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Статті в журналах з теми "Malignant Cells - Molecular Characetrization"

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Автор: Grafiati

Опубліковано: 7 вересня 2023

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1

Fredholm, Simon, Andreas Willerslev-Olsen, Özcan Met, Linda Kubat, Maria Gluud, Sarah L. Mathiasen, Christina Friese, et al. "SATB1 in Malignant T Cells." Journal of Investigative Dermatology 138, no. 8 (August 2018): 1805–15. http://dx.doi.org/10.1016/j.jid.2018.03.1526.

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2

Miller, W. H. "Molecular Targets of Arsenic Trioxide in Malignant Cells." Oncologist 7, no. 90001 (April 1, 2002): 14–19. http://dx.doi.org/10.1634/theoncologist.7-2004-14.

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3

Miller, Wilson H. "Molecular Targets of Arsenic Trioxide in Malignant Cells." Oncologist 7, S1 (April 2002): 14–19. http://dx.doi.org/10.1634/theoncologist.7-suppl_1-14.

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4

Suzme, R., J.-C. Tseng, B. Levin, S. Ibrahim, D. Meruelo, and A. Pellicer. "Sindbis viral vectors target hematopoietic malignant cells." Cancer Gene Therapy 19, no. 11 (September 7, 2012): 757–66. http://dx.doi.org/10.1038/cgt.2012.56.

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5

BALIS, M. EARL. "Adenosine Deaminase and Malignant Cells." Annals of the New York Academy of Sciences 451, no. 1 (October 1985): 142–49. http://dx.doi.org/10.1111/j.1749-6632.1985.tb27105.x.

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6

Cairo, Gaetano, Paolo Vezzoni, Lidia Bardella, Luisa Schiaffonati, Emilia Rappocciolo, Sonia Levi, Paolo Arosio, and Aldo Bernelli-Zazzera. "Regulation of ferritin synthesis in malignant and non-malignant lymphoid cells." Biochemical and Biophysical Research Communications 139, no. 2 (September 1986): 652–57. http://dx.doi.org/10.1016/s0006-291x(86)80040-7.

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7

Postovit, Lynne-Marie, Elisabeth A. Seftor, Richard EB Seftor, and Mary JC Hendrix. "Targeting Nodal in malignant melanoma cells." Expert Opinion on Therapeutic Targets 11, no. 4 (March 20, 2007): 497–505. http://dx.doi.org/10.1517/14728222.11.4.497.

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8

Cheng, Sun-Long, Rosa Huang-Liu, Jin-Nan Sheu, Shui-Tein Chen, Supachok Sinchaikul, and Gregory J. Tsay. "Toxicogenomics of A375 human malignant melanoma cells." Pharmacogenomics 8, no. 8 (August 2007): 1017–36. http://dx.doi.org/10.2217/14622416.8.8.1017.

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9

Katsoulidis, Efstratios, Surinder Kaur, and Leonidas C. Platanias. "Deregulation of Interferon Signaling in Malignant Cells." Pharmaceuticals 3, no. 2 (February 4, 2010): 406–18. http://dx.doi.org/10.3390/ph3020406.

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10

Too, Catherine K. L., Christine Lee, Shirley M. Sangster, and Peter W. Gout. "Malignant Progression of Rat Nb2 Lymphoma Cells." Cancer Genetics and Cytogenetics 110, no. 2 (April 1999): 115–23. http://dx.doi.org/10.1016/s0165-4608(98)00191-5.

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11

Testa, Joseph R., and Philip N. Tsichlis. "AKT signaling in normal and malignant cells." Oncogene 24, no. 50 (November 2005): 7391–93. http://dx.doi.org/10.1038/sj.onc.1209100.

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12

Lazarovici, Philip, Michael Bergel, Tsury Hasson, Ezra Rahamim, and Jacob Hochman. "Immunomagnetic separation and analysis of non-malignant variants and parental malignant mouse lymphoma cells." Journal of Molecular Recognition 4, no. 4 (July 1991): 143–49. http://dx.doi.org/10.1002/jmr.300040406.

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13

Liu, Peng, Liwei Zhao, Friedemann Loos, Caroline Marty, Wei Xie, Isabelle Martins, Sylvie Lachkar, et al. "Immunosuppression by Mutated Calreticulin Released from Malignant Cells." Molecular Cell 77, no. 4 (February 2020): 748–60. http://dx.doi.org/10.1016/j.molcel.2019.11.004.

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14

Bian, Jing, Jianyang Fu, Xin Wang, Jihye Lee, Gagandeep Brar, Freddy E. Escorcia, Maggie Cam, and Changqing Xie. "Characterization of Immunogenicity of Malignant Cells with Stemness in Intrahepatic Cholangiocarcinoma by Single-Cell RNA Sequencing." Stem Cells International 2022 (April 29, 2022): 1–14. http://dx.doi.org/10.1155/2022/3558200.

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Анотація:

Cancer stem cells (CSCs) are responsible for long-term maintenance of tumors and thought to play a role in treatment resistance. The interaction between stemness and immunogenicity of CSCs in the intrahepatic cholangiocarcinoma (iCCA) is largely unknown. Here, we used single-cell transcriptomic data to study immunogenicity of malignant cells in human iCCA. Using an established computerized method CytoTRACE, we found significant heterogeneity in stemness/differentiation states among malignant cells. We demonstrated that the high stemness malignant cells express much lower levels of major histocompatibility complex II molecules when compared to low stemness malignant cells, suggesting a role of immune evasion in high stemness malignant cells. In addition, high stemness malignant iCCA cells exhibited significant expression of certain cytokine members, including CCL2, CCL20, CXCL1, CXCL2, CXCL6, CXCL8, TNFRSF12A, and IL6ST, indicating communication with surrounding immune cells. These results indicate that high stemness malignant cells retain their intrinsic immunological feature that facilitate the escape of immune surveillance.

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15

Theobald, Matthias, and Rienk Offringa. "Anti-p53-directed immunotherapy of malignant disease." Expert Reviews in Molecular Medicine 5, no. 11 (March 28, 2003): 1–13. http://dx.doi.org/10.1017/s1462399403006173.

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Анотація:

Mutation and aberrant expression of the p53 tumour suppressor protein are the most frequent molecular alterations in human malignancy. Peptides derived from the p53 protein and presented by major histocompatibility complex molecules for T-cell recognition could serve as universal tumour-associated antigens for cancer immunotherapy. Because p53 normally functions as a ubiquitously expressed self-protein, controlling cell-cycle progression and apoptosis, it also represents a paradigm target molecule for tumour-reactive yet self-antigen-specific T cells. Tailoring p53-based cancer immunotherapy thus requires both interference with p53-specific self-tolerance and induction of the entire repertoire of p53-reactive T cells. Transferring selected T-cell receptor genes into human T cells offers a novel and appealing strategy to meet these requirements.

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16

Lekka, Małgorzata, Dorota Gil, Wojciech Dąbroś, Justyna Jaczewska, Andrzej J. Kulik, Janusz Lekki, Zbigniew Stachura, Jerzy Stachura, and Piotr Laidler. "Characterization of N-cadherin unbinding properties in non-malignant (HCV29) and malignant (T24) bladder cells." Journal of Molecular Recognition 24, no. 5 (July 26, 2011): 833–42. http://dx.doi.org/10.1002/jmr.1123.

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17

Keith, W. Nicol, Alan Bilsland, T. R. Jeffry Evans, and Rosalind M. Glasspool. "Telomerase-directed molecular therapeutics." Expert Reviews in Molecular Medicine 4, no. 10 (April 22, 2002): 1–25. http://dx.doi.org/10.1017/s1462399402004507.

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The management of malignant disease remains one of the most challenging areas of modern medicine. The lifetime risk of developing cancer in the western world is estimated to be as high as 1 in 3. Traditionally, surgery, chemotherapy and radiotherapy have been the primary choice of treatment for patients with malignant tumours. Despite advances in the use and development of conventional cytotoxic agents, the cure rate remains disappointing in most patients with advanced disease of the common solid tumours. Consequently, the development of novel anti-cancer therapies is a high priority in cancer medicine. In recent years, a new generation of cancer therapies has emerged, based on a growing understanding of the molecular events that contribute to malignant transformation. A major difference between normal and cancer cells is the ability of cancer cells to multiply in an unrestricted and ungoverned fashion. In this context, there is considerable interest in elucidating the mechanisms that allow this unrestricted proliferation and that ultimately result in immortal cancer cells. It is now clear that the enzyme telomerase confers immortality on cells in most types of cancer. With the cancer cell reliant on telomerase for its survival, telomerase represents an extremely attractive mechanism-based target for the development of new cancer therapeutics.

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18

Nitsch, Andreas, Caroline Sander, Benedikt Eggers, Martin Weiss, Eva Egger, Franz-Josef Kramer, Holger H. H. Erb, Alexander Mustea, and Matthias B. Stope. "Pleiotropic Devitalization of Renal Cancer Cells by Non-Invasive Physical Plasma: Characterization of Molecular and Cellular Efficacy." Cancers 15, no. 2 (January 12, 2023): 481. http://dx.doi.org/10.3390/cancers15020481.

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Renal cell carcinoma (RCC) is the third most common urological tumor and has an extremely poor prognosis after metastasis has occurred. Therapeutic options are highly restricted, primarily due to resistance to classical chemotherapeutics. The development of new, innovative therapeutic procedures is thus of great urgency. In the present study, the influence of non-invasive physical plasma (NIPP) on malignant and non-malignant renal cells is characterized. The biological efficacy of NIPP has been demonstrated in malignant renal cell lines (786-O, Caki-1) and non-malignant primary human renal epithelial cells (HREpC). The cell responses that were experimentally examined were cell growth (cell number determination, calculation of growth rate and doubling time), cell motility (scratch assay, invasiveness assay), membrane integrity (uptake of fluorescent dye, ATP release), and induction of apoptosis (TUNEL assay, caspase-3/7 assay, comet assay). A single NIPP treatment of the malignant cells significantly inhibited cell proliferation, invasiveness, and metastasis. This treatment has been attributed to the disruption of membrane functionality and the induction of apoptotic mechanisms. Comparison of NIPP sensitivity of malignant 786-O and Caki-1 cells with non-malignant HREpC cells showed significant differences. Our results suggest that renal cancer cells are significantly more sensitive to NIPP than non-malignant renal cells. Treatment with NIPP could represent a promising innovative option for the therapy of RCC and might supplement established treatment procedures. Of high clinical relevance would be the chemo-sensitizing properties of NIPP, which could potentially allow a combination of NIPP treatment with low-dose chemotherapy.

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19

Vatter, Sandra, Gudrun Pahlke, Joachim W. Deitmer, and Gerhard Eisenbrand. "Differential phosphodiesterase expression and cytosolic Ca2+in human CNS tumour cells and in non-malignant and malignant cells of rat origin." Journal of Neurochemistry 93, no. 2 (March 2, 2005): 321–29. http://dx.doi.org/10.1111/j.1471-4159.2005.03028.x.

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20

Steidl, Christian, Joseph M. Connors, and Randy D. Gascoyne. "Molecular Pathogenesis of Hodgkin's Lymphoma: Increasing Evidence of the Importance of the Microenvironment." Journal of Clinical Oncology 29, no. 14 (May 10, 2011): 1812–26. http://dx.doi.org/10.1200/jco.2010.32.8401.

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Hodgkin's lymphoma (HL) represents the most common subtype of malignant lymphoma in young people in the Western world. Most patients can be cured with modern treatment strategies, although approximately 20% will die after relapse or progressive disease. The histologic hallmark of the disease is the presence of the characteristic Hodgkin Reed-Sternberg (HRS) cells in classical HL and so-called lymphocyte-predominant (LP) cells in nodular lymphocyte-predominant HL. HL is unique among all cancers because malignant cells are greatly outnumbered by reactive cells in the tumor microenvironment and make up only approximately 1% of the tumor. Expression of a variety of cytokines and chemokines by the HRS and LP cells is believed to be the driving force for an abnormal immune response, perpetuated by additional factors secreted by reactive cells in the microenvironment that help maintain the inflammatory milieu. The malignant HRS and LP cells manipulate the microenvironment, permitting them to develop their malignant phenotype fully and evade host immune attack. Gene expression signatures derived from non-neoplastic cells correlate well with response to initial and subsequent therapies, reflecting their functional relevance. Recent biomarker studies have added texture to clinical outcome predictors, and their incorporation into prognostic models may improve our understanding of the biologic correlates of treatment failure. Moreover, recent preclinical and clinical studies have demonstrated that the tumor microenvironment represents a promising therapeutic target, raising hope that novel treatment strategies focused on the interface between malignant and reactive cells will soon emerge.

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21

Armstrong, Cheryl A., David C. Tara, Charles E. Hart, Andreas Kock, Thomas A. Luger, and John C. Ansel. "Heterogeneity of cytokine production by human malignant melanoma cells." Experimental Dermatology 1, no. 1 (February 1992): 37–45. http://dx.doi.org/10.1111/j.1600-0625.1992.tb00070.x.

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22

Kim, N.-Y., M.-C. Kim, and Y. Kim. "Hypomethylation reduced the aggressive potential of human malignant mesothelioma cells." Cancer Gene Therapy 23, no. 12 (November 18, 2016): 425–32. http://dx.doi.org/10.1038/cgt.2016.57.

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23

Yan, Ting, Wangwang Qiu, Jianlu Song, Youben Fan, and Zhili Yang. "ARHGAP36 regulates proliferation and migration in papillary thyroid carcinoma cells." Journal of Molecular Endocrinology 66, no. 1 (January 2021): 1–10. http://dx.doi.org/10.1530/jme-20-0230.

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The diagnosis and treatment of recurrence and metastasis in papillary thyroid carcinoma (PTC) are still clinical challenges. One of the key factors is the lack of specific diagnostic markers and therapeutic targets for recurrence and metastasis. Single-cell RNA sequencing (scRNA-seq) has emerged as a powerful approach to find specific biomarkers by dissecting expression profiling in human cancers at the resolution of individual cells. Here, we investigated cell profiles of the primary tumor and lymph node metastasis and paracancerous normal tissues in one PTC patient using scRNA-seq, and compared individual cell gene expression differences. The transcriptomes of 11,805 single cells were profiled, and malignant cells exhibited a profound transcriptional overlap between primary and metastatic lesions, but there were differences in the composition and quantity of non-malignant cells. ARHGAP36 was one of the genes that were highly expressed in almost all of the primary and metastatic malignant cells without non-malignant or normal follicular cells and was then confirmed by immunostaining in a sample cohort. Compared with the paracancerous normal tissue, the expression of ARHGAP36 in primary and metastatic carcinoma tissues was significantly higher as assayed by qRT-PCR. ARHGAP36 knockdown significantly inhibited the proliferation and migration of PTC cells in vitro and involved several proliferation and migration-associated signaling pathways by RNA seq. Our study demonstrated that ARHGAP36 is exclusively expressed in the malignant cells of primary PTC, as well as metastatic lesions, and regulates their proliferation and migration, meaning it can be used as a potential diagnostic marker and therapeutic target molecule.

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24

Mavletova, D. A., V. V. Ryapolov, and G. A. Dvorkin. "High-molecular-weight stress proteins in the cytoskeleton of malignant cells." Doklady Biochemistry and Biophysics 408, no. 1 (June 2006): 142–44. http://dx.doi.org/10.1134/s1607672906030094.

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25

Mitsiades, Nicholas, Constantine S. Mitsiades, Paul G. Richardson, Ciaran McMullan, Vassiliki Poulaki, Galinos Fanourakis, Robert Schlossman, et al. "Molecular sequelae of histone deacetylase inhibition in human malignant B cells." Blood 101, no. 10 (May 15, 2003): 4055–62. http://dx.doi.org/10.1182/blood-2002-11-3514.

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Abstract Histone acetylation modulates gene expression, cellular differentiation, and survival and is regulated by the opposing activities of histone acetyltransferases (HATs) and histone deacetylases (HDACs). HDAC inhibition results in accumulation of acetylated nucleosomal histones and induces differentiation and/or apoptosis in transformed cells. In this study, we characterized the effect of suberoylanilide hydroxamic acid (SAHA), the prototype of a series of hydroxamic acid–based HDAC inhibitors, in cell lines and patient cells from B-cell malignancies, including multiple myeloma (MM) and related disorders. SAHA induced apoptosis in all tumor cells tested, with increased p21 and p53 protein levels and dephosphorylation of Rb. We also detected cleavage of Bid, suggesting a role for Bcl-2 family members in regulation of SAHA-induced cell death. Transfection of Bcl-2 cDNA into MM.1S cells completely abrogated SAHA-induced apoptosis, confirming its protective role. SAHA did not induce cleavage of caspase-8, -9, or -3 in MM.1S cells during the early phase of apoptosis, and the pan-caspase inhibitor ZVAD-FMK did not protect against SAHA. Conversely, poly(ADP)ribose polymerase (PARP) was cleaved in a pattern indicative of calpain activation, and the calpain inhibitor calpeptin abrogated SAHA-induced cell death. Importantly, SAHA sensitized MM.1S cells to death receptor–mediated apoptosis and inhibited the secretion of interleukin 6 (IL-6) induced in bone marrow stromal cells (BMSCs) by binding of MM cells, suggesting that it can overcome cell adhesion–mediated drug resistance. Our studies delineate the mechanisms whereby HDAC inhibitors mediate anti-MM activity and overcome drug resistance in the BM milieu and provide the framework for clinical evaluation of SAHA, which is bioavailable, well tolerated, and bioactive after oral administration, to improve patient outcome.

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26

&NA;. "Use of molecular methods to screen urinary specimens for malignant cells." Advances in Anatomic Pathology 3, no. 5 (September 1996): 306. http://dx.doi.org/10.1097/00125480-199609000-00007.

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27

Pulciani, S., E. Santos, L. K. Long, V. Sorrentino, and M. Barbacid. "ras gene Amplification and malignant transformation." Molecular and Cellular Biology 5, no. 10 (October 1985): 2836–41. http://dx.doi.org/10.1128/mcb.5.10.2836-2841.1985.

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Анотація:

Morphologic transformation of NIH 3T3 mouse cells occurs upon transfection of these cells with large amounts (greater than or equal to 10 micrograms) of recombinant DNA molecules carrying the normal human H-ras-1 proto-oncogene. We provide experimental evidence indicating that transformation of these NIH 3T3 cells results from the combined effect of multiple copies of the H-ras-1 proto-oncogene rather than from spontaneous mutation of one of the transfected H-ras-1 clones (E. Santos, E.P. Reddy, S. Pulciani, R.J. Feldman, and M. Barbacid, Proc. Natl. Acad. Sci. USA 80:4679-4683, 1983). Levels of H-ras-1 RNA and p21 expression are highly elevated in the NIH 3T3 transformants, and in those cases examined, these levels correlate with the malignant properties of these cells. We have also investigated the presence of amplified ras genes in a variety of human carcinomas. In 75 tumor biopsies, we found amplification of the human K-ras-2 locus in one carcinoma of the lung. These results indicate that ras gene amplification is an alternative pathway by which ras genes may participate in the development of human neoplasia.

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28

Tie, Jun, Xiangyuan Zhang, and Daiming Fan. "Epigenetic roles in the malignant transformation of gastric mucosal cells." Cellular and Molecular Life Sciences 73, no. 24 (July 27, 2016): 4599–610. http://dx.doi.org/10.1007/s00018-016-2308-9.

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29

SHINDO, AYAKA, MIDORI KUSANO, HIROSHI SAKAGAMI, SHIGERU AMANO, MEGUMI INOMATA, MASAYO ABE, MASASHI OKAZAWA, and TAKAFUMI OOKA. "Comparison of UVC Sensitivity and Dectin-2 Expression Between Malignant and Non-malignant Cells." In Vivo 36, no. 5 (2022): 2116–25. http://dx.doi.org/10.21873/invivo.12937.

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30

De Abreu, Ronney, Lambert Lambooy, Elisabet Stet, Trude Vogels-Mentink, and Lambert Van Den Heuvel. "Thiopurine induced disturbance of DNA methylation in human malignant cells." Advances in Enzyme Regulation 35 (January 1995): 251–63. http://dx.doi.org/10.1016/0065-2571(94)00008-q.

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31

Matveeva, O. V., G. V. Kochneva, S. V. Netesov, S. B. Onikienko, and P. M. Chumakov. "Mechanisms of Oncolysis by Paramyxovirus Sendai." Acta Naturae 7, no. 2 (June 15, 2015): 6–16. http://dx.doi.org/10.32607/20758251-2015-7-2-6-16.

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Анотація:

Some viral strains of the Paramyxoviridae family may be used as anti-tumor agents. Oncolytic paramyxoviruses include attenuated strains of the measles virus, Newcastle disease virus, and Sendai virus. These viral strains, and the Sendai virus in particular, can preferentially induce the death of malignant, rather than normal, cells. The death of cancer cells results from both direct killing by the virus and through virus-induced activation of anticancer immunity. Sialic-acid-containing glycoproteins that are overexpressed in cancer cells serve as receptors for some oncolytic paramyxoviruses and ensure preferential interaction of paramyxoviruses with malignant cells. Frequent genetic defects in interferon and apoptotic response systems that are common to cancer cells ensure better susceptibility of malignant cells to viruses. The Sendai virus as a Paramyxovirus is capable of inducing the formation of syncytia, multinuclear cell structures which promote viral infection spread within a tumor without virus exposure to host neutralizing antibodies. As a result, the Sendai virus can cause mass killing of malignant cells and tumor destruction. Oncolytic paramyxoviruses can also promote the immune-mediated elimination of malignant cells. In particular, they are powerful inducers of interferon and other cytokynes promoting antitumor activity of various cell components of the immune response, such as dendritic and natural killer cells, as well as cytotoxic T lymphocytes. Taken together these mechanisms explain the impressive oncolytic activity of paramyxoviruses that hold promise as future, efficient anticancer therapeutics.

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32

Eum, Hye Hyeon, Minsuk Kwon, Daeun Ryu, Areum Jo, Woosung Chung, Nayoung Kim, Yourae Hong, et al. "Tumor-promoting macrophages prevail in malignant ascites of advanced gastric cancer." Experimental & Molecular Medicine 52, no. 12 (December 2020): 1976–88. http://dx.doi.org/10.1038/s12276-020-00538-y.

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Анотація:

AbstractGastric cancer (GC) patients develop malignant ascites as the disease progresses owing to peritoneal metastasis. GC patients with malignant ascites have a rapidly deteriorating clinical course with short survival following the onset of malignant ascites. Better optimized treatment strategies for this subset of patients are needed. To define the cellular characteristics of malignant ascites of GC, we used single-cell RNA sequencing to characterize tumor cells and tumor-associated macrophages (TAMs) from four samples of malignant ascites and one sample of cerebrospinal fluid. Reference transcriptomes for M1 and M2 macrophages were generated by in vitro differentiation of healthy blood-derived monocytes and applied to assess the inflammatory properties of TAMs. We analyzed 180 cells, including tumor cells, macrophages, and mesothelial cells. Dynamic exchange of tumor-promoting signals, including the CCL3–CCR1 or IL1B–IL1R2 interactions, suggests macrophage recruitment and anti-inflammatory tuning by tumor cells. By comparing these data with reference transcriptomes for M1-type and M2-type macrophages, we found noninflammatory characteristics in macrophages recovered from the malignant ascites of GC. Using public datasets, we demonstrated that the single-cell transcriptome-driven M2-specific signature was associated with poor prognosis in GC. Our data indicate that the anti-inflammatory characteristics of TAMs are controlled by tumor cells and present implications for treatment strategies for GC patients in which combination treatment targeting cancer cells and macrophages may have a reciprocal synergistic effect.

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33

Wang, Xiuxing, Briana C. Prager, Qiulian Wu, Leo J. Y. Kim, Ryan C. Gimple, Yu Shi, Kailin Yang, et al. "Reciprocal Signaling between Glioblastoma Stem Cells and Differentiated Tumor Cells Promotes Malignant Progression." Cell Stem Cell 22, no. 4 (April 2018): 514–28. http://dx.doi.org/10.1016/j.stem.2018.03.011.

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34

Thyrell, Lena, Sven Erickson, Boris Zhivotovsky, Katja Pokrovskaja, Olle Sangfelt, Juan Castro, Stefan Einhorn, and Dan Grandér. "Mechanisms of Interferon-alpha induced apoptosis in malignant cells." Oncogene 21, no. 8 (February 2002): 1251–62. http://dx.doi.org/10.1038/sj.onc.1205179.

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35

Fehrmann, Frauke, and Laimonis A. Laimins. "Human papillomaviruses: targeting differentiating epithelial cells for malignant transformation." Oncogene 22, no. 33 (August 2003): 5201–7. http://dx.doi.org/10.1038/sj.onc.1206554.

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36

Nadav-Dagan, Liat, Tal Shay, Nili Dezorella, Elizabeth Naparstek, Eytan Domany, Ben-Zion Katz, and Benjamin Geiger. "Adhesive Interactions Regulate Transcriptional Diversity in Malignant B Cells." Molecular Cancer Research 8, no. 4 (April 2010): 482–93. http://dx.doi.org/10.1158/1541-7786.mcr-09-0182.

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37

Khodyrev, Dmitriy A., Alexey S. Nikitin, Natalia S. Kulagina, and Alexander V. Averyanov. "Molecular genetic approaches in the diagnosis of lung cancer." Journal of Clinical Practice 6, no. 4 (November 15, 2015): 85–94. http://dx.doi.org/10.17816/clinpract83261.

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It is an acute problem for the 21st century to find effective and inexpensive methods for early detection of lung cancer. Patients, suspected of having a malignant disease of lungs, generally undergo clinical studies such as CT scans of the chest and bronchoscopy. The latter is mainly used to confirm the diagnosis. However, even when the signs, symptoms and radiological findings indicate that clinical diagnosis of malignant lung disease is evident, additional invasive procedures for obtaining the biological material suitable for the final confirmation of the presence of malignant cells are required. Currently, there is a clear understanding of the need to find biomarkers able to detect pre-clinical stage of cancer cells using minimally invasive procedures.

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Khodyrev, D. S., A. G. Nikitin, N. S. Kulagina, and A. V. Averyanov. "MOLECULAR GENETIC APPROACHES IN THE DIAGNOSIS OF LUNG CANCER." Journal of Clinical Practice 6, no. 3 (September 15, 2015): 85–94. http://dx.doi.org/10.17816/clinpract6385-94.

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Анотація:

It is an acute problem for the 21st century to find effective and inexpensive methods for early detection of lung cancer. Patients, suspected of having a malignant disease of lungs, generally undergo clinical studies such as CT scans of the chest and bronchoscopy. The latter is mainly used to confirm the diagnosis. However, even when the signs, symptoms and radiological findings indicate that clinical diagnosis of malignant lung disease is evident, additional invasive procedures for obtaining the biological material suitable for the final confirmation of the presence of malignant cells are required. Currently, there is a clear understanding of the need to find biomarkers able to detect pre-clinical stage of cancer cells using minimally invasive procedures.

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39

Medina, Vanina, Graciela Cricco, Mariel Nuñez, Gabriela Martín, Nora Mohamad, Florencia Correa-Fiz, Francisca Sanchez-Jiménez, Rosa Bergoc, and Elena S. Rivera. "Histamine-mediated signaling processes in human malignant mammary cells." Cancer Biology & Therapy 5, no. 11 (November 14, 2006): 1462–71. http://dx.doi.org/10.4161/cbt.5.11.3273.

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40

Kawasaki, Hajime, Carlos J. Carrera, and Dennis A. Carson. "Quantitative immunoassay of human deoxycytidine kinase in malignant cells." Analytical Biochemistry 207, no. 1 (November 1992): 193–96. http://dx.doi.org/10.1016/0003-2697(92)90522-9.

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Zhou, Fu-Xiang, Zheng-Kai Liao, Jing Dai, Jie Xiong, Cong-Hua Xie, Zhi-Guo Luo, Shi-Quan Liu, and Yun-Feng Zhou. "Radiosensitization effect of zidovudine on human malignant glioma cells." Biochemical and Biophysical Research Communications 354, no. 2 (March 2007): 351–56. http://dx.doi.org/10.1016/j.bbrc.2006.12.180.

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Burghardt, Isabel, Felix Tritschler, Christiane A. Opitz, Brigitte Frank, Michael Weller та Wolfgang Wick. "Pirfenidone inhibits TGF-β expression in malignant glioma cells". Biochemical and Biophysical Research Communications 354, № 2 (березень 2007): 542–47. http://dx.doi.org/10.1016/j.bbrc.2007.01.012.

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43

LIU, LIANG, ZHIXIONG LIU, HAO WANG, LONG CHEN, FUQIANG RUAN, JIHUI ZHANG, YI HU, HENGSHAN LUO, and SHUAI WEN. "Knockdown of PREX2a inhibits the malignant phenotype of glioma cells." Molecular Medicine Reports 13, no. 3 (January 19, 2016): 2301–7. http://dx.doi.org/10.3892/mmr.2016.4799.

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44

Ashfaq, R., and E. Fong. "Molecular profiling of metastatic breast cancer in body cavity fluids." Journal of Clinical Oncology 29, no. 27_suppl (September 20, 2011): 61. http://dx.doi.org/10.1200/jco.2011.29.27_suppl.61.

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61 Background: The diagnosis of malignant effusion signifies disease progression and is associated with a worse prognosis regardless of tumor origin. The cancer cells in fluids have unique genotypic and phenotypic characteristics that are uniquely different from the primary tumor. Therapeutic guidance should be based on the evaluation of tumor cells in effusions. This study reports the feasibility of molecular profiling for breast cancer metastasis in pleural and peritoneal fluids. Methods: A computer search was conducted to retrospectively identify malignant fluid samples or cell blocks for molecular profiling. A cell-block was either prepared or available for testing for all samples. An H&E slide was prepared from the cell- block and reviewed by a pathologist before any testing. Malignant cell percentages were determined for purpose of DNA microarray analysis and Sequencing. Appropriate clusters and malignant cells were marked for FISH. The results were reviewed and data compiled to calculate the yield of various molecular predictive tests. Results: We studied 172 fluid of which 28 were metastatic breast cancer (16.2%). Of the 28 breast cases, 10 IHC biomarkers could be performed in 20 (71.4 %), 1-9 in 1 (3.5 %), while 7 (25%) were insufficient. DNA microarray analysis was done in 10 (35.7%), FISH for EGFR 7 (25%), Her2 Neu FISH 11(39%), cMYC FISH 5 (17.8%) and TOPO2a by FISH 3 (10.7%). Combined IHC/FISH/MA data was available in 10, IHC and FISH data in 11 and IHC and MA data in 10 cases. Combined results of predictive markers provided information on therapeutic guidance in 21 of 28 cases. Conclusion: Molecular profiling of malignant fluids offers additional opportunities for testing those patients where other tissue samples such as needle core biopsy or resection samples are not available. Molecular profiling provides insight into the molecular characteristics of malignant cells in body cavity fluids and associated expression of unique therapeutic targets.

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45

Uziel, Orit, Gil Kanfer, Einat Beery, Dana Yelin, Daniel Shepshelovich, Mary Bakhanashvili, Jardena Nordenberg, and Meir Lahav. "The effects of erythropoietin signaling on telomerase regulation in non-erythroid malignant and non-malignant cells." Biochemical and Biophysical Research Communications 450, no. 1 (July 2014): 274–82. http://dx.doi.org/10.1016/j.bbrc.2014.05.105.

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46

Frigyesi, Ildikó, Jörgen Adolfsson, Mina Ali, Mikael Kronborg Christophersen, Ellinor Johnsson, Ingemar Turesson, Urban Gullberg, Markus Hansson, and Björn Nilsson. "Robust isolation of malignant plasma cells in multiple myeloma." Blood 123, no. 9 (February 27, 2014): 1336–40. http://dx.doi.org/10.1182/blood-2013-09-529800.

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Key Points Molecular characterization of myeloma requires isolation of malignant plasma cells, which is currently hampered by the instability of CD138. We identified CD319 and CD269 as robust replacements for CD138, facilitating molecular diagnostics in myeloma.

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47

Zhang, R., W. R. Wu, X. D. Shi, L. B. Xu, M. S. Zhu, H. Zeng, and C. Liu. "Dysregulation of Bmi1 promotes malignant transformation of hepatic progenitor cells." Oncogenesis 5, no. 2 (February 2016): e203-e203. http://dx.doi.org/10.1038/oncsis.2016.6.

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Marjanovic Vicentic, Jelena, Danijela Drakulic, Idoia Garcia, Vladanka Vukovic, Paula Aldaz, Nela Puskas, Igor Nikolic, et al. "SOX3 can promote the malignant behavior of glioblastoma cells." Cellular Oncology 42, no. 1 (September 12, 2018): 41–54. http://dx.doi.org/10.1007/s13402-018-0405-5.

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Grebenik, E. A., A. N. Generalova, A. V. Nechaev, E. V. Khaydukov, K. E. Mironova, O. A. Stremovskiy, E. N. Lebedenko, A. V. Zvyagin, and S. M. Deyev. "Specific Visualization of Tumor Cells Using Upconversion Nanophosphors." Acta Naturae 6, no. 4 (December 15, 2014): 48–53. http://dx.doi.org/10.32607/20758251-2014-6-4-48-53.

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The development of targeted constructs on the basis of photoluminescent nanoparticles with a high photo- and chemical stability and absorption/emission spectra in the transparency window of biological tissues is an important focus area of present-day medical diagnostics. In this work, a targeted two-component construct on the basis of upconversion nanophosphors (UCNPs) and anti-tumor 4D5 scFv was developed for selective labeling of tumor cells overexpressing the HER2 tumor marker characteristic of a number of human malignant tumors. A high affinity barnase : barstar (Bn : Bs) protein pair, which exhibits high stability in a wide range of pH and temperatures, was exploited as a molecular adapter providing self-assembly of the two-component construct. High selectivity for the binding of the two-component 4D5 scFv-Bn : UCNP-Bs construct to human breast adenocarcinoma SK-BR-3 cells overexpressing HER2 was demonstrated. This approach provides an opportunity to produce similar constructs for the visualization of different specific markers in pathogenic tissues, including malignant tumors.

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Whitfield, Holly J., Jean Berthelet, Stefano Mangiola, Caroline Bell, Robin L. Anderson, Bhupinder Pal, Anthony T. Papenfuss, Belinda Yeo, Delphine Merino, and Melissa J. Davis. "Abstract 6232: Defining the cellular composition and associated molecular phenotypes of malignant and non-malignant cells in breast cancer pleural effusions." Cancer Research 82, no. 12_Supplement (June 15, 2022): 6232. http://dx.doi.org/10.1158/1538-7445.am2022-6232.

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Abstract Malignant pleural effusions (MPE) are a common complication of advanced cancers, particularly those adjacent to the pleura such as lung and breast cancer and are a frequent complication in metastatic disease. The pathophysiology of MPE formation in advanced breast cancer remains poorly understood, and their composition and biology are understudied. To characterise the phenotypic diversity of malignant pleural effusion, we performed single-cell RNA sequencing on 10 MPEs from 7 metastatic breast cancer patients with diverse molecular subtypes: two triple negative (TNBC) patients, three luminal B patients including one with a rare inflammatory subtype, and two luminal A patients. For all patients, we sequenced cells from the entire MPE, without performing any enrichment or selection, in order to ascertain the cellular composition and molecular phenotypes in an unbiased manner. We identified pronounced differences in the relative proportions of malignant, mesothelial and immune cell populations: both TNBC and two Luminal B patients had extensive malignant cell populations, while the other three patients had few or no detectible malignant cells but extensive immune populations. We also observed heterogeneity in the expression of subtype-specific gene signatures and in copy number aberration patterns that captured variability across malignant cell populations both within and between patients. We observed that most malignant cells retained the molecular subtype diagnosed in the primary tumour, however sub-populations of malignant cells could be identified that mapped to different molecular subtypes, indicative of complexity in the molecular phenotypes of cancer cells disseminated to or metastasising in the pleural cavity. We distinguished mesothelial cell populations from malignant cells using key markers, expression of the PAM50 signatures, and copy number aberration patterns. We found that pleural mesothelial cells expressed a cancer associated fibroblast-like transcriptomic program that may support cancer growth within the pleural cavity through the secretion of growth factors that target malignant cells. Our dataset presents the first unbiased and unselected assessment of breast cancer associated MPEs at single cell resolution, providing the community with a vital resource for the study of MPEs. Our work highlights the molecular and cellular diversity captured in MPEs and advances the use of these clinically relevant biopsies both in monitoring disease progression and in the development of targeted therapeutics for patients with advanced breast cancer. Citation Format: Holly J. Whitfield, Jean Berthelet, Stefano Mangiola, Caroline Bell, Robin L. Anderson, Bhupinder Pal, Anthony T. Papenfuss, Belinda Yeo, Delphine Merino, Melissa J. Davis. Defining the cellular composition and associated molecular phenotypes of malignant and non-malignant cells in breast cancer pleural effusions [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 6232.

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