Bibliographies thématiques / Normal-tissues toxicity

Littérature scientifique sur le sujet « Normal-tissues toxicity »

Auteur : Grafiati
Publié le 10 mars 2023

Créez une référence correcte selon les styles APA, MLA, Chicago, Harvard et plusieurs autres

Choisissez une source :

Sommaire

Consultez les listes thématiques d’articles de revues, de livres, de thèses, de rapports de conférences et d’autres sources académiques sur le sujet « Normal-tissues toxicity ».

À côté de chaque source dans la liste de références il y a un bouton « Ajouter à la bibliographie ». Cliquez sur ce bouton, et nous générerons automatiquement la référence bibliographique pour la source choisie selon votre style de citation préféré : APA, MLA, Harvard, Vancouver, Chicago, etc.

Vous pouvez aussi télécharger le texte intégral de la publication scolaire au format pdf et consulter son résumé en ligne lorsque ces informations sont inclues dans les métadonnées.

Articles de revues sur le sujet "Normal-tissues toxicity"

1

Mortezaee, Keywan, Masoud Najafi, Bagher Farhood, Amirhossein Ahmadi, Dheyauldeen Shabeeb et Ahmed E. Musa. « NF‐κB targeting for overcoming tumor resistance and normal tissues toxicity ». Journal of Cellular Physiology 234, no 10 (25 mars 2019) : 17187–204. http://dx.doi.org/10.1002/jcp.28504.

Texte intégral
Styles APA, Harvard, Vancouver, ISO, etc.
2

Mortezaee, Keywan, Masoud Najafi, Bagher Farhood, Amirhossein Ahmadi, Dheyauldeen Shabeeb et Ahmed E. Musa. « Resveratrol as an Adjuvant for Normal Tissues Protection and Tumor Sensitization ». Current Cancer Drug Targets 20, no 2 (11 février 2020) : 130–45. http://dx.doi.org/10.2174/1568009619666191019143539.

Texte intégral
Résumé :
Cancer is one of the most complicated diseases in present-day medical science. Yearly, several studies suggest various strategies for preventing carcinogenesis. Furthermore, experiments for the treatment of cancer with low side effects are ongoing. Chemotherapy, targeted therapy, radiotherapy and immunotherapy are the most common non-invasive strategies for cancer treatment. One of the most challenging issues encountered with these modalities is low effectiveness, as well as normal tissue toxicity for chemo-radiation therapy. The use of some agents as adjuvants has been suggested to improve tumor responses and also alleviate normal tissue toxicity. Resveratrol, a natural flavonoid, has attracted a lot of attention for the management of both tumor and normal tissue responses to various modalities of cancer therapy. As an antioxidant and anti-inflammatory agent, in vitro and in vivo studies show that it is able to mitigate chemo-radiation toxicity in normal tissues. However, clinical studies to confirm the usage of resveratrol as a chemo-radioprotector are lacking. In addition, it can sensitize various types of cancer cells to both chemotherapy drugs and radiation. In recent years, some clinical studies suggested that resveratrol may have an effect on inducing cancer cell killing. Yet, clinical translation of resveratrol has not yielded desirable results for the combination of resveratrol with radiotherapy, targeted therapy or immunotherapy. In this paper, we review the potential role of resveratrol for preserving normal tissues and sensitization of cancer cells in combination with different cancer treatment modalities.
Styles APA, Harvard, Vancouver, ISO, etc.
3

Najafi, Masoud, Elahe Motevaseli, Alireza Shirazi, Ghazale Geraily, Abolhasan Rezaeyan, Farzad Norouzi, Saeed Rezapoor et Hamid Abdollahi. « Mechanisms of inflammatory responses to radiation and normal tissues toxicity : clinical implications ». International Journal of Radiation Biology 94, no 4 (7 mars 2018) : 335–56. http://dx.doi.org/10.1080/09553002.2018.1440092.

Texte intégral
Styles APA, Harvard, Vancouver, ISO, etc.
4

Picut, Catherine A., et George A. Parker. « Postnatal Organ Development as a Complicating Factor in Juvenile Toxicity Studies in Rats ». Toxicologic Pathology 45, no 1 (17 octobre 2016) : 248–52. http://dx.doi.org/10.1177/0192623316671609.

Texte intégral
Résumé :
Toxicologic pathologists must evaluate tissues of immature animals from a number of types of nonclinical toxicity studies. The pathologist who is familiar with normal postnatal organ development is in a better position to appropriately detect and differentiate between abnormal, delayed, or precocious development. Vacuolation and apoptosis in multiple tissue types are normal components of development that could influence the interpretation of some tissues. Unique postnatal features such as the germal matrix in the brain, gonocytes in the testes, and saccules in the lung may complicate the histopathological evaluation. With the knowledge of normal organ development and critical windows therein, it is possible to design targeted studies to identify xenobiotic toxicity.
Styles APA, Harvard, Vancouver, ISO, etc.
5

Lee, F. Y., et P. Workman. « Misonidazole protects mouse tumour and normal tissues from the toxicity of oral CCNU ». British Journal of Cancer 51, no 1 (janvier 1985) : 85–91. http://dx.doi.org/10.1038/bjc.1985.12.

Texte intégral
Styles APA, Harvard, Vancouver, ISO, etc.
6

Linard, Christine, et Maâmar Souidi. « PPARs in Irradiation-Induced Gastrointestinal Toxicity ». PPAR Research 2010 (2010) : 1–12. http://dx.doi.org/10.1155/2010/528327.

Texte intégral
Résumé :
The use of radiation therapy to treat cancer inevitably involves exposure of normal tissues. Although the benefits of this treatment are well established, many patients experience distressing complications due to injury to normal tissue. These side effects are related to inflammatory processes, and they decrease therapeutic benefit by increasing the overall treatment time. Emerging evidence indicates that PPARs and their ligands are important in the modulation of immune and inflammatory reactions. This paper discusses the effects of abdominal irradiation on PPARs, their role and functions in irradiation toxicity, and the possibility of using their ligands for radioprotection.
Styles APA, Harvard, Vancouver, ISO, etc.
7

&NA;. « Amifostine protects a broad range of normal tissues from chemotherapy- and radiotherapy-associated toxicity ». Drugs & ; Therapy Perspectives 17, no 21 (octobre 2001) : 1–5. http://dx.doi.org/10.2165/00042310-200117210-00001.

Texte intégral
Styles APA, Harvard, Vancouver, ISO, etc.
8

Taylor, C. W., L. M. Wang, A. F. List, D. Fernandes, G. D. Paine-Murrieta, C. S. Johnson et R. L. Capizzi. « Amifostine protects normal tissues from paclitaxel toxicity while cytotoxicity against tumour cells is maintained ». European Journal of Cancer 33, no 10 (septembre 1997) : 1693–98. http://dx.doi.org/10.1016/s0959-8049(97)00221-9.

Texte intégral
Styles APA, Harvard, Vancouver, ISO, etc.
9

Chen, Nan, Yuping Han, Yao Luo, Yanfeng Zhou, Xingjie Hu, Yun Yu, Xiaodong Xie et al. « Nanodiamond-based non-canonical autophagy inhibitor synergistically induces cell death in oxygen-deprived tumors ». Materials Horizons 5, no 6 (2018) : 1204–10. http://dx.doi.org/10.1039/c8mh00993g.

Texte intégral
Styles APA, Harvard, Vancouver, ISO, etc.
10

Ke, Yong, Keqiang Ye, Hans E. Grossniklaus, David R. Archer, Harish C. Joshi et Judith A. Kapp. « Noscapine inhibits tumor growth with little toxicity to normal tissues or inhibition of immune responses ». Cancer Immunology, Immunotherapy 49, no 4-5 (19 juin 2000) : 217–25. http://dx.doi.org/10.1007/s002620000109.

Texte intégral
Styles APA, Harvard, Vancouver, ISO, etc.
Plus de sources

Thèses sur le sujet "Normal-tissues toxicity"

1

MANGONI, MONICA. « PHARMACOLOGICAL MODULATION OF NORMAL TISSUES RESPONSETO RADIATION-INDUCED DAMAGES ». Doctoral thesis, 2009. http://hdl.handle.net/2158/599071.

Texte intégral
Styles APA, Harvard, Vancouver, ISO, etc.
2

Ingram, N., L. E. McVeigh, R. H. Abou-Saleh, J. Maynard, S. A. Peyman, J. R. McLaughlan, M. Fairclough et al. « Ultrasound-triggered therapeutic microbubbles enhance the efficacy of cytotoxic drugs by increasing circulation and tumour drug accumulation and limiting bioavailability and toxicity in normal tissues ». 2020. http://hdl.handle.net/10454/17999.

Texte intégral
Résumé :
Yes
Most cancer patients receive chemotherapy at some stage of their treatment which makes improving the efficacy of cytotoxic drugs an ongoing and important goal. Despite large numbers of potent anti-cancer agents being developed, a major obstacle to clinical translation remains the inability to deliver therapeutic doses to a tumor without causing intolerable side effects. To address this problem, there has been intense interest in nanoformulations and targeted delivery to improve cancer outcomes. The aim of this work was to demonstrate how vascular endothelial growth factor receptor 2 (VEGFR2)-targeted, ultrasound-triggered delivery with therapeutic microbubbles (thMBs) could improve the therapeutic range of cytotoxic drugs. Methods: Using a microfluidic microbubble production platform, we generated thMBs comprising VEGFR2-targeted microbubbles with attached liposomal payloads for localised ultrasound-triggered delivery of irinotecan and SN38 in mouse models of colorectal cancer. Intravenous injection into tumor-bearing mice was used to examine targeting efficiency and tumor pharmacodynamics. High-frequency ultrasound and bioluminescent imaging were used to visualise microbubbles in real-time. Tandem mass spectrometry (LC-MS/MS) was used to quantitate intratumoral drug delivery and tissue biodistribution. Finally, 89Zr PET radiotracing was used to compare biodistribution and tumor accumulation of ultrasound-triggered SN38 thMBs with VEGFR2 targeted SN38 liposomes alone. Results: ThMBs specifically bound VEGFR2 in vitro and significantly improved tumor responses to low dose irinotecan and SN38 in human colorectal cancer xenografts. An ultrasound trigger was essential to achieve the selective effects of thMBs as without it, thMBs failed to extend intratumoral drug delivery or demonstrate enhanced tumor responses. Sensitive LC-MS/MS quantification of drugs and their metabolites demonstrated that thMBs extended drug exposure in tumors but limited exposure in healthy tissues, not exposed to ultrasound, by persistent encapsulation of drug prior to elimination. 89Zr PET radiotracing showed that the percentage injected dose in tumors achieved with thMBs was twice that of VEGFR2-targeted SN38 liposomes alone. Conclusions: thMBs provide a generic platform for the targeted, ultrasound-triggered delivery of cytotoxic drugs by enhancing tumor responses to low dose drug delivery via combined effects on circulation, tumor drug accumulation and exposure and altered metabolism in normal tissues.
EPSRC funding (EP/I000623/1, EP/K023845/1 and EP/P023266/1) and the MRC for a Confidence in Concept award and MR/L01629X. L.E. McVeigh was funded by an EPSRC PhD Studentship (EP/L504993/1).
Styles APA, Harvard, Vancouver, ISO, etc.

Chapitres de livres sur le sujet "Normal-tissues toxicity"

1

« High dose therapy (autologus transplant) ». Dans Oxford Handbook of Cancer Nursing, sous la direction de Mike Tadman et Dave Roberts, 261–68. Oxford University Press, 2007. http://dx.doi.org/10.1093/med/9780198569244.003.0020.

Texte intégral
Résumé :
Principles and uses 262 Conditioning 264 Nursing issues of high dose therapy 266 Many haematological cancers are treated more effectively by higher doses of chemotherapy and radiotherapy than by lower doses. Continuing to escalate the dose given will theoretically increase the cure rate. However, the dose-limiting factor is the toxicity to normal tissues. The first tissue to be seriously affected is the bone marrow. Bone marrow suppression results in:...
Styles APA, Harvard, Vancouver, ISO, etc.
2

Balzano, Tiziano, et Omar El Hiba. « Metal Toxicity and Brain-Liver Axis ». Dans Advances in Environmental Engineering and Green Technologies, 216–35. IGI Global, 2019. http://dx.doi.org/10.4018/978-1-5225-7775-1.ch011.

Texte intégral
Résumé :
The liver is the main detoxifier organ of the body. When normal liver function is compromised, other systems in the body can be affected, including the brain. Hepatocerebral disorder is the term used to describe some neuropsychiatric conditions that result from liver failure and characterized by the accumulation of these toxic metals in brain. Examples of such disorders are Wilson's disease (WD), an autosomal recessive disorder that is characterized by the deposition of copper in liver and brain tissues and acquired (non-Wilsonian) hepatocerebral degeneration (AHCD), a complication that occurs most frequently in patients with hepatic coma or that suffered multiple episodes of severe HE. AHCD is characterized by accumulation in brain of manganese. This chapter will focus on the crucial importance of relationship between liver and brain functioning and on the effects produced when this relationship is compromised. Specifically, the chapter will discuss on the physiopathology of WD and AHCD and on the role that toxic metals play on neurological symptoms in such disorders.
Styles APA, Harvard, Vancouver, ISO, etc.
3

Sweeney, Connor, Lynn Quek, Betty Gration et Paresh Vyas. « Cancer stem cells ». Dans Oxford Textbook of Cancer Biology, sous la direction de Francesco Pezzella, Mahvash Tavassoli et David J. Kerr, 283–300. Oxford University Press, 2019. http://dx.doi.org/10.1093/med/9780198779452.003.0020.

Texte intégral
Résumé :
The concept of cancer stem cells (CSCs) emerged from our understanding of the way in which normal tissues are generated from multipotent stem cells. Regenerative tissues exhibit a cellular hierarchy of differentiation, which is maintained by stem cells. Evidence from experimental models has indicated that a similar hierarchy is seen in at least some cancers, where CSCs give rise to disordered and dysfunctional tissues, leading to disease. The CSC model proposes that tumours can be divided into at least two distinct populations. The stem cells are a specialized population of cancer cells with the unique property of long-term self-renewal that maintain the growth of the cancerous clone. These stem cells give rise to the second population of cells, which form the bulk of the tumour, and lack indefinite self-renewal. Recently, our understanding of CSCs has been refined through combining genetic, epigenetic, and functional models of tumorigenesis. Malignant transformation occurs as the result of sequential acquisition of genetic mutations. Capacity for self-renewal is essential for a clone to survive and progress to become cancerous. If an oncogenic mutation occurs in a cell that is incapable of self-renewal, the clone will become exhausted through differentiation. CSCs may survive anticancer chemotherapy and increasing evidence indicates their role in mediating treatment resistance and relapse. Therefore, strategies to eradicate cancers must effectively target the stem cells that maintain their growth. CSC-directed therapeutic strategies are currently being explored in experimental studies and clinical trials but reducing toxicity to normal tissue stem cells represents a significant challenge.
Styles APA, Harvard, Vancouver, ISO, etc.
4

Janapati, Yasodha Krishna, Sunil Junapudi et Sudharshan Reddy Dachani. « Overview of Nano-Strategies for Combating Cancer ». Dans Handbook of Research on Nano-Strategies for Combatting Antimicrobial Resistance and Cancer, 250–70. IGI Global, 2021. http://dx.doi.org/10.4018/978-1-7998-5049-6.ch012.

Texte intégral
Résumé :
Cancer is one of the prime rationales for mortality in humanity and remains a difficult disease to treat. Contemporary problems allied with conventional cancer chemotherapies embrace the insolubility of drugs in an aqueous medium, delivery of sub-therapeutic doses to target cells, lack of bioavailability, and most importantly, non-specific toxicity to normal tissues. Recent advances in nanotechnology investigation tackle potential solutions to these riddles. However, there are challenges regarding targeting specific sites, tracking the delivery system and control over the release of the drug to the target site. The nanodevices are 100 to 1000 times smaller than cells in humans; their size is comparable to the enzymes, the receptors. This enables them to have a large surface area and ability to interact with biomolecules on both the surface and inside cells. Nanomedicines between 8-100 nm have an enhanced permeability and retention (EPR) effect, which make these medicines to target passively the solid tumours.
Styles APA, Harvard, Vancouver, ISO, etc.
5

Saltzman, W. Mark. « Objecives of Tissue Engineering ». Dans Tissue Engineering. Oxford University Press, 2004. http://dx.doi.org/10.1093/oso/9780195141306.003.0006.

Texte intégral
Résumé :
Tissue exchange is an ancient art, but tissue engineering is a new concept. The new thinking about tissue engineering is supported by technologies that were developed during the twentieth century, including advanced cell culture, gene transfer, and materials synthesis. Tissue engineering arose from a diverse group of historical precedents that included pharmacology, surgery, and materials science; each historical line of inquiry engaged different motivations and diverse tools. Therefore, as a substitute for a single definition, this chapter observes tissue engineering from several different angles and attempts to illustrate the field by practical example. The field of tissue engineering can be subdivided in various ways; usually it is organized by organ system, as in hepatic tissue engineering or bone tissue engineering, which are concerned with engineering replacements for liver and bone function, respectively. A coarse subdivision can also be made according to the general objective; most tissue engineering strategies involve replacement of a tissue’s metabolic function, structural function, or both. Here, several overlapping views of tissue engineering are presented: tissue engineering as a logical extension of contemporary medical and surgical therapies; tissue engineering as a method for controlling the normal healing response of tissues; tissue engineering as an effort to repopulate the cellular component of tissues without replacement of the whole organ; tissue engineering as a variety of controlled drug delivery; and tissue engineering as a new method for developing models of human physiology. Metabolism is a coordinated ensemble of chemical transformations that are individually regulated by the action of enzymes. Many metabolic disorders are caused by the defective production of a single enzyme. It is sometimes possible to identify, produce, and use enzymes to reconstitute missing elements of metabolism. For example, the enzyme adenosine deaminase (ADA) is involved in the degradation of purine nucleosides; individuals who lack the gene for ADA cannot produce the enzyme in their bodies. As a result, high concentrations of certain purine nucleoside metabolites accumulate within cells; toxicity due to these metabolites is particularly harmful to B and T lymphocytes.
Styles APA, Harvard, Vancouver, ISO, etc.
6

Springs, Clark L. « Corneal Complications ». Dans Complications of Glaucoma Surgery. Oxford University Press, 2013. http://dx.doi.org/10.1093/oso/9780195382365.003.0042.

Texte intégral
Résumé :
The desired effects of antifibrotic agents 5-fluorouracil (5-FU) and mitomycin-C (MMC) in glaucoma filtration surgery result from their ability to limit postoperative scarring by inhibiting vascular proliferation and fibroblastic transformation. However, these same mechanisms of action can have deleterious effects on surrounding normal tissues such as the cornea. Knowing how to use these agents is important in preventing antifibrotic-related complications. 5-FU is an inhibitor of DNA synthesis, specifically thymidylate synthetase, and blocks thymidine from being incorporated into DNA. In addition to affecting DNA synthesis, 5-FU also may be incorporated into RNA, interfering with RNA synthesis and therefore protein synthesis. Thus, it is more toxic to actively proliferating cells. In glaucoma filtration surgery, 5-FU is generally administered intraoperatively (50 mg/mL for 5 minutes). 5-FU can also be administered as a subconjunctival injection postoperatively with a dosage of 5.0–7.5 mg in 0.1–0.15 mL solution directly from the 50 mg/mL bottle. A series of injections may be given over several weeks and titrated based on clinical response. In addition to glaucoma filtration surgery, 5-FU has also been used for other ophthalmic applications such as pterygium surgery, lacrimal surgery, and during vitrectomy to prevent proliferative vitreoretinopathy. MMC is an alkylating agent that crosslinks DNA. It requires enzymatic activation via cytochrome p450 prior to exerting its inhibitory effects on DNA synthesis. MMC activity is independent of cell cycle and affects both actively replicating and nonreplicating cells. However, variations in enzymatic activity among individuals may contribute to the differences in efficacy, as well as toxicity of MMC. In glaucoma filtration surgery, MMC is typically administered as a single intraoperative application. It is applied after dissection of the conjunctival flap and prior to the formation of the scleral flap. Most surgeons use a dose of 0.1–0.5 mg/mL with an exposure time of 1–5 minutes depending upon the clinical indication. MMC use has also been well established for refractive surgery to prevent corneal haze after photorefractive keratectomy in patients at high risk of developing corneal haze, pterygium surgery, and corneal intraepithelial neoplasia. For more information on 5-FU and MMC in glaucoma surgery, see Chapter 3.
Styles APA, Harvard, Vancouver, ISO, etc.

Actes de conférences sur le sujet "Normal-tissues toxicity"

1

Ambati, Srikanth R., Shieh JaeHung, Benet Pera, Elissa W. P. Wong, Eloisi Caldas Lopes, Elizabeth Peguero, Tsann-Long Su et Malcolm A. S. Moore. « Abstract 1625 : Ureidomustine, a novel DNA-crosslinking agent shows activity in sarcoma preclinical models and lacks toxicity in normal tissues ». Dans Proceedings : AACR 106th Annual Meeting 2015 ; April 18-22, 2015 ; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-1625.

Texte intégral
Styles APA, Harvard, Vancouver, ISO, etc.
2

Cogdill, Alexandria P., Alina Boesteanu, Kathleen Haines, Joseph Fraietta, John Scholler, Andreas Loew, Pramod Thekkat et al. « Abstract B05 : A biologic screen to evaluate potential toxicity of chimeric antigen receptor modified T cells against primary normal human tissues ». Dans Abstracts : AACR Special Conference : Tumor Immunology and Immunotherapy : A New Chapter ; December 1-4, 2014 ; Orlando, FL. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/2326-6074.tumimm14-b05.

Texte intégral
Styles APA, Harvard, Vancouver, ISO, etc.
3

Schoor, Oliver, Jens Fritsche, Sarah Kutscher, Andrea Mahr, Lea Stevermann, Annika Sonntag, Franziska Hoffgaard et al. « Abstract 2291 : On- and off target toxicity profiling for adoptive cell therapy by mass spectrometry-based immunopeptidome analysis of primary human normal tissues ». Dans Proceedings : AACR 107th Annual Meeting 2016 ; April 16-20, 2016 ; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-2291.

Texte intégral
Styles APA, Harvard, Vancouver, ISO, etc.
4

Benammar, Sarra, Fatima Mraiche, Jensa Mariam Joseph et Katerina Gorachinova. « Glucose and Transferrin Liganded PLGA Nanoparticles Internalization in Non-Small Lung Cancer Cells ». Dans Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2020. http://dx.doi.org/10.29117/quarfe.2020.0227.

Texte intégral
Résumé :
Introduction: Recently, after a decade of confusing results, several studies pointed out that overexpression of GLUT1 (glucose transporter 1) is a biomarker of worse prognosis in NSCLC. Nonetheless, the presence of transferrin (Tf receptor), which is overexpressed in most cancer tissues and most lung cancers as well, in NSCLC is also an indicator of very poor prognosis. Therefore, these ligands can be used for active targeting of lung cancer cells and improved efficacy of internalization of cancer therapy using nanomedicines. Objectives: Having the background, the main goal of the project was the assessment of the influence of the glucose and transferrin ligands on the efficacy of internalization of the designed (i) glucose decorated PLGA (poly lactic-coglycolic acid) nanoparticles (Glu-PLGA NPs) and (ii) transferrin decorated PLGA nanoparticles (Tf-PLGA NPs) in comparison to (iii) non-liganded PLGA NPs using a A549 lung cancer cells. Methods: Glu-PLGA NPs, Tf-PLGA NPs and PLGA NP - fluorescently labelled), were designed using a sonication assisted nanoprecipitation method. Further, physicochemical properties characterization (particle size analysis, zeta potential, FTIR analysis, DSC analysis), cytotoxicity evaluation using MTT test, and cell internalization studies of DTAF labelled NPs using fluorimetry in A549 NSCLC cell line were performed. Results: The results pointed to a significantly improved internalization rate of the liganded compared to PLGA NPs. Glu-PLGA NPs showed higher internalization rate compared to Tf-PLGA and PLGA NPs, in the serum-supplemented and serumfree medium even at normal levels of glucose in the cell growth medium. Conclusion: The developed nanocarriers offer unique advantages of enhanced targetability, improved cell internalization and decreased toxicity, which makes them promising solution for current therapeutic limitations.
Styles APA, Harvard, Vancouver, ISO, etc.

Rapports d'organisations sur le sujet "Normal-tissues toxicity"

1

Morrow, Charles S. Turning Chemopreventive Agents Against Breast Cancer : Sensitizing Cancers to Therapeutics While Protecting Normal Tissues from Toxicity. Fort Belvoir, VA : Defense Technical Information Center, juillet 2012. http://dx.doi.org/10.21236/ada589289.

Texte intégral
Styles APA, Harvard, Vancouver, ISO, etc.
Vous pouvez également être intéressé par les bibliographies sur le sujet « Normal-tissues toxicity » pour d’autres types de sources :
Articles de revues
Nous offrons des réductions sur tous les plans premium pour les auteurs dont les œuvres sont incluses dans des sélections littéraires thématiques. Contactez-nous pour obtenir un code promo unique!

Vers la bibliographie