33-38.
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Lung cancer is the leading cause of cancer death globally. Non-small cell lung cancer (NSCLC) constitutes more than 80% of all lung cancers, and patients with distant metastasis have much higher mortality. The survival times of NSCLC patients with metastasis have been reported in early studies, however, it remains unclear whether there are variations or patterns in survival times of patients with different metastases. Therefore, we assessed risk factors for distant metastases and the effects of different organ metastasis on overall survival (OS) in patients with NSCLC. Methods: demographics and clinical data of NSCLC patients with and without distant metastasis were collected from the Surveillance, Epidemiology, and End Result (SEER) database between 2010 and 2016. We investigated risk factors for distant metastasis patients and compared the difference in OS of NSCLC patients with different metastatic sites. Results: a total of 3849 patients diagnosed with NSCLC were screened from the SEER database with 41% (1577) of the patients having distant metastasis. During the follow-up period, 3221 (83.7%) patients died and, of all the deceased patients, 2935 (88.4%) died of lung cancer while only 286 (11.6%) died from other diseases or causes. The occurrence of distant metastasis was closely related to the patient’s age, primary tumour site, tumour grade, T stage, N stage, surgery of primary site, radiation therapy, and chemotherapy (p<0.05). Compared to patients without metastasis, whose median OS was 13 months, the median OS of patients with metastasis was 6 months (lung), 5 months (liver), 5 months (bone), 4 months (brain), and 3 months (multiple organs). Conclusions: distant metastasis indicates a poor prognosis in NSCLC patients. There were significant differences in the prognosis of different metastatic sites and the order of their OS from high to low was: no metastasis > lung metastasis, liver metastasis, bone metastasis > brain metastasis, multiple organ metastasis.
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V., Ramya, and Sahayaraj J. "Transitional cell carcinoma of urinary bladder with cervical lymph node metastasis: a case report and review of literature." International Journal of Advances in Medicine 6, no. 1 (January 23, 2019): 194. http://dx.doi.org/10.18203/2349-3933.ijam20190130.
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Bladder cancer usually spreads via the lymphatic and hematogenous routes, the common sites of metastases of urinary bladder cancers being the regional lymph nodes, liver, lung, bone, peritoneum, pleura, kidney, adrenal gland and intestines. Metastasis to non-regional lymph nodes especially cervical lymph nodes is extremely rare presentation. Metastasis to head and neck region is associated with poor prognosis and low survival rate. Here-in we report a case of cervical lymph node metastasis in patient with muscle invasive bladder cancer.
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Apanovich, Natalya, Maria Peters, Pavel Apanovich, Danzan Mansorunov, Anna Markova, Vsevolod Matveev, and Alexander Karpukhin. "The Genes—Candidates for Prognostic Markers of Metastasis by Expression Level in Clear Cell Renal Cell Cancer." Diagnostics 10, no. 1 (January 8, 2020): 30. http://dx.doi.org/10.3390/diagnostics10010030.
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The molecular prognostic markers of metastasis are important for personalized approaches to clear cell renal cell carcinoma (ccRCC) treatment but markers for practical use are still missing. To address this gap we studied the expression of ten genes—CA9, NDUFA4L2, VWF, IGFBP3, BHLHE41, EGLN3, SAA1, CSF1R, C1QA, and FN1—through RT-PCR, in 56 ccRCC patients without metastases and with metastases. All of these, excluding CSF1R, showed differential and increased (besides SAA1) expression in non-metastasis tumors. The gene expression levels in metastasis tumors were decreased, besides CSF1R, FN1 (not changed), and SAA1 (increased). There were significant associations of the differentially expressed genes with ccRCC metastasis by ROC analysis and the Fisher exact test. The association of the NDUFA4L2, VWF, EGLN3, SAA1, and C1QA expression with ccRCC metastasis is shown for the first time. The CA9, NDUFA4L2, BHLHE4, and EGLN3 were distinguished as the strongest candidates for ccRCC metastasis biomarkers. We used an approach that presupposed that the metastasis marker was the expression levels of any three genes from the selected panel and received sensitivity (88%) and specificity (73%) levels with a relative risk of RR > 3. In conclusion, a panel of selected genes—the candidates in biomarkers of ccRCC metastasis—was created for the first time. The results might shed some light on the ccRCC metastasis processes.
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Del Vecchio, Sharon, Robert Ellis, Kylie Gallagher, Keng Lim Ng, Li Ma, Geoffrey Strutton, and Simon Wood. "A Rare Case of Solitary Kidney Metastasis following Primary Laryngeal Squamous Cell Carcinoma." Journal of Kidney Cancer and VHL 4, no. 2 (May 2, 2017): 6–9. http://dx.doi.org/10.15586/jkcvhl.2017.68.
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Laryngeal cancer is the 14th most common malignancy worldwide, and its common subtype squamous cell carcinoma (SCC) is highly associated with tobacco use and long-term alcohol consumption. The incidence of distant metastasis from a primary laryngeal cancer has been reported to be very low, between 6.5% and 8.5%, according to published tumour registry data. Distant metastases of laryngeal SCC most commonly involve the lung, liver, bone and mediastinum, seldom involving the kidney. Renal metastasis has been well established in many other cancers such as lymphoma, lung, breast and gastric carcinoma. This report discusses the rare case of a solitary renal metastasis following a primary laryngeal SCC.
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Namad, Tariq, Jiang Wang, Annemarie Tilton, and Nagla Abdel Karim. "Bilateral Choroidal Metastasis from Non-Small Cell Lung Cancer." Case Reports in Oncological Medicine 2014 (2014): 1–5. http://dx.doi.org/10.1155/2014/858265.
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Breast and lung cancers are the most common primary neoplasms to manifest with choroidal metastases. The incidence of choroidal metastases from metastatic lung cancer was reported to be 2–6.7%. We report a case of bilateral choroidal metastasis from non-small cell lung cancer. A 59-year-old Caucasian female patient, never a smoker, was diagnosed with stage IV lung adenocarcinoma metastatic to the pleura, bones, and the brain. Her initial scan of the chest showed innumerable soft tissue nodules and mediastinal adenopathy compatible with metastatic disease. Her initial brain MRI showed numerous small enhancing lesions consistent with extensive disease. Unfortunately, during her follow-up visits, she presented with bulge on her left eye. Simultaneously, her follow-up chest scan showed increase in the size of the lung nodules. She continued to have a reasonable performance status at that time, except for mild increase in her dyspnea. The choroidal metastases require a multidisciplinary care and should be among the differential patients with malignancy who present with ocular symptoms.
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Zhao, Yu, Huiqin Guo, Jiangyang Lu, David C. Christiani, Xihong Lin, and Zhaoxi Wang. "Association of brain metastasis in non-small cell lung cancer." Journal of Clinical Oncology 31, no. 15_suppl (May 20, 2013): e19081-e19081. http://dx.doi.org/10.1200/jco.2013.31.15_suppl.e19081.
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e19081 Background: Brain metastases are the main cause of non-small cell lung cancer (NSCLC) relapse and death. However, it is difficult to predict which NSCLC patient will develop brain metastasis. We have observed and summarized the relationship between the clinical and molecular biological features including EGFR mutation status and brain metastases in a prospectively enrolled case series, and developed a multivariable model in this study. Methods: The study enrolled 184 Chinese NSCLC patients with at least 18 months follow-up period. Clinical information including age, smoking history, lymph node status, pathological stage, primary location and histological type of the tumor and EGFR (including exon 19 and 21) and KRAS mutation status were collected and analyzed. Univariate and multivariate Cox regression analysis was run to investigate risk factors of brain metastasis from these features. A risk model based on these risk factors was constructive. Results: 13.0% (24/184) patients were diagnosed as brain metastasis. EGFR mutation (P=0.026), younger age (P=0.034) and lymph node metastasis (P=0.038) were associated with brain metastasis. A Cox model based on these 3 factors was founded and the risk of brain metastasis was 1.9% (1/53), 8.3% (5/60) and 25.4 % (18/71) in low, intermediate and high risk group, respectively (P<0.001). Conclusions: EGFR mutation, younger age and lymph node metastasis are associated with brain metastasis in NSCLC patients. If confirmed in clinical trials, high risk patients may be considered for prophylactic cranial irradiation therapy in future clinical trials
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Valiente, Manuel, Amanda Van Swearingen, Carey Anders, Amos Bairoch, Adrienne Boire, Paula Bos, Diana Cittelly, et al. "52. BrMPANEL: A PUBLIC RESOURCE OF ORGANOTROPIC CELL LINES." Neuro-Oncology Advances 2, Supplement_2 (August 2020): ii10—ii11. http://dx.doi.org/10.1093/noajnl/vdaa073.040.
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Abstract Central nervous system (CNS), notably brain, metastases are most prevalent in lung cancer (20–56% of patients), breast cancer (5–20%) and melanoma (7–16%). Lesions occur in both the brain parenchyma and the meninges. To mechanistically understand CNS metastasis formation and develop preventive and therapeutic strategies, it is essential to use model systems that, as much as possible, faithfully recapitulate the clinical disease process. Furthermore, the complexities of brain metastases dictate that studies should utilize multiple model systems in various stages of brain metastases progression. To facilitate brain metastasis research, 19 laboratories around the world have compiled comprehensive information on their brain metastasis mouse models. Each lab has provided details on the cell lines that they have generated or characterized as being capable of forming metastatic colonies in the brain, as well as principle methodologies of brain metastasis research. This Brain Metastasis Cell Lines Panel (BrMPanel, https://apps.cnio.es/app/BrainMetastasis/CellLines) represents the first of its class and includes information about each cell line, how tropism to the brain was established, and the behavior of each model in vivo. The BrMPanel is composed of 60 cell lines, derived from patients (32 cell lines, 53%), mouse (27, 45%) or rat (1, 2%), and represent the three main cancer types that result in brain metastasis: breast cancer (38 cell lines, 63%), lung cancer (8, 13%) and melanoma (14, 23%). This resource is intended to assist investigators in choosing the most suitable model for research on brain metastasis, and is available to the entire scientific community. The ultimate goal of this effort is to facilitate research on this unmet clinical need, to improve models through a collaborative environment, and to promote the exchange of information on these valuable resources. We invite other collaborators to contribute their models to the BrMPanel to grow this resource.
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Ali Mohammed Hammamy, Riyadh, Khalid Farooqui, and Wisam Ghadban. "Sclerotic Bone Metastasis in Pulmonary Adenocarcinoma." Case Reports in Medicine 2018 (June 12, 2018): 1–5. http://dx.doi.org/10.1155/2018/1903757.
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Pulmonary adenocarcinoma is one of the major types of lung cancers in which metastasis is very common and it accounts approximately to one-third of all primary pulmonary cancers. Although a minority of patients with lung cancer are asymptomatic, which gets usually detected in routine chest radiography, most of the patients present with some symptoms. Lung cancer metastasis may occur virtually in every organ system. Patients with non-small-cell lung cancer commonly have extrathoracic metastases to the adrenal glands, liver, brain, bones, and lymph nodes at presentation. Approximately one-third of patients with lung cancer will present with symptoms related to extrathoracic spread. Metastasis to the bone is not uncommon in lung cancer; however, osteoblastic bone metastasis is very rare. Here we present a 30-year-old female diagnosed to have pulmonary adenocarcinoma with multiple sclerotic bony lesions in the vertebra.
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Iijima, Yoshihito, Masahito Ishikawa, Shun Iwai, Nozomu Motono, Shigeki Yamagishi, Kiyoshi Koizumi, and Hidetaka Uramoto. "Is extrathoracic metastasis screening necessary for clinical stage IA non-small cell lung cancer?" Science Progress 105, no. 1 (January 2022): 003685042210851. http://dx.doi.org/10.1177/00368504221085152.
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Background: Detecting distant metastases when staging lung cancer is critical to avoid unnecessary surgery and provide appropriate multidisciplinary treatment. However, it is controversial as to whether staging studies should be performed routinely for patients with early-stage lung cancer who have no evidence of distant metastasis. Thus, this study aimed to examine the need for extrathoracic metastasis screening in patients with clinical stage IA non-small cell lung cancer, understand the association between extrathoracic metastasis and other clinical features, and evaluate the diagnostic efficiency of imaging screening for preoperative extrathoracic metastasis in patients with early-stage lung cancer. Methods: From 2010 to 2019, 510 patients diagnosed with clinical T1N0 lung cancer, excluding contralateral lung metastases, pleural dissemination, malignant pleural effusion, and malignant pericardial effusion, were treated for primary lung cancer. Patients were divided into two groups, and their clinicopathological characteristics were investigated. Results: Five patients (1.0%) had extrathoracic metastases. The histological types were adenocarcinoma in three of the cases, and squamous cell carcinoma and large cell neuroendocrine carcinoma in the other two cases. The T factor was T1b in one case and T1c in four cases. Four patients had solid tumors and one had a solid predominant tumor with an average tumor diameter of 23.0 ± 2.9 mm. The size of solid tumors with extrathoracic metastases was larger than their counterparts. Conclusion: When evaluating stage IA non-small cell lung cancer with a solid component diameter < 22 mm, or clinical T1mi-1bN0 in computed tomography evaluation, screening for preoperative extrathoracic metastasis may be omitted.
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Recio, Susana Garcia, Toshinori Hinoue, Gregory L. Wheeler, Benjamin J. Kelly, Justin M. Balko, Katherine A. Hoadley, Peter W. Laird, Elaine R. Mardis, and Charles M. Perou. "Abstract LB176: Multiplatform analysis of matched primary and metastatic breast tumors from the AURORA US Network identifies microenvironment features as drivers of metastasis." Cancer Research 82, no. 12_Supplement (June 15, 2022): LB176. http://dx.doi.org/10.1158/1538-7445.am2022-lb176.
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Abstract Background: Metastatic breast cancer (MBC) patients often have short survival, and successful treatment represents one of the most challenging aspects of cancer care. This poor prognosis is likely multifactorial, including increased clonal heterogeneity, drug resistance mechanisms, and alterations of the tumor microenvironment. Methods: The primary data source was multi-platform data coming from the AURORA US Project that includes RNAseq, DNAseq, and DNA methylation arrays, which assayed 55 MBC patients representing 51 primary cancers and 102 linked metastatic specimens. In addition, RNA sequencing data from two other datasets of primary tumor-metastasis pairs were also used (i.e. UNC Tumor Donation Program/RAP dataset (24 primary and 74 metastasis specimens), and the GEICAM/2009-03 ConvertHER trial dataset (102 primaries and 102 metastatic pairs)). In total, this combined RNAseq dataset contained 177 primary tumors and 278 metastases, including 28 liver, 18 lung, 12 brain, and 24 lymph node metastases. We used these data to address two pressing questions, namely: 1) do gene expression features vary in primary tumors vs metastases according to PAM50 expression subtype, and 2) do gene expression features vary according to site of metastasis. Results: Using the AURORA multi-platform data, we determined that 17% of metastatic tumors (mainly TNBC/Basal-like) showed reduced expression of HLA-A that was associated with DNA methylation and/or focal DNA deletions near the HLA-A locus; these methylated tumors also showed concomitant lower immune cell infiltrates. Reduced expression of HLA-A gene and immune cell infiltrates were also validated at the RNA level in RAP dataset. Next, RNA expression differences were examined using the combined data set and varied according to tumor subtype. ER+/Luminal metastases had lower fibroblast and endothelial cell content, while triple negative (TNBC)/Basal-like metastases showed a dramatic decrease in T cell and B cell signatures/features. Comparative analyses between primary and site-specific metastasis (i.e., primary vs liver metastasis) or between sites of metastases (i.e., liver vs lung metastasis) revealed that both liver and brain, on average, had low immune cell features regardless of the primary tumor phenotype. Even within the same patient, we detected low immune cell features in brain and liver metastases compared to lung and lymph node metastases. Lastly, liver metastases showed a gain of Luminal B/HER2E gene expression features and MYC targets, and brain TNBC metastasis showed a gain of cell differentiation/Luminal-related gene signatures. Conclusions: These findings could have direct implications for the treatment of MBC patients with immune-based therapies and suggest new therapeutic avenues depending upon the tumor metastasis phenotype, and site of metastasis. Citation Format: Susana Garcia Recio, Toshinori Hinoue, Gregory L. Wheeler, Benjamin J. Kelly, Justin M. Balko, Katherine A. Hoadley, Peter W. Laird, Elaine R. Mardis, Charles M. Perou. Multiplatform analysis of matched primary and metastatic breast tumors from the AURORA US Network identifies microenvironment features as drivers of metastasis [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2022; 2022 Apr 8-13. Philadelphia (PA): AACR; Cancer Res 2022;82(12_Suppl):Abstract nr LB176.
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Mansour, Hager, Ghmkin Hassan, Said M. Afify, Ting Yan, Akimasa Seno, and Masaharu Seno. "Metastasis Model of Cancer Stem Cell-Derived Tumors." Methods and Protocols 3, no. 3 (August 21, 2020): 60. http://dx.doi.org/10.3390/mps3030060.
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Metastasis includes the dissemination of cancer cells from a malignant tumor and seed in distant sites inside the body forming secondary tumors. Metastatic cells from the primary tumor can move even before the cancer is detected. Therefore, metastases are responsible for more than 90% of cancer-related deaths. Over recent decades there has been adequate evidence suggesting the existence of CSCs with self-renewing and drug-resistant potency within heterogeneous tumors. Cancer stem cells (CSCs) act as a tumor initiating cells and have roles in tumor retrieve and metastasis. Our group recently developed a unique CSC model from mouse induced pluripotent stem cells cultured in the presence of cancer cell-conditioned medium that mimics tumors microenvironment. Using this model, we demonstrated a new method for studying metastasis by intraperitoneal transplantation of tumors and investigate the metastasis ability of cells from these segments. First of all, CSCs were injected subcutaneously in nude mice. The developed malignant tumors were minimized then transplanted into the peritoneal cavity. Following this, the developed tumor in addition to lung, pancreas and liver were then excised and analyzed. Our method showed the metastatic potential of CSCs with the ability of disseminated and moving to blood circulation and seeding in distant organs such as lung and pancreas. This method could provide a good model to study the mechanisms of metastasis according to CSC theory.
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Gowrishankar, Banumathy, Manickam Janakiraman, Chung-Han Lee, Venkata Jaganmohan Thodima, Ana M. Molina, Premal H. Patel, Theresa Margaret Gold, et al. "Metastasis-associated mutations in clear cell renal cell carcinoma." Journal of Clinical Oncology 34, no. 2_suppl (January 10, 2016): 600. http://dx.doi.org/10.1200/jco.2016.34.2_suppl.600.
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600 Background: Over 30% of patients with clear cell renal cell carcinoma (ccRCC) exhibit metastasis at the time of diagnosis and exhibit poor outcome. About 20-50% of patients with localized disease eventually develop metastasis after nephrectomy. The goal of the current study was to identify target gene mutations associated with ccRCC metastasis. Methods: In this IRB approved study, genomic DNA from 128 ccRCC resected specimens (128 unique patients) were profiled using a custom targeted next-generation sequencing (NGS) panel comprising 70 frequently mutated genes and prognostic SNPs in renal cancer. The specimen cohort consisted of 78 primary (29 stage I-III, 30 stage IV, 19 unknown) and 50 metastatic (10 lung, 9 bone, 25 other sites, 6 unknown) lesions. Following hybrid capture, sequencing was performed (MiSeq, Illumina) and variants identified using CLCbio (Qiagen). Chi-square test was used to test for significance. Results: The median specimen had 4 non-synonymous mutations (123/128 samples had at least one mutation). 66 genes showed a non-synonymous mutation in at least one specimen. There was no significant difference between total mutation count between primary and metastatic specimens (Mann-Whitney test). TSC1 mutation was significantly enriched in metastatic (8/50) compared with primary lesions (3/78). No TSC1 mutation was found in the 29 localized (stage I-III) primary lesions. Interestingly, TSC1 maps to 9q34 and our prior copy number studies indicated that loss of 9q is also enriched in metastatic lesions. Of the 11 specimens bearing TSC1 mutation in this cohort, 5 also had loss of 9q. In 44 specimens with known sites of resection, SETD2 and TSC1 mutations were not found in metastases to the lung but found in 30-40% of lesions at other sites, KDM5C and TSC1 mutations were not found in metastases to the bone while 25-30% of lesions at other sites exhibited these mutations. Due to the limited sample size, significance could not be determined for these associations. Conclusions: Preliminary results of this study implicated TSC1 in the metastasis of ccRCC. Since TSC1 mutation is known to confer sensitivity to mTOR inhibitors, our initial finding of absence of TSC1 mutation in lung and bone sites of metastasis may have therapeutic implications.
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Tanaka, Mai, Samantha S. Dykes, and Dietmar W. Siemann. "Inhibition of the Axl pathway impairs breast and prostate cancer metastasis to the bones and bone remodeling." Clinical & Experimental Metastasis 38, no. 3 (March 31, 2021): 321–35. http://dx.doi.org/10.1007/s10585-021-10093-z.
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AbstractApproximately 90% of cancer-related deaths result from cancer metastasis. In prostate and breast cancers, bone is the most common site of cancer cell dissemination. Key steps in the metastatic cascade are promoted through upregulation of critical cell signaling pathways in neoplastic cells. The present study assessed the role of the receptor tyrosine kinase Axl in prostate and breast cancer cell metastasis to bones using (i) Axl knockdown neoplastic cells and osteoclast progenitor cells in vitro, (ii) intracardiac injection of Axl knockdown tumor cells in vivo, and (iii) selective Axl inhibitor BGB324. Axl inhibition in neoplastic cells significantly decreased their metastatic potential, and suppression of Axl signaling in osteoclast precursor cells also reduced the formation of mature osteoclasts. In vivo, Axl knockdown in prostate and breast cancer cells significantly suppressed the formation and progression of bone metastases. Hence, therapeutic targeting of Axl may impair tumor metastasis to the bones through neoplastic and host cell signaling axes.
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Rattan, Ramandeep, Rouba Ali Fehmi, and Adnan Munkarah. "Metformin: An Emerging New Therapeutic Option for Targeting Cancer Stem Cells and Metastasis." Journal of Oncology 2012 (2012): 1–12. http://dx.doi.org/10.1155/2012/928127.
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Metastasis is an intricate process by which a small number of cancer cells from the primary tumor site undergo numerous alterations, which enables them to form secondary tumors at another and often multiple sites in the host. Transition of a cancer cell from epithelial to mesenchymal phenotype is thought to be the first step in the progression of metastasis. Recently, the recognition of cancer stem cells has added to the perplexity in understanding metastasis, as studies suggest cancer stem cells to be the originators of metastasis. All current and investigative drugs have been unable to prevent or reverse metastasis, as a result of which most metastatic cancers are incurable. A potential drug that can be considered is metformin, an oral hypoglycemic drug. In this review we discuss the potential of metformin in targeting both epithelial to mesenchymal transition and cancer stem cells in combating cancer metastases.
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Yang, Yi Ming, Lin Ye, Fiona Ruge, Ziqian Fang, Ke Ji, Andrew J. Sanders, Shuqin Jia, et al. "Activated Leukocyte Cell Adhesion Molecule (ALCAM), a Potential ‘Seed’ and ‘Soil’ Receptor in the Peritoneal Metastasis of Gastrointestinal Cancers." International Journal of Molecular Sciences 24, no. 1 (January 3, 2023): 876. http://dx.doi.org/10.3390/ijms24010876.
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Activated Leukocyte Cell Adhesion Molecule (ALCAM/CD166) is a cell–cell adhesion protein conferring heterotypic and homotypic interactions between cells of the same type and different types. It is aberrantly expressed in various cancer types and has been shown to be a regulator of cancer metastasis. In the present study, we investigated potential roles of ALCAM in the peritoneal transcoelomic metastasis in gastrointestinal cancers, a metastatic type commonly occurred in gastro-intestinal and gynaecological malignancies and resulting in poor clinical outcomes. Specifically, we studied whether ALCAM acts as both a ‘seed’ receptor in these tumour cells and a ‘soil’ receptor in peritoneal mesothelial cells during cancer metastasis. Gastric cancer and pancreatic cancer tissues with or without peritoneal metastasis were compared for their levels of ALCAM expression. The impact of ALCAM expression in these tumours was also correlated to the patients’ clinical outcomes, namely peritoneal metastasis-free survival. In addition, cancer cells of gastric and pancreatic origins were used to create cell models with decreased or increased levels of ALCAM expression by genetic knocking down or overexpression, respectively. Human peritoneal mesothelial cells were also genetically transfected to generate cell models with different profiles of ALCAM expression. These cell models were used in the tumour-mesothelial interaction assay to assess if and how the interaction was influenced by ALCAM. Both gastric and pancreatic tumour tissues from patients who developed peritoneal metastases had higher levels of ALCAM transcript than those without. Patients who had tumours with high levels of ALCAM had a much shorter peritoneal metastasis free survival compared with those who had low ALCAM expression (p = 0.006). ALCAM knockdown of the mesothelial cell line MET5A rendered the cells with reduced interaction with both gastric cancer cells and pancreatic cancer cells. Likewise, levels of ALCAM in both human gastric and pancreatic cancer cells were also a determining factor for their adhesiveness to mesothelial cells, a process that was likely to be triggered the phosphorylation of the SRC kinase. A soluble ALCAM (sALCAM) was found to be able to inhibit the adhesiveness between cancer cells and mesothelial cells, mechanistically behaving like a SRC kinase inhibitor. ALCAM is an indicator of peritoneal metastasis in both gastric and pancreatic cancer patients. It acts as not only a potential peritoneal ‘soil’ receptor of tumour seeding but also a ‘soil’ receptor in peritoneal mesothelial cells during cancer metastasis. These findings have an important therapeutic implication for treating peritoneal transcoelomic metastases.
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Meiliana, Anna, Nurrani Mustika Dewi, and Andi Wijaya. "Targeting Metastatic Cancer: Disseminated Tumor Cells and Premetastatic Niches." Indonesian Biomedical Journal 14, no. 4 (December 1, 2022): 329–48. http://dx.doi.org/10.18585/inabj.v14i4.2035.
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BACKGROUND: Metastases are simply known as cancers spread to another part of the body, and often be responsible for the severity of cancer prognosis. Somehow, the complex mechanisms of metastases are not fully understood yet.CONTENT: The characteristic of cancer is akin to a never-healing wound. Cancer cells are plastic and dynamic as they build their niches and developed into metastases, even when they seem dormant. Therefore, cancer cells can survive the immune system. Recent research has shown the distinct biology of metastasis-initiating cell, which leads to tumor development in distant organs, immune surveillance evasion, and co-option of metastatic micro-environments. Effective cancer therapies must consider the regenerative states of metastatic malignancies and have careful observation of patient phenotypes.SUMMARY: This review aimed to provide an insight on genesis and characteristics of metastases, starting from its seeding and dormancy, until the advance phase. Thus, developing therapy for cancer metastases should not start as it grows, but even as earlier strategies since the primary tumor was detected.KEYWORDS: cancer metastasis, DTC, CTC, CSC, dormancy, pre-metastatic niche, plasticity
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Martini, Stefania, Francesca Arcadipane, Pierfrancesco Franco, Giuseppe C. Iorio, Sara Bartoncini, Elena Gallio, Alessia S. Guarneri, and Umberto Ricardi. "Radiation therapy for oligometastatic oropharyngeal cancer." BJR|case reports 6, no. 1 (March 2020): 20190021. http://dx.doi.org/10.1259/bjrcr.20190021.
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At presentation, isolated metastasis from oropharyngeal squamous cell carcinoma is rare. Liver is a relatively uncommon first site of failure, especially in the absence of other distant metastases, particularly without diagnosis of lung metastases. We report on a case of HPV-related oropharyngeal squamous cell carcinoma with synchronous liver metastasis treated with radiation therapy. This condition, defined as "oligometastatic state," describes a subset of patients with limited volume metastatic disease in whom favorable outcomes were reported with the use of local ablative therapies on both the primary tumor and metastatic sites. As a definitive treatment, we offered the patient, ineligible for other therapeutic approaches, exclusive radiation treatment on the head and neck region and a stereotactic ablative approach targeted to the liver metastasis.
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KARATAŞ, Fatih, Süleyman ŞAHİN, Aydın AYTEKİN, Bekir HACIOĞLU, and Mustafa ALTINBAŞ. "The Probable Relation Between Asbestos and Isolated Pleural Metastasis in Renal Cell Cancer." Akdeniz Medical Journal 2, no. 1 (January 30, 2016): 49–50. http://dx.doi.org/10.17954/amj.2016.46.
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Tantraworasin, Apichat, Somcharoen Saeteng, Nirush Lertprasertsuke, Nuttapon Arayawudhikule, Choosak Kasemsarn, and Jayanton Patumanond. "Completely Resected N0 Non-Small Cell Lung Cancer: Prognostic Factors Affecting Long-Term Survival." ISRN Surgery 2013 (August 29, 2013): 1–7. http://dx.doi.org/10.1155/2013/175304.
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Background. Although early stage non-small cell lung cancer (NSCLC) has an excellent outcome and correlated with good long-term survival, up to 15 percent of patients still relapse postoperatively and die. This study is conducted to identify prognostic factors that may affect the long-term survival in completely resected N0 NSCLC. Methods. Medical records of 124 patients with completely resected N0 NSCLC were retrospectively reviewed. Prognostic factors affecting long-term survival were analyzed by the Kaplan-Meier method and Cox proportional hazards analysis. Results. Overall five-year survival rate was 48 percent. Multivariable analysis revealed stage of disease, tumor necrosis, tumor recurrence, brain metastasis, adrenal metastases, and skin metastases as significant prognostic factors affecting long-term survival. The hazard ratio (HR) of tumor necrosis, tumor recurrence, brain metastasis, adrenal metastases, and skin metastases was 2.0, 2.3, 7.6, 4.1, and 8.3, respectively, and all P values were less than 0.001. Conclusions. Our study shows stage of disease, tumor necrosis, tumor recurrence, brain metastasis, adrenal metastasis, and skin metastasis as the independent prognostic factors of long-term survival in pathological N0 NSCLC. Early stage NSCLC patients without nodal involvement or presented with tumor necrosis should benefit from adjuvant chemotherapy, and sites of metastasis could predict the long-term survival as described.
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Winkler, Juliane, Weilun Tan, Angela O. Pisco, Andrei Goga, Spyros Darmanis, and Zena Werb. "Abstract 964: Tumor cell plasticity promotes metastasis across heterogeneous tumors." Cancer Research 82, no. 12_Supplement (June 15, 2022): 964. http://dx.doi.org/10.1158/1538-7445.am2022-964.
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Abstract Metastasis, the growth of secondary tumors in distant organs, is the major cause of cancer-related deaths due to insufficient therapeutic effects of conventional treatment. Individual tumor cells exhibit heterogeneous features and growth potentials within the same tumor that may influence metastasis formation. During the metastatic cascade, tumor cells adapt their phenotype to various microenvironments that are distinct from their original site resulting in heterogeneous metastatic cells that often are resistant to conventional treatment. The underlying mechanisms of why some tumor cells can give rise to metastases, whereas others cannot are remarkably poorly understood. We established patient-derived xenograft (PDX) models of breast cancer with different metastatic potential and preserved tumor heterogeneity. We analyzed the intrinsic cellular programs of individual tumor cells that influence the metastatic potential of breast cancers using different single-cell RNA-sequencing protocols (MULTI-Seq and Smart-Seq2). Using gene expression profiling of matched primary tumor and metastatic cells of 13 human breast cancers, we demonstrated that while human tumors showed profound inter-patient heterogeneity, they also shared signatures of differentially expressed genes between primary tumor and metastatic cells. Tumors with similar metastatic capabilities shared similar signatures, suggesting potential targets to directly treat metastasis. Additionally, we found that the plasticity of tumor cells is a common feature across tumors that is beneficial for the formation of metastasis. Tumors with higher levels of plastic tumor cells have a greater ability to form metastases. Moreover, we identified a subset of tumor cells expressing both markers of epithelial and mesenchymal characteristics, demonstrating in-vivo evidence for tumor epithelial-mesenchymal plasticity (EMP) in the metastatic cascade. The EMP is a continuum of states with epithelial and mesenchymal cell states as the two extremes of this continuum. The identified transition cells express distinct markers suggesting that these cells may represent a novel and overlooked cell type within the EMP continuum. Given the importance of tumor plasticity in the metastatic cascade, inhibiting the subset of tumor cells that are currently undergoing EMP may represent a novel treatment strategy for metastasis. Citation Format: Juliane Winkler, Weilun Tan, Angela O. Pisco, Andrei Goga, Spyros Darmanis, Zena Werb. Tumor cell plasticity promotes metastasis across heterogeneous tumors [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2022; 2022 Apr 8-13. Philadelphia (PA): AACR; Cancer Res 2022;82(12_Suppl):Abstract nr 964.
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Aksarin, A. A., M. D. Ter-Ovanesov, A. A. Mordovsky, S. M. Kopeyka, and P. P. Troyan. "LOBE-SPECIFIC METASTASIS IN NON-SMALL CELL LUNG CANCER." Siberian journal of oncology 20, no. 5 (October 31, 2021): 31–40. http://dx.doi.org/10.21294/1814-4861-2021-20-5-31-40.
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Aim: to identify the pathways of lymph node metastases in non-small cell lung cancer (NSCLC).Material and Methods. The frequency of mediastinal lymph node metastases and treatment outcomes were analyzed in 327 patients with stage I–III non-small cell lung carcinoma (NSCLC), who underwent lung resection with systematic lymph node dissection (SLND) between 2007 and 2011.Results. In cases with tumor location in any lobe of the right lung, metastasis occurred in the superior and inferior mediastinal lymph nodes. In left-side tumors, the main pathways of lymphatic spread of tumors were superior and inferior mediastinal nodes as well as aortic lymph nodes. Left lower lobe tumors metastasized most often to inferior mediastinal lymph nodes. Skip metastases were observed at any location of the tumor. Routine examination of all ipsilateral mediastinal lymph nodes overstaged NSCLC in 19.5 % of cases. The overall 5-and 10-year survival rates in patients with stage I–III NSCLC with SND were 61.5 % and 49.2 %, respectively. The median survival time was 103 months.Conclusion. Despite typical metastatic patterns of mediastinal lymph nodes in patients with NSCLC, non-specific metastasis was observed at any location of the tumor, which required mandatory systematic nodal dissection.
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Summers, Matthew A., Michelle M. McDonald, and Peter I. Croucher. "Cancer Cell Dormancy in Metastasis." Cold Spring Harbor Perspectives in Medicine 10, no. 4 (September 23, 2019): a037556. http://dx.doi.org/10.1101/cshperspect.a037556.
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Liotta, Lance A. "Cancer Cell Invasion and Metastasis." Scientific American 266, no. 2 (February 1992): 54–63. http://dx.doi.org/10.1038/scientificamerican0292-54.
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Zhang, Di, Feng Feng, Ruping Liu, Wenjia Zhu, and Li Yao. "Mechanochemistry in cancer cell metastasis." Chinese Chemical Letters 30, no. 1 (January 2019): 7–14. http://dx.doi.org/10.1016/j.cclet.2018.06.011.
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Sato, Ryo, Teppei Nakano, Mari Hosonaga, Oltea Sampetrean, Ritsuko Harigai, Takashi Sasaki, Ikuko Koya, et al. "RNA Sequencing Analysis Reveals Interactions between Breast Cancer or Melanoma Cells and the Tissue Microenvironment during Brain Metastasis." BioMed Research International 2017 (2017): 1–10. http://dx.doi.org/10.1155/2017/8032910.
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Metastasis is the main cause of treatment failure and death in cancer patients. Metastasis of tumor cells to the brain occurs frequently in individuals with breast cancer, non–small cell lung cancer, or melanoma. Despite recent advances in our understanding of the causes and in the treatment of primary tumors, the biological and molecular mechanisms underlying the metastasis of cancer cells to the brain have remained unclear. Metastasizing cancer cells interact with their microenvironment in the brain to establish metastases. We have now developed mouse models of brain metastasis based on intracardiac injection of human breast cancer or melanoma cell lines, and we have performed RNA sequencing analysis to identify genes in mouse brain tissue and the human cancer cells whose expression is associated specifically with metastasis. We found that the expressions of the mouse genes Tph2, Sspo, Ptprq, and Pole as well as those of the human genes CXCR4, PLLP, TNFSF4, VCAM1, SLC8A2, and SLC7A11 were upregulated in brain tissue harboring metastases. Further characterization of such genes that contribute to the establishment of brain metastases may provide a basis for the development of new therapeutic strategies and consequent improvement in the prognosis of cancer patients.
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Shopov, Spasimir. "Endobronchial localization - arena of two tumors: a case report." Folia Medica 64, no. 6 (December 31, 2022): 1003–6. http://dx.doi.org/10.3897/folmed.64.e71252.
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The lung is a common arena for metastases of tumors with different localization, but endobronchial localization of metastases is very rare. The most common tumors with endobronchial localization of metastasis are renal, breast, and colorectal cancer. We report a man presenting with cough and hemoptysis. Endobronchial biopsy showed renal cell carcinoma and micro-invasive bronchogenic squamous cell carcinoma. Endobronchial metastases from renal cell carcinoma are rare. The squamous cell lung cancer is one of the most common cancers in men, but the combination of renal cell carcinoma and micro-invasive squamous cell carcinoma with endobronchial localization is a casuistic case.
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Ebert, Matthias P. A., Jun Yu, Juliane Hoffmann, Alba Rocco, Christoph Röcken, Sabine Kahmann, Oliver Müller, Murray Korc, Joseph J. Sung, and Peter Malfertheiner. "Loss of Beta-Catenin Expression in Metastatic Gastric Cancer." Journal of Clinical Oncology 21, no. 9 (May 1, 2003): 1708–14. http://dx.doi.org/10.1200/jco.2003.10.017.
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Purpose: Beta-catenin (β-catenin) participates in intercellular adhesion and is an integral part of the Wnt signaling pathway. The role of β-catenin in the pathogenesis of gastric cancer and its metastasis is largely unknown. Patients and Methods: Immunohistochemistry and Western blot analysis were used to analyze the expression of β-catenin in 87 human gastric cancers, in metastasis and cancer cell lines. The β-catenin and the adenomatous polyposis coli (APC) genes were analyzed for gene mutations. Furthermore, methylation of the β-catenin promoter in cell lines was assessed by treatment with 5′-azadeoxycytidine and sodium bisulfite genomic sequencing. Results: β-Catenin expression was present at either the cell membrane or the cytoplasm in 34 of 75 primary gastric cancers. Expression of β-catenin was significantly more frequent in intestinal-type (P = .0049) and well-differentiated gastric cancers (P < .001). There were no quantitative differences between gastric cancers and the nonmalignant gastric tissues, as determined by Western blot analysis. One of 18 metastatic cancer lesions and four of five gastric cancer cell lines expressed β-catenin protein. N87 cells, derived from the liver metastasis of a gastric cancer, did not express β-catenin. Treatment with 5′-azadeoxycytidine restored β-catenin protein levels in this cell line, which exhibited significantly more 5-methylcytosines in the β-catenin promoter compared with the other cell lines. Conclusion: β-Catenin expression is lost in a subgroup of primary gastric cancers, is frequently absent in metastases, and exhibits nuclear localization in cancers with either β-catenin or APC gene mutations. Interestingly, the loss of β-catenin expression in metastatic gastric cancers may result from hypermethylation of the β-catenin promoter.
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Kamiyoshihara, Mitsuhiro, Osamu Kawashima, Shuji Sakata, Susumu Ishikawa, and Yasuo Morishita. "Non-Small Cell Lung Cancer with Ipsilateral Intrapulmonary Metastasis." Asian Cardiovascular and Thoracic Annals 8, no. 2 (June 2000): 141–45. http://dx.doi.org/10.1177/021849230000800212.
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From 1981 through 1997, lobectomy or pneumonectomy with mediastinal lymph node dissection was performed in 604 patients with non-small cell lung cancer, of whom 42 (7%) were diagnosed as having ipsilateral pulmonary metastasis. There were 23 males and 19 females, the mean age was 66 years. Lobectomy was carried out in 37 cases and pneumonectomy in 5. Postoperative histology identified 29 adenocarcinomas, 11 squamous cell carcinomas, 1 large cell carcinoma, and 1 adenosquamous cell carcinoma. Two cases were classified as pathologic stage I, 1 as stage II, 26 as IIIA, and 13 as IIIB. Blood vessel invasion was present in 33 cases and absent in 2 cases. Five and 10-year survival rates were 34.3% and 17.1%, respectively. Patients with pulmonary metastasis had a poorer prognosis than those without metastasis; there were local recurrences in 6 patients, distant metastases in 9, and 15 deaths. There were no significant differences in recurrence sites between patients with and without pulmonary metastasis. Multivariate analysis showed that lymph node involvement and blood vessel invasion were useful prognostic factors. Ipsilateral pulmonary metastasis in the same lobe was regarded as local invasion for which surgical resection is the optimal treatment.
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Petrova, Yuliya I., Leslayann Schecterson, and Barry M. Gumbiner. "Roles for E-cadherin cell surface regulation in cancer." Molecular Biology of the Cell 27, no. 21 (November 2016): 3233–44. http://dx.doi.org/10.1091/mbc.e16-01-0058.
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The loss of E-cadherin expression in association with the epithelial–mesenchymal transition (EMT) occurs frequently during tumor metastasis. However, metastases often retain E-cadherin expression, an EMT is not required for metastasis, and metastases can arise from clusters of tumor cells. We demonstrate that the regulation of the adhesive activity of E-cadherin present at the cell surface by an inside-out signaling mechanism is important in cancer. First, we find that the metastasis of an E-cadherin–expressing mammary cell line from the mammary gland to the lung depends on reduced E-cadherin adhesive function. An activating monoclonal antibody to E-cadherin that induces a high adhesive state significantly reduced the number of cells metastasized to the lung without affecting the growth in size of the primary tumor in the mammary gland. Second, we find that many cancer-associated germline missense mutations in the E-cadherin gene in patients with hereditary diffuse gastric cancer selectively affect the mechanism of inside-out cell surface regulation without inhibiting basic E-cadherin adhesion function. This suggests that genetic deficits in E-cadherin cell surface regulation contribute to cancer progression. Analysis of these mutations also provides insights into the molecular mechanisms underlying cadherin regulation at the cell surface.
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Liang, Zhengfang, Fengwei Nong, Jingjie Zhao, Dalong Wei, Qianli Tang, Jian Song, and Lingzhang Meng. "Heterogeneity in NK Cell Subpopulations May Be Involved in Kidney Cancer Metastasis." Journal of Immunology Research 2022 (August 22, 2022): 1–8. http://dx.doi.org/10.1155/2022/6378567.
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Although substantial progress has been made in the immunotherapy of kidney cancer, its efficacy varies from patient to patient, with many responding suboptimally or even developing metastases. Thus, research on the tumour immune microenvironment and immune cell heterogeneity is essential for kidney cancer treatment. In this study, natural killer (NK) cell populations were isolated using signature genes from the single-cell sequencing data of clear cell renal cell carcinoma (ccRCC) and normal kidney tissues and divided into three subpopulations according to the differences in gene expression profiles: NK(GZMH), NK(EGR1), and NK(CAPG). Gene set enrichment analysis revealed that NK(EGR1) and NK(CAPG) were closely related to tumour metastasis, as shown by kidney cancer metastasis to Hodgkin lymphoma, T-cell leukaemia, and Ki-1+ anaplastic large cell lymphoma. Thus, these two NK cell subpopulations are promising targets for inhibiting metastasis in ccRCC. Our findings revealed heterogeneity in the infiltrating NK cells of kidney cancer, which can serve as a reference for the mechanisms underlying metastasis in kidney cancer.
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Mitsimponas, Nikolaos, Maria Mitsogianni, Felipe Crespo, Karl-Axel Hartmann, Stefan Diederich, Bernd Klosterhalfen, and Aristoteles Giagounidis. "Isolated Splenic Metastasis from Non-Small-Cell Lung Cancer: A Case Report and Review of the Literature." Case Reports in Oncology 10, no. 2 (July 11, 2017): 638–43. http://dx.doi.org/10.1159/000478002.
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Metastases to the spleen are rare but have been reported for different tumor entities, including breast cancer, lung cancer, colorectal cancer, ovarian cancer, and melanoma. As an isolated event, splenic metastasis from non-small-cell lung cancer (NSCLC) is exceedingly rare. Until now, only 28 cases have been reported in the medical literature. We report the case of a 66-year-old woman with NSCLC (adenocarcinoma) who presented with a synchronous, isolated splenic metastasis. Operative removal of both primary tumor and metastasis was not possible due to multiple comorbidities. Therefore, treatment was limited to combined systemic chemotherapy and simultaneous radiation of the primary tumor, which led to partial remission of the disease. Isolated metastasis to the spleen in NSCLC has been reported only 28 times in the medical literature, most often in male patients with right-sided lung tumors, most of which were adenocarcinomas. The majority of patients were asymptomatic with respect to splenic metastasis. About half of the reported cases were isolated metachronous splenic metastases. Splenectomy seems to confer a survival advantage. We review the pertinent medical literature.
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Shimizu, Reiko, Tomomari Kinoshita, Naomichi Sasaki, Mao Uematsu, Yusuke Sugita, Toshiyuki Shima, Masahiko Harada, Tsunekazu Hishima, and Hirotoshi Horio. "Clinicopathological Factors Related to Recurrence Patterns of Resected Non-Small Cell Lung Cancer." Journal of Clinical Medicine 9, no. 8 (August 1, 2020): 2473. http://dx.doi.org/10.3390/jcm9082473.
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Even after complete resection, non-small cell lung cancer (NSCLC) shows preferential recurrence in the mediastinal lymph nodes, lungs, brain, bone, liver, and adrenal gland. However, the relationship between clinicopathological factors and recurrence patterns after resection has not been well-evaluated. Among 688 NSCLC cases with complete resection between 2004 and 2016, 233 cases recurred at our institute. On multivariate analyses, NSCLCs with lymph node metastasis and pulmonary metastasis at surgery commonly recurred in the mediastinal lymph nodes and lungs, respectively. Young age, adenocarcinoma, and vascular invasion were correlated with brain metastasis. Although no variable was associated with bone metastasis, vascular invasion was correlated with postoperative liver and adrenal gland metastasis. Pathologically proven stage II or III NSCLC, adenocarcinoma, and the presence of lymphatic permeation would result in multiple metastases. Vascular invasion, larger invasive size, and advanced stage were independent risk factors of early recurrence. Considering survival, vascular invasion, elderly age, and non-adenocarcinoma were unfavorable prognostic factors after recurrence. Some clinicopathological variables were correlated with organ-specific metastasis and post-recurrence survival. Particularly, vascular invasion was a biomarker of brain, liver, and adrenal gland metastases and a prognostic marker after recurrence among completely resected NSCLC. This information is useful for more frequent patient follow-up and identifying organ-specific distant metastasis.
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Macara, Ian G., and Luke McCaffrey. "Cell polarity in morphogenesis and metastasis." Philosophical Transactions of the Royal Society B: Biological Sciences 368, no. 1629 (November 5, 2013): 20130012. http://dx.doi.org/10.1098/rstb.2013.0012.
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Most human cancers arise either from epithelial cells or their progenitors. Epithelial cells possess a distinctive apical–basal polarity and loss of polarity is frequently assumed to be a common feature of cancer progression. In particular, cancer cell dissemination to ectopic sites, and metastatic growth at those sites, is often considered to require a mesenchymal transition in which the transformed epithelial cells lose their apical–basal polarity. However, many cancers retain epithelial characteristics, and until recently there has been little conclusive evidence for an involvement of the cell polarity machinery in tumour growth and metastasis. In this article, we discuss evidence that polarity proteins can be potent invasion suppressors but that loss of epithelial character is not essential either for tumour growth and invasion, or metastatic colonization.
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Tkachenko, R., O. Kuryk, A. Golovko, and O. Rudnytska. "DISTANT METASTASIS TO THE THYROID GLAND: CLINICAL REVIEW." Клінічна та профілактична медицина 4, no. 14 (December 20, 2020): 105–13. http://dx.doi.org/10.31612/2616-4868.4(14).2020.10.
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Background. Metastasis to the thyroid from non-thyroid sites is an uncommon clinical presentation in oncology practice. Renal cell carcinoma is most common primary cancer, followed by breast cancer metastases, small cell lung carcinoma, colorectal cancer, malignant melanoma, malignancies of the gastrointestinal cancer. However, given that thyroid nodules are most common in women, and women with a history of urogenital malignancy are at higher risk of developing thyroid cancer, the possibility of metastatic thyroid cancer must be considered while evaluating a thyroid lump.
Aim: to investigate patient management while finding distant metastases to the thyroid and identification of the most common complications.
Material and methods. Identified reports of patients with thyroid metastasis were analyzed in the current literature review. Both clinical and autopsy series were included.
Results. Metastases to the thyroid gland may be discovered at the time of diagnosis of the primary cancer, after preoperative investigation or due to histological examination of an operative specimen. In autopsy series, the most common primary site of metastatic thyroid tumors is lung cancer. In a clinical setting, renal cell carcinoma is the most common. Otherwise, when patients present with isolated metastases during follow-up of indolent disease, surgery might provide central neck control and even long-term cure. Prognosis may also vary according to the morphological features of primary cancer, time interval between initial diagnosis and metastasis and presence of extrathyroid invasion.
Conclusions. Although the thyroid gland is highly vascularized, metastasis of malignant tumors to the thyroid is relatively rare and detection of metastasis shows a low frequency. A past history of malignant neoplasm should raise the index of suspicious of metastatic disease in patients with thyroid nodules with or without cervical lymphadenopathy. In such patients communication among clinicians treating the thyroid and the primary tumor is essential, as there are differences in treatment protocols and prognosis when compared to primary thyroid cancers. The setting is complex, and decisions must be made considering the localization of primary site, features of the primary tumor and comorbidities. Careful balancing of these factors influences effective patient management and long-term survival.
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Lorenzo-Herrero, Seila, Alejandro López-Soto, Christian Sordo-Bahamonde, Ana Gonzalez-Rodriguez, Massimo Vitale, and Segundo Gonzalez. "NK Cell-Based Immunotherapy in Cancer Metastasis." Cancers 11, no. 1 (December 28, 2018): 29. http://dx.doi.org/10.3390/cancers11010029.
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Metastasis represents the leading cause of cancer-related death mainly owing to the limited efficacy of current anticancer therapies on advanced malignancies. Although immunotherapy is rendering promising results in the treatment of cancer, many adverse events and factors hampering therapeutic efficacy, especially in solid tumors and metastases, still need to be solved. Moreover, immunotherapeutic strategies have mainly focused on modulating the activity of T cells, while Natural Killer (NK) cells have only recently been taken into consideration. NK cells represent an attractive target for cancer immunotherapy owing to their innate capacity to eliminate malignant tumors in a non-Major Histocompatibility Complex (MHC) and non-tumor antigen-restricted manner. In this review, we analyze the mechanisms and efficacy of NK cells in the control of metastasis and we detail the immunosubversive strategies developed by metastatic cells to evade NK cell-mediated immunosurveillance. We also share current and cutting-edge clinical approaches aimed at unleashing the full anti-metastatic potential of NK cells, including the adoptive transfer of NK cells, boosting of NK cell activity, redirecting NK cell activity against metastatic cells and the release of evasion mechanisms dampening NK cell immunosurveillance.
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Kodama, Koichi, Tetsuya Imao, and Kazuto Komatsu. "Metastatic Ureteral Involvement of Non-Small Cell Lung Cancer." Case Reports in Medicine 2011 (2011): 1–3. http://dx.doi.org/10.1155/2011/394326.
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Metastases from a variety of malignant tumors can involve the ureters, but ureteral involvement by lung cancer is extremely rare and usually described at autopsy. We report a rare case of a 76-year-old man who presented with a three-month history of right flank dullness and was noted to have a nonhomogeneous retroperitoneal mass with hydronephrosis of the right kidney on computed tomography of the abdomen. Computed tomography of the thorax showed a nodule in the lower lobe, measuring3×2 cm, in the right lung. After excluding the presence of other primary tumors and metastases, we reached a final diagnosis of solitary retroperitoneal metastasis of adenocarcinoma of the lung. Although rare, in patients of non-small cell lung cancer, presence of hydronephrosis should alert the physician to the possibility of metastasis.
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Markovic, Marina, Dalibor Jovanovic, Zeljko Todorovic, Marija Zivkovic, Aleksandar Dagovic, Slobodanka Mitrović, Marina Petrović, and Jelena Nešić. "Primary Small Cell Carcinoma Of Lung With Metachronous Breast Metastasis." Serbian Journal of Experimental and Clinical Research 18, no. 3 (October 26, 2017): 263–67. http://dx.doi.org/10.1515/sjecr-2016-0087.
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Abstract Breast metastases from an extra-mammary malignancy are rare. Among the lung malignancies that metastasise in the breasts, previous literature has described approximately 30 cases of NSCLC and only a few cases of SCLC. Here, we present a 54-year-old woman with metachronous breast metastasis from pulmonary small cell carcinoma. She presented with a soft tissue mass in the right lung hilum. After bronchoscopy with biopsy, SCLC was verified. Th e patient was given 4 cycles of etoposide and cisplatin followed by radiation therapy. Seven months after the diagnosis of primary lung cancer, the patient palpated a mass in her right breast. Clinical examination and further diagnostics revealed the suspected malignancy, and a radical mastectomy was performed. Immunohistochemical findings suggested metastatic SCLC in the breast. Differentiation between primary and metastatic cancer in the breast is very important for therapeutic planning
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Cheung, Kevin J., Veena Padmanaban, Vanesa Silvestri, Koen Schipper, Joshua D. Cohen, Amanda N. Fairchild, Michael A. Gorin, et al. "Polyclonal breast cancer metastases arise from collective dissemination of keratin 14-expressing tumor cell clusters." Proceedings of the National Academy of Sciences 113, no. 7 (February 1, 2016): E854—E863. http://dx.doi.org/10.1073/pnas.1508541113.
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Recent genomic studies challenge the conventional model that each metastasis must arise from a single tumor cell and instead reveal that metastases can be composed of multiple genetically distinct clones. These intriguing observations raise the question: How do polyclonal metastases emerge from the primary tumor? In this study, we used multicolor lineage tracing to demonstrate that polyclonal seeding by cell clusters is a frequent mechanism in a common mouse model of breast cancer, accounting for >90% of metastases. We directly observed multicolored tumor cell clusters across major stages of metastasis, including collective invasion, local dissemination, intravascular emboli, circulating tumor cell clusters, and micrometastases. Experimentally aggregating tumor cells into clusters induced a >15-fold increase in colony formation ex vivo and a >100-fold increase in metastasis formation in vivo. Intriguingly, locally disseminated clusters, circulating tumor cell clusters, and lung micrometastases frequently expressed the epithelial cytoskeletal protein, keratin 14 (K14). RNA-seq analysis revealed that K14+ cells were enriched for desmosome and hemidesmosome adhesion complex genes, and were depleted for MHC class II genes. Depletion of K14 expression abrogated distant metastases and disrupted expression of multiple metastasis effectors, including Tenascin C (Tnc), Jagged1 (Jag1), and Epiregulin (Ereg). Taken together, our findings reveal K14 as a key regulator of metastasis and establish the concept that K14+ epithelial tumor cell clusters disseminate collectively to colonize distant organs.
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Wen, Lei, Changguo Shan, Da Liu, Cheng Zhou, and Linbo Cai. "BSCI-09. Multiomic single cell analysis reveals emerging principles of tumor immune microenvironment inherent to NSCLC brain metastases." Neuro-Oncology Advances 3, Supplement_3 (August 1, 2021): iii3. http://dx.doi.org/10.1093/noajnl/vdab071.008.
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Abstract Brain is one of the most common sites for distant metastasis of lung cancer. Treatment naïve lung cancer patients diagnosed with brain metastasis are left with very limited options. Checkpoint inhibition is a powerful immunotherapy strategy but delivers benefit only to a small population of patients. Here we harnessed the power and resolution of single cell RNA sequencing and single cell TCR/BCR sequencing to investigate the tumor immune microenvironment (TIME) of NSCLC brain metastases. We enrolled treatment naïve lung cancer patients with brain metastasis. The enrolled subjects covered different histology types and driver gene mutation status. We revealed the emerging principles of innate and adaptive immune components inherent to NSCLC brain metastases. We also uncovered several significant intercellular communication patterns that potentiates cancer cell seeding and fosters cancer cell proliferation. Those results served as a starting point to design optimal immunotherapy strategies for advanced lung cancer patients with limited options.
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Segkos, Konstantinos, Carl Schmidt, and Fadi Nabhan. "Isolated Liver Metastasis in Hürthle Cell Thyroid Cancer Treated with Microwave Ablation." Case Reports in Endocrinology 2017 (2017): 1–4. http://dx.doi.org/10.1155/2017/2790741.
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Hürthle cell thyroid cancer (HCTC) is a less common form of differentiated thyroid cancer. It rarely metastasizes to the liver, and when it does, the metastasis is almost never isolated. Here we report a 62-year-old male with widely invasive Hürthle cell thyroid cancer, who underwent total thyroidectomy and received adjuvant treatment with I-131 with posttreatment scan showing no evidence of metastatic disease. His thyroglobulin however continued to rise after that and eventually an isolated liver metastasis was identified. He underwent laparoscopic microwave ablation of the liver metastasis, with dramatic decline in thyroglobulin and no structural disease identified to date. This case highlights the rare occurrence of isolated liver metastasis from HCTC and also illustrates the utility of thermoablation as an alternative to surgical resection in the treatment of small isolated liver metastases from HCTC.
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McCann, Brendan, Kiran Bhatti, and Vivienne MacLaren. "Incidence of brain metastasis in esophageal cancer." Journal of Clinical Oncology 33, no. 3_suppl (January 20, 2015): 46. http://dx.doi.org/10.1200/jco.2015.33.3_suppl.46.
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46 Background: Brain metastasis in oesophageal cancer is a rare but often fatal complication. In previous studies the incidence has ranged from 1.4% - 13% with the largest studies from China and Japan that have been retrospectively based over fifteen to twenty years. (Ogawa K, Toita T, Sueyama H. Brain metastases from esophageal carcinoma: natural history, prognostic factors, and outcome. Cancer. 2002 Feb 1;94(3):759-64.) With improving diagnostic techniques and differing histology of oesophageal cancer from Eastern countries we undertook a study to determine the incidence of brain metastases in oesophageal cancers in the West of Scotland. Methods: Data from all the new patients diagnosed with oesophageal cancer was obtained with permission from the Regional Managed Clinical Network from the years 2011 and 2012 yielding a total of 701 patients. The individual clinical records were examined to ascertain if the patient developed brain metastases on CT/MRI scan, their tumour type and management. Results: Of the 701 patients diagnosed with oesophageal cancer, 19 developed brain metastasis demonstrating an incidence of 2.7%. 12 of these patients primary diagnosis was adenocarcinoma. The others were small cell (3), neuroendocrine (2), squamous (1) and no histology (1). At the time of writing 17 out of 19 patients had died from their oesophageal cancer. The 2 surviving patients had a single brain metastasis that was resected and treated with adjuvant radiotherapy. 6 other patients had whole brain radiotherapy, 1 patient had partial brain radiotherapy and 10 were managed with best supportive care. Mean survival from diagnosis of brain metastasis for best supportive care was 26 +/- 14 days versus mean survival for radiotherapy treatment from 100+/- 57 days (p = 0.003) demonstrating a difference between the groups. Conclusions: The incidence of brain metastasis in oesophageal cancer in the West of Scotland was 2.7% with the prognosis generally poor unless resected.
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Yamada, Hideki, Takuya Akahane, Atsushi Horiuchi, Ryu Shimada, Hajime Shibuya, Tamuro Hayama, Keijirou Nozawa, Souichirou Ishihara, Keiji Matsuda, and Toshiaki Watanabe. "A Case of Lung Squamous Cell Carcinoma With Metastases to the Duodenum and Small Intestine." International Surgery 96, no. 2 (April 1, 2011): 176–81. http://dx.doi.org/10.9738/1380.1.
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Abstract Gastrointestinal metastasis of lung cancer is fairly rare, and metastasis to the duodenum is very uncommon. We report a case of duodenum and small intestine metastases of lung squamous cell carcinoma. The patient was a 66-year-old man. He was diagnosed with lung squamous cell carcinoma (T4N3M1 [mediastinum, cervical lymph node, and duodenum metastases], stage IV). He noted a sense of abdominal fullness on the evening of the day chemoradiotherapy was given, and emergency surgery was performed for suspected perforation of the digestive tract. Intraoperative findings included a tumor in the small intestine with a perforation at the tumor site; partial resection of the small intestine, including the tumor, was performed. Small intestine metastasis of lung cancer was diagnosed following histopathologic examination. When lung cancer patients complain of abdominal symptoms, it is important to consider gastrointestinal metastases in diagnosis and treatment.
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Gründker, Carsten, Matthias Läsche, Johanna Hellinger, and Günter Emons. "Mechanisms of Metastasis and Cell Mobility – The Role of Metabolism." Geburtshilfe und Frauenheilkunde 79, no. 02 (February 2019): 184–88. http://dx.doi.org/10.1055/a-0805-9113.
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AbstractTumour metastasis is responsible for more than 90% of tumour-associated mortality. About one third of breast cancer patients in the early stage develop metastases. The transformation in tumour development referred to as the “metastatic cascade” or “metastatic cycle” is a complex and multi-stage event. While it is generally recognised that epithelial-mesenchymal transformation (EMT) plays a crucial role in cancer progression and metastasis, the metabolic events in this process have received little attention to date. We would therefore like to provide a brief overview here of the influence of the metabolism on the progression and metastasis of tumours.
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Heyde, Alexander, Johannes G. Reiter, Kamila Naxerova, and Martin A. Nowak. "Consecutive seeding and transfer of genetic diversity in metastasis." Proceedings of the National Academy of Sciences 116, no. 28 (June 25, 2019): 14129–37. http://dx.doi.org/10.1073/pnas.1819408116.
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During metastasis, only a fraction of genetic diversity in a primary tumor is passed on to metastases. We calculate this fraction of transferred diversity as a function of the seeding rate between tumors. At one extreme, if a metastasis is seeded by a single cell, then it inherits only the somatic mutations present in the founding cell, so that none of the diversity in the primary tumor is transmitted to the metastasis. In contrast, if a metastasis is seeded by multiple cells, then some genetic diversity in the primary tumor can be transmitted. We study a multitype branching process of metastasis growth that originates from a single cell but over time receives additional cells. We derive a surprisingly simple formula that relates the expected diversity of a metastasis to the diversity in the pool of seeding cells. We calculate the probability that a metastasis is polyclonal. We apply our framework to published datasets for which polyclonality has been previously reported, analyzing 68 ovarian cancer samples, 31 breast cancer samples, and 8 colorectal cancer samples from 15 patients. For these clonally diverse metastases, under typical metastasis growth conditions, we find that 10 to 150 cells seeded each metastasis and left surviving lineages between initial formation and clinical detection.