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Sunday, May 17, 2020 | History

2 edition of Mechanisms for establishment of taxol resistance in human breast tumour cells found in the catalog.

Mechanisms for establishment of taxol resistance in human breast tumour cells

Leigh Arseneau

Mechanisms for establishment of taxol resistance in human breast tumour cells

by Leigh Arseneau

  • 390 Want to read
  • 3 Currently reading

Published by Laurentian University in Sudbury, Ont .
Written in English


Edition Notes

StatementLeigh Arseneau.
The Physical Object
Pagination47 l. :
Number of Pages47
ID Numbers
Open LibraryOL22161055M

You can write a book review and share your experiences. Other readers will always be interested in your opinion of the books you've read. Whether you've loved the book or not, if you give your honest and detailed thoughts then people will find new books that are right for them. Full text of "Molecular Biology Of Cancer Mechanisms, Third Edition Lauren Pecorino" See other formats.

Thus, more investigations have been implemented to identify the potential SLCO1B3-related mechanisms of cancer drug resistance. In this review, we focus on the emerging roles of SLCO1B3 protein in the development of cancer chemotherapy resistance and briefly discuss the mechanisms of resistance. A new human breast cancer cell line, KPL-1 secretes tumour-associated antigens and grows rapidly in female athymic nude mice. Brit. J. Cancer , Kurebayashi J, Sonoo H, Shimozuma K. Timing of surgery in relation to the menstrual cycle and its influence on the survival of Japanese women with operable breast cancer.

  Triple-negative breast cancer (TNBC) represents an aggressive subtype with limited therapeutic options. Experimental preclinical models that recapitulate their tumors of origin can accelerate target identification, thereby potentially improving therapeutic efficacy. Patient-derived xenografts (PDXs), due to their genomic and transcriptomic fidelity to the tumors from Cited by: 4. METHODS: A comparative analysis of effects of MPs isolated from human breast cancer cells and non-malignant human brain endothelial cells were examined on THP-1 derived macrophages in vitro. MP-mediated effects on cell phenotype and functionality was assessed by cytokine analysis, cell chemotaxis and phagocytosis, immunolabelling, flow.


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Mechanisms for establishment of taxol resistance in human breast tumour cells by Leigh Arseneau Download PDF EPUB FB2

Sensitization of breast cancer cells to taxol by inhibition of taxol resistance gene 1 Article (PDF Available) in Oncology letters 3(1) June with 14 Reads How we measure 'reads'.

Taxol suppresses dynamics of individual microtubules in living human tumor cells. Mol Biol C Link, Google Scholar; Zasadil LM, Andersen KA, Yeum D, Rocque GB, Wilke LG, Tevaarwerk AJ, Raines RT, Burkard ME, Weaver BA ().

Cytotoxicity of paclitaxel in breast cancer is due to chromosome missegregation on multipolar spindles. Overcoming methotrexate resistance in breast cancer tumour cells by the use of a new cell-penetrating peptide Article in Biochemical Pharmacology 71(4).

Abnormal Akt-Related Pathways in Resistance to Cancer Therapy. Undoubtedly, the development of malignant cells with enhanced resistance to chemo- and/or radiotherapy is one of the most pressing issues for the field of oncology [62, –].The onset of cancer cell variants with increased resistance to therapy may cause the relapse of the illness, which is often Cited by: The panel consisted of human tumors of the breast, colon, and lung, in addition to the murine L leukemia and B16 melanoma syngeneic models.

22 These syngeneic models involved inoculation of tumor cells by i.p., subcutaneous (s.c.), or intravenous (i.v.) routes, whereas human tumor xenografts were grown under the renal subcapsule. 25 Cited by: Molecular Biology of the Cell Vol.

25, Interfering cellular lactate homeostasis overcomes Taxol resistance of breast cancer cells through the microRNAmediated lactate transporter (MCT1) inhibition. Neurotoxic mechanisms of paclitaxel are local to the distal axon and independent of transport defects.

A first step, which prolongs the concept of ‘virtual patients’ reviewed in Chapter 7, is the establishment not only of the detailed ‘social’ architecture of the human immune cells but also of a detailed nosotaxonomy to clarify disease maps with the view to facilitate indication discovery and a general taxonomy of cytokine networks as Author: Alain A.

Vertès. FADD was initially described as an adaptor molecule for death receptor-mediated apoptosis, but subsequently it has been implicated in nonapoptotic cellular processes such as proliferation and cell cycle control.

During the last decade, FADD has been shown to play a pivotal role in most of the signalosome complexes, such as the necroptosome and the inflammasome.

Interestingly, Author: José L Marín-Rubio, Laura Vela-Martín, José Fernández-Piqueras, María Villa-Morales. Survivin, also called baculoviral inhibitor of apoptosis repeat-containing 5 or BIRC5, is a protein that, in humans, is encoded by the BIRC5 gene. NCBI Reference Sequence: NG_ Survivin is a member of the inhibitor of apoptosis (IAP) family.

The survivin protein functions to inhibit caspase activation, thereby leading to negative regulation of apoptosis or programmed Aliases: BIRC5, API4, EPR-1, baculoviral IAP repeat.

Multidrug resistance (MDR) is a phenomenon whereby cells confer drug resistance to structurally and functionally unrelated compounds. P-glycoprotein (P-gp; MDR1 or ABCB1), a member of the ATP-binding cassette transporter superfamily, has been particularly recognized for its contribution to MDR in the field of cancer ed expression of P-gp has been documented Author: Adrian P.

Turner, Camille Alam, Reina Bendayan. The lack of response to pharmacological treatment constitutes a substantial limitation in the handling of patients with primary liver cancers (PLCs).

The existence of active mechanisms of chemoresistance (MOCs) in hepatocellular carcinoma, cholangiocarcinoma, and hepatoblastoma hampers the usefulness of chemotherapy.

A better understanding of MOCs is needed to Author: Jose J. Marin, Elisa Herraez, Elisa Lozano, Rocio I. Macias, Oscar Briz. Trastuzumab, sold under the brand name Herceptin among others, is a monoclonal antibody used to treat breast cancer and stomach cancer.

It is specifically used for cancer that is HER2 receptor positive. It may be used by itself or together with other chemotherapy medication. Trastuzumab is given by slow injection into a vein and injection just under the ncy category: AU: D, US: N (Not classified yet).

Cancer stem cells are tumour-initiating, chemo-resistant cells that show great promise as a potential target cell though which novel cancer treatments can be developed. However, in recent years it has been shown that most malignancies are composed of multiple independent or inter-related hierarchies of stem and progenitor cells, which.

Cancer cell lines have been widely used for research purposes and proved to be a useful tool in the genetic approach, and its characterization shows that they are, in fact, an excellent model for the study of the biological mechanisms involved in cancer [].Examples areshown in table use of cancer cell lines allowed an increment of the information about the deregulated genes Cited by: Cancer: New Insights for the Healthcare Professional: Edition is a ScholarlyEditions™ eBook that delivers timely, authoritative, and comprehensive information about Cancer.

The editors have built Cancer: New Insights for the Healthcare Professional: Edition on the vast information databases of ScholarlyNews.™ You can expect the information about Cancer in Reviews: 1.

Yu D, Liu B, Tan Met pression of c-erbB-2/neu in breast cancer cells confers increased resistance to Taxol via mdr- I-independent mechanisms. Oncogene, –, Oncogene, –, Cited by: Furthermore, in human lung cancer cells induced p53 expression enhanced the cytotoxic effect of cisplatin whereas p21 waf1 overexpression surprisingly lead to increased drug resistance.

Similarly, cisplatin-resistant human non-small cell lung cancer (NSCLC) cells could be sensitized to drug-induced senescence by re-expressing p16 Ink4a [ ].Cited by: 2. Title:ABC Transporters: Regulation and Association with Multidrug Resistance in Hepatocellular Carcinoma and Colorectal Carcinoma VOLUME: 26 ISSUE: 7 Author(s):María Paula Ceballos, Juan Pablo Rigalli, Lucila Inés Ceré, Mariana Semeniuk, Viviana Alicia Catania and María Laura Ruiz* Affiliation:Institute of Experimental Physiology, Faculty of Biochemical and Cited by: 8.

Over the last 40 years, advances in the development of breast cancer drugs have led to improved treatments and outcomes for patients [1, 2].However, mortality, which is generally attributed to metastatic disease and resistance to chemotherapy, has remained relatively unchanged over the same period [3, 4].In addition, many cancer drugs have significant toxicity, Cited by:   The effect of PUFAs on tumour cell motility and motogen-stimulated motility has been recently reported.

Figure 9A. Effects of GLA on the expression of maspin and motility of cancer cells. Human colon cancer cells were treated with different fatty acids (left), GLA at different concentrations (middle), or with GLA for different time periods/5.

van Ark-Otte J, Samelis G, Rubio G, Lopez Saez JB, Pinedo HM, Giaccone G () Effects of tubulin-inhibiting agents in human lung and breast cancer cell lines with different multidrug resistance by: dividing cancer cells over normal cells.

Interestingly, mechanistic studies on the very first generation of anticancer drugs discovered in the 20th century revealed them to do just that. It is no surprise then that most of the first half of the book is devoted to anticancer drugs targeting DNA or related processes either as anti.In addition, the field of oncology is currently addressing the function of rare subpopulation of cancer cells with stem cell-like properties, or cancer stem cells, in the process of carcinogenesis, spreading of metastasis, regeneration of the tumor mass, and development of malignant cells with enhanced resistance to chemo and/or radiotherapy Cited by: