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Journal articles on the topic 'Tumor Formation'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 February 2022

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1

Easter, Stephanie L., Elizabeth H. Mitchell, Sarah E. Baxley, Renee Desmond, Andra R. Frost, and Rosa Serra. "Wnt5a Suppresses Tumor Formation and Redirects Tumor Phenotype in MMTV-Wnt1 Tumors." PLoS ONE 9, no. 11 (November 17, 2014): e113247. http://dx.doi.org/10.1371/journal.pone.0113247.

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2

Riede, Isolde. "Genes in Tumor Formation." Journal of Hematology and Oncology Research 3, no. 2 (October 22, 2019): 18–22. http://dx.doi.org/10.14302/issn.2372-6601.jhor-19-2986.

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With the definition of four gene classes, all differences between tumor cells and normal cells can be explained. Proliferative mutations induce a shortcut, forcing the cell to divide. They allow replication without control, induce somatic pairing defects of chromosomes and genome instability. Intact Tumor Supressors or mutant Switch Functions can inhibit this process. Oncogene mutations optimize the growth of the cells.

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3

Korneva, Yulia S., and Roman V. Ukrainets. "Principles of premetastatic niche formation." Journal of Modern Oncology 21, no. 4 (May 7, 2020): 6–9. http://dx.doi.org/10.26442/18151434.2019.4.190715.

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The article is devoted to premetastatic niche as a complex term, including stromal cells, vessels, extracellular matrix and their changes during interaction with the primary tumor. On example of different malignant tumors authors describe as primary tumor through tumor exosomes prepares certain organs-recipients to metastatic clone implantation. In the area of premetastatic niche under the influence of tumorous exosomes polarization of macrophages towards M2 type takes place. The cells are the main agents, providing survival as well as migration of tumorous cells. Affecting extracellular matrix, macrophages change the microcirculatory bed permeability. This mechanism is directed towards increase of its permeability to entrance of metastatic clone cells form vessels into premetastatic niche. Besides macrophages fibroblasts and polypotent bone marrow stem cells are also reprogrammed, that results in metabolism and local immunity changes at the place of future implantation. As a result, only when tissue of recipient-organ is prepared for contact with metastatic clone, their interaction take place with consequent formation of secondary tumor metastatic niche. Thus, this review describes pathogenesis of metastasis, different from its early understanding as spread of metastatic clone with lymph and blood. These peculiarities may in future have significant impact in practical medicine, Blockage of signal spread from primary tumor through exosomes is one of the promising directions in pathogenetic therapy of malignant tumors. Investigation of principles of premetastatic niche formation may become a theoretical substantiation for prophylaxis of metastatic disease and inhibition of micrometastasis to macrometastasis transformation.

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4

Baggenstos, Martin A., John A. Butman, Edward H. Oldfield, and Russell R. Lonser. "Role of edema in peritumoral cyst formation." Neurosurgical Focus 22, no. 5 (May 2007): 1–7. http://dx.doi.org/10.3171/foc.2007.22.5.10.

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✓Peritumoral cysts (those arising immediately adjacent to the tumor mass) are frequently associated with benign and malignant tumors of the brain and spinal cord (syringomyelia). The cystic component of central nervous system (CNS) tumors and associated peritumoral cysts are often the cause of clinical symptoms. Because of the common occurrence of peritumoral cysts with CNS neoplasms and the morbidity associated with them, advanced imaging, histological, and molecular techniques have been used to determine the mechanism underlying cyst formation and propagation. Based on evidence from such studies, edema appears to be a common precursor to peritumoral cyst formation in the CNS. Mediators of vascular permeability acting locally in the tumor and/or hydrodynamic forces within abnormal tumor vascula-ture appear to drive fluid extravasation. When these forces overcome the ability of surrounding tissue to resorb fluid, edema and subsequent cyst formation occur. These findings support the concept that the tumor itself is the source of the edema that precedes cyst formation and that resection of tumors or medical therapies directed at decreasing their vascular permeability will result in the resolution of edema and cysts.

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5

Mamedova, S. M., M. A. Qarashova, E. M. Aliyeva, and S. Q. Sultanova. "The condition of the hypothalamic-pituitary-adrenal-ovarian system in women with tumors and tumoral formations of the organs of the reproductive system in the postmenopausal period." HEALTH OF WOMAN, no. 7(133) (September 30, 2018): 96–99. http://dx.doi.org/10.15574/hw.2018.133.96.

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The objective: of the study was to study the state of the hypothalamic-pituitary-adrenal-ovarian system in women with benign preinvasive and tumor-like formations of the reproductive system organs in the postmenopausal period. Materials and methods. 130 women with various tumors and tumoral formations of reproductive system organs in the postmenopausal period were examined. The parameters of follicle stimulating, luteinizing hormones, estradiol, estrone, prolactin, progesterone, testosterone, dehydroepiandosterone sulfate were studied. Results. It was established that out of 130 women with various tumors and tumoral formations of the organs of the reproductive system in the postmenopausal period, uterine myoma was defined in 39 (39%), endometrial hyperplasia in 23 (17.7%), tumor-like formation of ovaries in 17 (13.1%). It was found that in the postmenopausal period, the presence of hyperandrogenia, hyperprolactinemia, and a significant increase in the level of estrone were noted in women with benign, preinvasive and tumor-like formations of the organs of the reproductive system, regardless of tumor origin. Conclusion. The obtained results allowed to conclude that in the postmenopausal period the presence of uterine fibroids, endometrial hyperplasia and ovarian tumor formation is accompanied by hyperprolactinemia, hyperandrogenism and hyperestrogenism due to an increase in estrone level. Key words: postmenopausal period, uterine myoma, endometrial hyperplasia, tumor-like formations, hyperandrogenia, hyperprolactinaemia, estrone.

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6

Samara, Ghassan, Michael Hurwitz, Mark Sawicki, and Edward Passaro. "Molecular mechanisms of tumor formation." American Journal of Surgery 164, no. 4 (October 1992): 389–96. http://dx.doi.org/10.1016/s0002-9610(05)80911-0.

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7

Vinnitsky, V. B. "Oncogerminative hypothesis of tumor formation." Medical Hypotheses 40, no. 1 (January 1993): 19–27. http://dx.doi.org/10.1016/0306-9877(93)90191-r.

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8

Lee, Thomas C., and Shizuo Mukai. "Molecular Events in Tumor Formation." International Ophthalmology Clinics 37, no. 4 (1997): 215–32. http://dx.doi.org/10.1097/00004397-199703740-00018.

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9

Purkayastha, Sudarshana, Alexandra Berliner, Suraj Shawn Fernando, Buddima Ranasinghe, Indrani Ray, Hussnain Tariq, and Probal Banerjee. "Curcumin blocks brain tumor formation." Brain Research 1266 (April 2009): 130–38. http://dx.doi.org/10.1016/j.brainres.2009.01.066.

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10

Xu, Daozhi, Peixin Dong, Ying Xiong, Junming Yue, Kei Ihira, Yosuke Konno, Noriko Kobayashi, Yukiharu Todo, and Hidemichi Watari. "MicroRNA-361: A Multifaceted Player Regulating Tumor Aggressiveness and Tumor Microenvironment Formation." Cancers 11, no. 8 (August 7, 2019): 1130. http://dx.doi.org/10.3390/cancers11081130.

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MicroRNA-361-5p (miR-361) expression frequently decreases or is lost in different types of cancers, and contributes to tumor suppression by repressing the expression of its target genes implicated in tumor growth, epithelial-to-mesenchymal transition (EMT), metastasis, drug resistance, glycolysis, angiogenesis, and inflammation. Here, we review the expression pattern of miR-361 in human tumors, describe the mechanisms responsible for its dysregulation, and discuss how miR-361 modulates the aggressive properties of tumor cells and alter the tumor microenvironment by acting as a novel tumor suppressor. Furthermore, we describe its potentials as a promising diagnostic or prognostic biomarker for cancers and a promising target for therapeutic development.

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11

Poh, Boonmin, Hideto Koso, Hiroyuki Momota, Takashi Komori, Yutaka Suzuki, Nobuaki Yoshida, Yasushi Ino, Tomoki Todo, and Sumiko Watanabe. "Foxr2 promotes formation of CNS-embryonal tumors in a Trp53-deficient background." Neuro-Oncology 21, no. 8 (April 12, 2019): 993–1004. http://dx.doi.org/10.1093/neuonc/noz067.

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Abstract Background Embryonal tumors in the central nervous system (CNS) are primary, aggressive, and poorly differentiated pediatric brain tumors. We identified forkhead box R2 (Foxr2) as an oncogene for medulloblastoma through a transposon-based insertional mutagenesis screen. Foxr2 translocation has been identified in a subset of human embryonal tumors of the CNS, designated as CNS neuroblastoma with Foxr2 activation (CNS NB-Foxr2); however, the in vivo functions of Foxr2 remain elusive. Methods We analyzed the effect of Foxr2 overexpression in the mouse brain by generating a transgenic strain that expresses Foxr2 in the entire brain under a transformation related protein 53 (Trp53)–deficient background. We performed histological analysis of tumors and characterized tumor-derived sphere-forming cells. We investigated gene expression profiles of tumor-derived cells. Results Foxr2 and Trp53 loss promoted tumor formation in the olfactory bulb (OB) and brainstem (BS). The tumors showed the common morphological features of small round blue cell tumors, exhibiting divergent, mainly neuronal and glial, patterns of differentiation, which corresponds to the definition of CNS-embryonal tumors. Importantly, all mice developed CNS-embryonal tumors. In the OB, early proliferative lesions consisting of oligodendrocyte transcription factor 2 (Olig2+) cells were observed, indicating that Foxr2 expression expanded Olig2+ cells in the OB. Tumor-derived cells formed spheres in vitro and induced tumors that recapitulated the parental tumor upon transplantation, indicating the presence of tumor-initiating cells. Gene expression profiling revealed that OB and BS tumor cells were enriched for the expression of the genes specific to CNS NB-Foxr2. Conclusion Our data demonstrate that Foxr2 plays a causative role in the formation of CNS-embryonal tumors.

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12

Amereh, Meitham, Roderick Edwards, Mohsen Akbari, and Ben Nadler. "In-Silico Modeling of Tumor Spheroid Formation and Growth." Micromachines 12, no. 7 (June 25, 2021): 749. http://dx.doi.org/10.3390/mi12070749.

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Mathematical modeling has significant potential for understanding of biological models of cancer and to accelerate the progress in cross-disciplinary approaches of cancer treatment. In mathematical biology, solid tumor spheroids are often studied as preliminary in vitro models of avascular tumors. The size of spheroids and their cell number are easy to track, making them a simple in vitro model to investigate tumor behavior, quantitatively. The growth of solid tumors is comprised of three main stages: transient formation, monotonic growth and a plateau phase. The last two stages are extensively studied. However, the initial transient formation phase is typically missing from the literature. This stage is important in the early dynamics of growth, formation of clonal sub-populations, etc. In the current work, this transient formation is modeled by a reaction–diffusion partial differential equation (PDE) for cell concentration, coupled with an ordinary differential equation (ODE) for the spheroid radius. Analytical and numerical solutions of the coupled equations were obtained for the change in the radius of tumor spheroids over time. Human glioblastoma (hGB) cancer cells (U251 and U87) were spheroid cultured to validate the model prediction. Results of this study provide insight into the mechanism of development of solid tumors at their early stage of formation.

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13

Leonard, Gurgas, Doru-Popescu Nelu, Hangan Tony, Chirila Sergiu, Moroianu Olimpia, and Roşoiu Natalia. "Electron Microscopy Study of Nodular Basal Cell Carcinoma." ARS Medica Tomitana 24, no. 2 (May 1, 2018): 90–95. http://dx.doi.org/10.2478/arsm-2018-0017.

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Abstract The electron microscopic study represent the changes in the skin layers in the malignant tumor, the nodular basal cell epithelioma. Comparisons were made between normal cells found in the normal skin at the periphery of the tumor, the cells located near the tumor and the tumors located in the depth of the carcinoma. The microscopic analysis of the tumor formation revealed the characteristics of the pigmented nodular basal cell epitheliu. To the exterior of the carcinoma were evidenced numerous globular formations limiting the peripheral extension of the tumor, which explains its evolution in years.

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14

Ladisch, S., S. Kitada, and E. F. Hays. "Gangliosides shed by tumor cells enhance tumor formation in mice." Journal of Clinical Investigation 79, no. 6 (June 1, 1987): 1879–82. http://dx.doi.org/10.1172/jci113031.

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15

Zhu, Yin, Yi Hu, Ming Cheng, Chun-Yan Zeng, Zhen Yang, Xiao-Dong Zhou, Jiang Chen, and Nong-Hua Lu. "Establishment and Characterization of a Nude Mouse Model of Subcutaneously Implanted Tumors and Abdominal Metastasis in Gastric Cancer." Gastroenterology Research and Practice 2017 (2017): 1–6. http://dx.doi.org/10.1155/2017/6856107.

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A mouse gastric cancer model is an important tool for studying the mechanisms of gastric cancer. To establish subcutaneously implanted tumors, MKN-45 cell suspensions and tumor tissues were implanted into the middle of the right armpit of nude mice. To generate an abdominal metastasis model, MKN-45 cell suspensions and tumor tissue homogenates were implanted into the middle of the lower abdomen. We measured the weights of the nude mice and the longest dimension, shortest dimension, thickness, and volume of the tumor. We also analyzed the rate of tumor formation, the time required for tumor formation, and the number and size of abdominal tumors in the mice. The rates of formation of the subcutaneously implanted tumors were 100%, 0%, and 100% in the nude mice inoculated with 2 × 107cells/mL or 1 × 107cells/mL of the MKN-45 cell suspension or the tumor tissue homogenate (2 × 107cells/mL), respectively. The rates of metastatic abdominal tumor formation were 100%, 50%, and 75% in mice inoculated with 5 × 107cells/mL or 1 × 107cells/mL of the tumor tissue homogenate or the MKN-45 cell suspension (5 × 107cells/mL), respectively. We derived tumor tissues and tumor tissue homogenates from nude mice prior to establishing the subcutaneous model of implanted tumors and the abdominal metastasis model of gastric cancer, respectively.

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16

Cho, Bong Jun, Hans H. Kim, David J. Lee, Eun Jung Choi, Yeo Hyun Hwang, Sun Ha Chun, and In Ah Kim. "MicroRNA-21 inhibitor potentiates anti-tumor effect of radiation therapy in vitro and in vivo." Tumor Microenvironment and Therapy 2, no. 1 (January 10, 2014): 1–13. http://dx.doi.org/10.2478/tumor-2014-0001.

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AbstractMicroRNA-21 (miR-21) plays important roles in carcinogenesis and is highly expressed in diverse human cancers. We evaluated the potential of targeting miRNA-21 to overcome the radioresistance of human cancer cells having an activated EGFR2-associated signaling and also aimed to elucidate the mechanisms of radiosensitization, and the effect on epithelial- mesenchymal transition (EMT). Ectopic overexpression of miR-21 up-regulated EGFR/HER2-associated signaling and increased radioresistance of a panel of human cancer cells (U251, U87, and A549 cells). In contrast, a specific inhibitor of miR-21 attenuated this signaling and radiosensitized a panel of human cancer cells. Inhibition of miR-21 was associated with persistent γH2AX foci formation. Inhibition of miR-21 decreased the typical features of EMT, such as invasion and migration and vascular tube formation. Treatment with anti-miR-21 decreased tumor burden in nude mice bearing intracranial U251 xenografts compared to controls. Combined treatment of anti-miR-21 and radiation further decreased tumor burden compared to each treatment alone. In summary, miR-21 is an important onco-miR, which confers radioresistance and diverse features of EMT. Inhibition of miR-21 could be a potential strategy for improving the efficacy of radiation therapy via unique modulation of pro-survival signaling implicated in radiation response and EMT.

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17

Sutoh, Mihoko, Yasuhiro Hashimoto, Takahiro Yoneyama, Hayato Yamamoto, Shingo Hatakeyama, Takuya Koie, Akiko Okamoto, et al. "Invadopodia Formation by Bladder Tumor Cells." Oncology Research Featuring Preclinical and Clinical Cancer Therapeutics 19, no. 2 (February 1, 2010): 85–92. http://dx.doi.org/10.3727/096504010x12875107808008.

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18

Esko, J., K. Rostand, and J. Weinke. "Tumor formation dependent on proteoglycan biosynthesis." Science 241, no. 4869 (August 26, 1988): 1092–96. http://dx.doi.org/10.1126/science.3137658.

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19

Dieter, Raymond A., George B. Kuzycz, Jeff Huml, and Lenora Su. "Tracheobronchial Tumor Cast Formation and Pneumothorax." Chest 120, no. 5 (November 2001): 1741–42. http://dx.doi.org/10.1378/chest.120.5.1741.

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20

Deng, Chu-Xia. "Tumor formation inBrca1 conditional mutant mice." Environmental and Molecular Mutagenesis 39, no. 2-3 (2002): 171–77. http://dx.doi.org/10.1002/em.10069.

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21

Lubkin, S. R., and T. Jackson. "Multiphase Mechanics of Capsule Formation in Tumors." Journal of Biomechanical Engineering 124, no. 2 (March 29, 2002): 237–43. http://dx.doi.org/10.1115/1.1427925.

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The presence of a capsule around a tumor is known to be correlated with benign status, and the absence of a capsule often has negative implications for patient prognosis. A mechanical description is presented of the growth of a tumor and the resulting deformations of surrounding normal tissue. A mathematical model of the mechanics is analyzed using physical parameters measured in vivo and in vitro. The model has only three dimensionless parameters, and its results are very robust with respect to parameter variation. We show that the presence of contractility in the surrounding tissue, corresponding to a host defense, can make an existing capsule denser and constrain the tumor better, but cannot be responsible for the observed pressure gradients in encapsulated tumors. Some implications for treatment are discussed.

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22

FUJITA, Tomomichi. "Screening of Genes Related to Tumor Formation in Tobacco Genetic Tumors." Plant tissue culture letters 11, no. 3 (1994): 171–77. http://dx.doi.org/10.5511/plantbiotechnology1984.11.171.

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23

Nacov, Emil. "Tumor angiogenesis formation of vessels de novo at germ cell tumors." Cancer 66, no. 5 (September 1, 1990): 916–22. http://dx.doi.org/10.1002/1097-0142(19900901)66:5<916::aid-cncr2820660517>3.0.co;2-m.

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24

Francis, J. L., and M. Amirkhosravi. "Coagulation Activation by MC28 Fibrosarcoma Cells Facilitates Lung Tumor Formation." Thrombosis and Haemostasis 73, no. 01 (1995): 059–65. http://dx.doi.org/10.1055/s-0038-1653726.

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SummaryTumor cells interact with the hemostatic system in various ways and may thus influence malignant growth and spread. MC28 fibrosarcoma cells possess a potent procoagulant activity (PCA) and form lung tumors following intravenous injection. The aim of this work was to study the relationship between PCA, intravascular coagulation and lung seeding in the MC28 model. MC28 cells were injected into control, warfarinized and heparinized hooded Lister rats. Coagulation changes were monitored by thromboelastography (TEG) and Sonoclot™ analysis (SA), lung fibrin formation by light and electron microscopy, tumor seeding by macroscopic counting and tumor cell and platelet deposition in the lungs by radiolabelling. PCA was measured by chromogenic assay. MC28 PCA was characterized as a tissue factorfactor VIIa complex that probably arose during cell culture or disaggregation of solid tumors. Injection of tumor cells caused marked coagulopathy and was rapidly (within 30 min) followed by fibrin deposition in the lungs and accumulation of radiolabelled platelets. Heparin and warfarin significantly reduced lung seeding (p <0.001) and reduced retention of radiolabelled tumor cells in the pulmonary circulation (p <0.01). Inhibition of cellular PCA by prior treatment with con- canavalin A markedly reduced intravascular coagulation and lung seeding.We conclude that MC28 cells cause intravascular coagulation as a direct result of their procoagulant activity. The data suggest that tumor cells form complexes with platelets and fibrin which are retained in the lungs long enough for extravasation and seeding to occur.Anticoagulation reduces tumor cell-platelet-fibrin complex formation, decreasing the time spent in the lungs and thereby reduces seeding. Thus, the antitumor effect of warfarin, at least in the MC28 model, is due to its anticoagulant action.

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Eichenlaub, Teresa, Stephen M. Cohen, and Héctor Herranz. "Cell Competition Drives the Formation of Metastatic Tumors in a Drosophila Model of Epithelial Tumor Formation." Current Biology 26, no. 4 (February 2016): 419–27. http://dx.doi.org/10.1016/j.cub.2015.12.042.

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26

Kuziel, Genevra, Victoria Thompson, Joseph V. D’Amato, and Lisa M. Arendt. "Stromal CCL2 Signaling Promotes Mammary Tumor Fibrosis through Recruitment of Myeloid-Lineage Cells." Cancers 12, no. 8 (July 28, 2020): 2083. http://dx.doi.org/10.3390/cancers12082083.

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Obesity is correlated with breast tumor desmoplasia, leading to diminished chemotherapy response and disease-free survival. Obesity causes chronic, macrophage-driven inflammation within breast tissue, initiated by chemokine ligand 2 (CCL2) signaling from adipose stromal cells. To understand how CCL2-induced inflammation alters breast tumor pathology, we transplanted oncogenically transformed human breast epithelial cells with breast stromal cells expressing CCL2 or empty vector into murine mammary glands and examined tumor formation and progression with time. As tumors developed, macrophages were rapidly recruited, followed by the emergence of cancer-associated fibroblasts (CAFs) and collagen deposition. Depletion of CD11b + myeloid lineage cells early in tumor formation reduced tumor growth, CAF numbers, and collagen deposition. CCL2 expression within developing tumors also enhanced recruitment of myeloid progenitor cells from the bone marrow into the tumor site. The myeloid progenitor cell population contained elevated numbers of fibrocytes, which exhibited platelet-derived growth factor receptor-alpha (PDGFRα)-dependent colony formation and growth in vitro. Together, these results suggest that chronic inflammation induced by CCL2 significantly enhances tumor growth and promotes the formation of a desmoplastic stroma through early recruitment of macrophages and fibrocytes into the tumor microenvironment. Fibrocytes may be a novel target in the tumor microenvironment to reduce tumor fibrosis and enhance treatment responses for obese breast cancer patients.

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Park, Jung-Woo. "Foam cell formation associated with a borderline ovarian tumor: a case report." Current Gynecologic Oncology 18, no. 2 (December 31, 2020): e57-e59. http://dx.doi.org/10.15557/cgo.2020.0011.

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Foam cell formation is a very common pathologic finding in atherosclerosis, often found in some major organs. However, the involvement of the retroperitoneal organs is very rare and foam cell formation associated with borderline ovarian tumor has not been reported. Borderline ovarian tumors are epithelial ovarian tumors with a low growth rate, low potential to invade or metastasize, and excellent prognosis. Still, a rapidly growing borderline ovarian tumor can exert pressure on the retroperitoneal organs. It may cause retroperitoneal irritation and inflammation, and form a mass lesion in adjacent organs. We report the case of a 41-year-old woman with a borderline ovarian tumor and foam cell infiltration.

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Levina, Vera, Yunyun Su, and Elieser Gorelik. "Immunological and Nonimmunological Effects of Indoleamine 2,3-Dioxygenase on Breast Tumor Growth and Spontaneous Metastasis Formation." Clinical and Developmental Immunology 2012 (2012): 1–12. http://dx.doi.org/10.1155/2012/173029.

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The role of the tryptophan-catabolizing enzyme, indoleamine 2,3-dioxygenase (IDO1), in tumor escape and metastasis formation was analyzed using two pairs ofIdo1+andIdo1−murine breast cancer cell lines.Ido1expression in 4T1 cells was knocked down by shRNA, andIdo1expression in NT-5 cells was upregulated by stable transfection. Growth ofIdo1−tumors and spontaneous metastasis formation were inhibited in immunocompetent mice. A higher level of cytotoxic T lymphocytes was generated by spleen cells from mice bearingIdo1−tumors thanIdo1+tumors. Tumor and metastatic growth was enhanced in immunodeficient mice, confirming an intensified immune response in the absence ofIdo1expression. However,Ido1+tumors grow faster thanIdo1−tumors in immunodeficient SCID/beige mice (lacking T, B, and NK cells) suggesting that someIdo1-controlled nonimmunological mechanisms may be involved in tumor cell growth regulation.In vitroexperiments demonstrated that downregulation ofIdo1in tumor cells was associated with decreased cell proliferation, increased apoptosis, and changed expression of cell cycle regulatory genes, whereas upregulation ofIdo1in the cells had the opposite effects. Taken together, our findings indicate thatIdo1expression could exert immunological and nonimmunological effects in murine breast tumor cells.

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Nisato, Riccardo, Jean-Christophe Tille, and Michael Pepper. "Lymphangiogenesis and tumor metastasis." Thrombosis and Haemostasis 90, no. 10 (2003): 591–97. http://dx.doi.org/10.1160/th03-04-0206.

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SummaryIn several human cancers, increased expression in primary tumors of vascular endothelial growth factor-C (VEGF-C) is correlated with regional lymph node metastasis. Studies using transgenic mice overexpressing VEGF-C, or xenotransplantation of VEGF-C-expressing tumor cells into immunodeficient mice, have demonstrated a role for VEGF-C in tumor lymphangiogenesis and the subsequent formation of lymph node metastasis. However, at variance with data obtained in animal models, there is at present very little evidence for lymphangiogenesis in human tumors. Nonetheless, the striking correlation between levels of VEGF-C in primary human tumors and lymph node metastases exists, which suggests that VEGF-C may serve functions other than lymphangiogenesis. Thus, VEGF-C may activate pre-existing lymphatics which in turn become directly involved in tumor cell chemotaxis, intralymphatic intravasation and distal dissemination. A reciprocal dialogue is therefore likely to exist between tumor and lymphatic endothelial cells which results in the formation of lymph node metastases.This publication was partially financed by Serono Foundation for the Advancement of Medical Science.Part of this paper was originally presented at the 2nd International Workshop on New Therapeutic Targets in Vascular Biology from February 6-9, 2003 in Geneva, Switzerland.

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Qin, Z., S. Krüger-Krasagakes, U. Kunzendorf, H. Hock, T. Diamantstein, and T. Blankenstein. "Expression of tumor necrosis factor by different tumor cell lines results either in tumor suppression or augmented metastasis." Journal of Experimental Medicine 178, no. 1 (July 1, 1993): 355–60. http://dx.doi.org/10.1084/jem.178.1.355.

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Tumor necrosis factor (TNF) produced by tumor cells after gene transfer can effectively suppress the growth of locally growing tumors. We wanted to test the effects of "local" TNF on the growth of a highly metastatic cell line. Therefore, a recombinant retrovirus allowing expression of the TNF gene by the beta-actin promotor has been constructed and used to infect the two tumor cell lines EB and ESB, which grow as solid tumor or metastasize, respectively. Expression of TNF by EB cells resulted in their rapid and dose-dependent rejection. In sharp contrast, mice injected with ESB cells producing similar amounts of TNF showed no signs of tumor suppression, but rather had reduced survival rates that correlated with enhanced hepatic metastases. The accelerated formation of liver metastases by ESB TNF cells could be reversed by an anti-TNF mAb. These results demonstrate the opposite effects TNF may have on tumor growth: suppression of a locally growing tumor and promotion of metastasis formation.

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Kampa, Kerstin M., Jared D. Acoba, Dexi Chen, Kelly Beemer, Joel Gay, Zhiyi Zhu, Emerson Padiernos, et al. "ASPP2 Haploinsufficiency Promotes Tumor Formation in a Mouse Model." Blood 108, no. 11 (November 16, 2006): 4333. http://dx.doi.org/10.1182/blood.v108.11.4333.4333.

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Abstract ASPP2 interacts with the tumor suppressor protein p53 and promotes damage-induced apoptosis in part through stimulation of p53-mediated apoptosis. We have previously demonstrated that low ASPP2 levels correlate with poor clinical outcome in patients with diffuse large B-cell lymphoma treated with anthracycline-based chemotherapy. Moreover, reduced ASPP2 expression has been demonstrated in other tumor types. These findings led us to hypothesize that ASPP2 may function as a tumor suppressor. To further explore this, we targeted the ASPP2 allele in a mouse by homologous recombination using a knockout vector that replaced exons 10–17 with a neoR gene. Two separate ES clones were used for blastocyst injections to generate several chimeras that were used to generate ASPP2 heterozygous mice. ASPP2+/− mice appear developmentally normal and reproduce. However ASPP2−/− mice could not be generated. Genotype analysis as early as Ed 6.5 did not detect ASPP2−/− embryos---which implies an early embryonic lethal defect in the homozygote. ASPP2+/− (n=135) and ASPP2+/+ (n=63) sibling mice were observed for spontaneous tumor formation. Overall median tumor-free survival was 117 weeks in the ASPP2+/− mice verses 125 weeks in the ASPP2+/+mice (p = 0.035 log-rank test). Overall tumor incidence (at 115 weeks) for ASPP2+/− and ASPP2+/+ mice was 43% and 22%, respectively. The incidence of tumor types, from all tumors detected, was similar between ASPP2+/− and ASPP2+/+ mice: 34% versus 33% (lymphoma), 18% versus 14% (sarcoma), and 47% versus 52% (carcinoma), respectively. Compound p53+/−;ASPP2+/− mice did not exhibit accelerated tumor formation relative to p53+/−;ASPP2+/+ mice. Additionally, a tet-Myc:ASPP2+/− lymphoma mouse model did not exhibit accelerated lymphomagenesis. However, preliminary data suggests that ASPP2+/− mice may have an increased incidence of irradiation-induced leukemia/lymphoma when compared to ASPP2+/+ mice, and confirmatory studies are ongoing. In response to ionizing radiation, doxorubicin, or serum-starvation, preliminary analysis reveals a G0/G1 checkpoint defect in ASPP2+/− MEFs compared to ASPP2+/+ MEFs. Our results provide in vivo evidence that ASPP2 can function as a tumor suppressor. Further studies are underway to determine the mechanism of this observation.

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Alicke, Bruno, Klara Totpal, Jill M. Schartner, Amy M. Berkley, Sophie M. Lehar, Aude-Hélène Capietto, Rafael A. Cubas, and Stephen E. Gould. "Immunization associated with primary tumor growth leads to rejection of commonly used syngeneic tumors upon tumor rechallenge." Journal for ImmunoTherapy of Cancer 8, no. 2 (July 2020): e000532. http://dx.doi.org/10.1136/jitc-2020-000532.

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The recent success of multiple immunomodulating drugs in oncology highlights the potential of relieving immunosuppression by directly engaging the immune system in the tumor bed to target cancer cells. Durable responses to immune checkpoint inhibitors experienced by some patients may be indicative of the formation of a T cell memory response. This has prompted the search for preclinical evidence of therapy-induced long-term immunity as part of the evaluation of novel therapeutics. A common preclinical method used to document long-term immunity is the use of tumor rechallenge experiments in which tumor growth is assessed in mice that have previously rejected tumors in response to therapy. Failure of rechallenge engraftment, typically alongside successful engraftment of the same tumor in naive animals as a control, is often presented as evidence of therapy-induced tumor immunity. Here, we present evidence that formation of tumor immunity often develops independent of therapy. We observed elevated rates of rechallenge rejection following surgical resection of primary tumors for four of five commonly used models and that such postexcision immunity could be adoptively transferred to treatment-naïve mice. We also show that tumor-specific cytolytic T cells are induced on primary tumor challenge independent of therapeutic intervention. Taken together these data call into question the utility of tumor rechallenge studies and the use of naïve animals as controls to demonstrate therapy-induced formation of long-term tumor immunity.

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Wagner, Kay-Dietrich, Siyue Du, Luc Martin, Nathalie Leccia, Jean-François Michiels, and Nicole Wagner. "Vascular PPARβ/δ Promotes Tumor Angiogenesis and Progression." Cells 8, no. 12 (December 12, 2019): 1623. http://dx.doi.org/10.3390/cells8121623.

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Peroxisome proliferator-activated receptors (PPARs) are nuclear receptors, which function as transcription factors. Among them, PPARβ/δ is highly expressed in endothelial cells. Pharmacological activation with PPARβ/δ agonists had been shown to increase their angiogenic properties. PPARβ/δ has been suggested to be involved in the regulation of the angiogenic switch in tumor progression. However, until now, it is not clear to what extent the expression of PPARβ/δ in tumor endothelium influences tumor progression and metastasis formation. We addressed this question using transgenic mice with an inducible conditional vascular-specific overexpression of PPARβ/δ. Following specific over-expression of PPARβ/δ in endothelial cells, we induced syngenic tumors. We observed an enhanced tumor growth, a higher vessel density, and enhanced metastasis formation in the tumors of animals with vessel-specific overexpression of PPARβ/δ. In order to identify molecular downstream targets of PPARβ/δ in the tumor endothelium, we sorted endothelial cells from the tumors and performed RNA sequencing. We identified platelet-derived growth factor receptor beta (Pdgfrb), platelet-derived growth factor subunit B (Pdgfb), and the tyrosinkinase KIT (c-Kit) as new PPARβ/δ -dependent molecules. We show here that PPARβ/δ activation, regardless of its action on different cancer cell types, leads to a higher tumor vascularization which favors tumor growth and metastasis formation.

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Costantini, V., and L. R. Zacharski. "Blood Coagulation Activation in Cancer: Challenges for Cancer Treatment." Hämostaseologie 15, no. 01 (January 1995): 14–20. http://dx.doi.org/10.1055/s-0038-1655282.

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SummaryIt has been known for over a century that blood coagulation and fibrinolysis pathways are activated systemically in patients with malignancy. Recent studies have revealed evidence for two distinct pathways of interaction between tumor cells and the host coagulation mechanism that include production of either initiators of thrombin formation or expression of plasminogen activators by the tumor cells in situ within intact tumor tissue. Studies in specific in vitro and animal models of malignancy have implicated either tumor cell procoagulants or urokinase in mechanisms of tumor cell proliferation, invasion, and metastasis. We have formulated a classification of human tumor types based on detection of components of either of these pathways in situ. Type I tumors are those in which the tumor cells are associated with an intact coagulation pathway that leads to thrombin formation at the tumor periphery but in which the tumor cells lack urokinase. Type II tumors are those in which the tumor cells express urokinase but lack an associated coagulation pathway leading to thrombin formation. Type III tumors are those that express neither of these pathways, or exhibit some other pattern of interaction. Evidence suggests that anticoagulant therapy is capable of ameliorating the clinical course of a procoagulant tumor type namely, small cell carcinoma of the lung. This approach may be effective in other type I tumors. Clinical trials of agents capable of inhibiting urokinase-initiated proteolysis are required to clarify cause/effect relationships in urokinase-expressing tumors. Exploration of the coagulation-cancer interaction holds considerable promise for imaginative new approaches to cancer treatment that are not only relatively nontoxic and low cost, but also effective because they may interrupt fundamental mechanisms of malignant growth control.

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Okamoto, Rika, Masaya Ueno, Yoshihiro Yamada, Naoko Takahashi, Hideto Sano, Toshio Suda, and Nobuyuki Takakura. "Hematopoietic cells regulate the angiogenic switch during tumorigenesis." Blood 105, no. 7 (April 1, 2005): 2757–63. http://dx.doi.org/10.1182/blood-2004-08-3317.

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Abstract Hematopoietic cells (HCs) promote blood vessel formation by producing various proangiogenic cytokines and chemokines and matrix metalloproteinases. We injected mouse colon26 colon cancer cells or human PC3 prostate adenocarcinoma cells into mice and studied the localization of HCs during tumor development. HCs were distributed in the inner tumor mass in all of the tumor tissues examined; however, the localization of HCs in the tumor tissue differed depending on the tumor cell type. In the case of colon26 tumors, as the tumor grew, many mature HCs migrated into the tumor mass before fine capillary formation was observed. On the other hand, although very few HCs migrated into PC3 tumor tissue, c-Kit+ hematopoietic stem/progenitor cells accumulated around the edge of the tumor. Bone marrow suppression induced by injection of anti–c-Kit neutralizing antibody suppressed tumor angiogenesis by different mechanisms according to the tumor cell type: bone marrow suppression inhibited the initiation of sprouting angiogenesis in colon26 tumors, while it suppressed an increase in the caliber of newly developed blood vessels at the tumor edge in PC3 tumors. Our findings suggest that HCs are involved in tumor angiogenesis and regulate the angiogenic switch during tumorigenesis.

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Kuang, Dong-Ming, Yan Wu, Nini Chen, Jiasen Cheng, Shi-Mei Zhuang, and Limin Zheng. "Tumor-derived hyaluronan induces formation of immunosuppressive macrophages through transient early activation of monocytes." Blood 110, no. 2 (July 15, 2007): 587–95. http://dx.doi.org/10.1182/blood-2007-01-068031.

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Abstract Macrophages (Mφ) in most solid tumors exhibit a distinct immunosuppressive phenotype, but the mechanisms that allow tumor microenvironments to “educate” Mφ are incompletely understood. Here, we report that culture supernatants (TSNs) from several types of tumor cell lines can drive monocytes to become immunosuppressive Mφ. Kinetic experiments revealed that soon after exposure to these TSNs, monocytes began to provoke transient proinflammatory responses and then became refractory to subsequent stimulation. Other TSNs that failed to cause such temporary preactivation did not alter Mφ polarization. Consistent with these results, we observed that the monocytes/Mφ in different areas of human tumor samples exhibited distinct activation patterns. Moreover, we found that hyaluronan fragments constitute a common factor produced by various tumors to induce the formation of immunosuppressive Mφ, and also that upregulation of hyaluronan synthase-2 in tumor cells is correlated with the ability of the cells to cause Mφ dysfunction. These results indicate that soluble factors derived from tumor cells, including hyaluronan fragments, co-opt the normal development of Mφ to dynamically educate the recruited blood monocytes in different niches of a tumor. The malignant cells can thereby avoid initiation of potentially dangerous Mφ functions and create favorable conditions for tumor progression.

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Schmitt, Adam M., and Bakhtiar Yamini. "Nfkb1 suppresses DNA alkylation-induced tumor formation." Molecular & Cellular Oncology 2, no. 1 (January 2, 2015): e968073. http://dx.doi.org/10.4161/23723548.2014.968073.

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38

Godovanets, O., I. Marchuk, and T. Muryniuk. "EPULIS AS A TUMOR FORMATION. CLINICAL CASE." Neonatology, surgery and perinatal medicine 9, no. 3(33) (November 11, 2019): 131–34. http://dx.doi.org/10.24061/2413-4260.ix.3.33.2019.12.

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39

Di Leva, Gianpiero, and Carlo M. Croce. "Roles of small RNAs in tumor formation." Trends in Molecular Medicine 16, no. 6 (June 2010): 257–67. http://dx.doi.org/10.1016/j.molmed.2010.04.001.

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40

Yamashiro, H., M. Yamamoto, and R. van Woesik. "Tumor formation on the coral Montipora informis." Diseases of Aquatic Organisms 41 (2000): 211–17. http://dx.doi.org/10.3354/dao041211.

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41

Dai, Ziwei, and Jason W. Locasale. "Metabolic pattern formation in the tumor microenvironment." Molecular Systems Biology 13, no. 2 (February 2017): 915. http://dx.doi.org/10.15252/msb.20167518.

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42

Danis, Judit, and Márta Széll. "Functional relevance of pyknons in tumor formation." Non-coding RNA Investigation 2 (2018): 3. http://dx.doi.org/10.21037/ncri.2017.12.05.

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43

Song, Shilin, Diana Andrejeva, Flávia C. P. Freitas, Stephen M. Cohen, and Héctor Herranz. "dTcf/Pangolinsuppresses growth and tumor formation inDrosophila." Proceedings of the National Academy of Sciences 116, no. 28 (June 24, 2019): 14055–64. http://dx.doi.org/10.1073/pnas.1816981116.

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Wnt/Wingless (Wg) signaling controls many aspects of animal development and is deregulated in different human cancers. The transcription factor dTcf/Pangolin (Pan) is the final effector of the Wg pathway inDrosophilaand has a dual role in regulating the expression of Wg target genes. In the presence of Wg, dTcf/Pan interacts with β-catenin/Armadillo (Arm) and induces the transcription of Wg targets. In absence of Wg, dTcf/Pan partners with the transcriptional corepressor TLE/Groucho (Gro) and inhibits gene expression. Here, we use the wing imaginal disk ofDrosophilaas a model to examine the functions that dTcf/Pan plays in a proliferating epithelium. We report a function of dTcf/Pan in growth control and tumorigenesis. Our results show that dTcf/Pan can limit tissue growth in normal development and suppresses tumorigenesis in the context of oncogene up-regulation. We identify the conserved transcription factorsSox box protein 15(Sox15) andFtz transcription factor 1(Ftz-f1) as genes controlled by dTcf/Pan involved in tumor development. In conclusion, this study reports a role for dTcf/Pan as a repressor of normal and oncogenic growth and identifies the genes inducing tumorigenesis downstream of dTcf/Pan.

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Kazeem, A. A. "The immunological aspects of keloid tumor formation." Journal of Surgical Oncology 38, no. 1 (May 1988): 16–18. http://dx.doi.org/10.1002/jso.2930380106.

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45

Xu, R. K., X. M. Wu, A. K. Di, J. N. Xu, C. S. Pang, and S. F. Pang. "Pituitary Prolactin-Secreting Tumor Formation: Recent Developments." Neurosignals 9, no. 1 (2000): 1–20. http://dx.doi.org/10.1159/000014618.

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46

Jessberger, R. "New Insights into Germ Cell Tumor Formation." Hormone and Metabolic Research 40, no. 5 (May 2008): 342–46. http://dx.doi.org/10.1055/s-2008-1073168.

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47

Dang, L., X. Fan, A. Chaudhry, M. Wang, N. Gaiano, and C. G. Eberhart. "Notch3 signaling initiates choroid plexus tumor formation." Oncogene 25, no. 3 (September 26, 2005): 487–91. http://dx.doi.org/10.1038/sj.onc.1209074.

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48

Eckert, Mark A., Thinzar M. Lwin, Andrew T. Chang, Jihoon Kim, Etienne Danis, Lucila Ohno-Machado, and Jing Yang. "Twist1-Induced Invadopodia Formation Promotes Tumor Metastasis." Cancer Cell 19, no. 3 (March 2011): 372–86. http://dx.doi.org/10.1016/j.ccr.2011.01.036.

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49

Campanero, Miguel R. "Mechanisms involved in Burkitt’s lymphoma tumor formation." Clinical and Translational Oncology 10, no. 5 (May 2008): 250–55. http://dx.doi.org/10.1007/s12094-008-0193-x.

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50

Rhim, Andrew D., Emily T. Mirek, Nicole M. Aiello, Anirban Maitra, Jennifer M. Bailey, Florencia McAllister, Maximilian Reichert, et al. "EMT and Dissemination Precede Pancreatic Tumor Formation." Cell 148, no. 1-2 (January 2012): 349–61. http://dx.doi.org/10.1016/j.cell.2011.11.025.

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