Drug Resistance: The Clinical Perspective

Da, Anthoney; Sb, Kaye

doi:10.1385/1-59259-687-8:1

Cited by 4 publications

(2 citation statements)

References 38 publications

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“…These lesions upon formation are able to be recognized by DNA proteins that trigger DNA damage repair and/or apoptosis signaling and the platinum caused cell death is mediated by cell cycle arrest that occurs in the G2 phase of the mitotic cycle [47]. DNA repair includes the nucleotide excision repair pathway (NER) [48,49], the DNA mismatch repair mechanism (MMR) [50,51], and the homologous recombination repair pathway [52]. Other chemotherapeutic agents include cyclophosphamide, doxorubicin, melphalan, busulphan etc, that act in various ways in achieving their effect on the target cells [53][54][55].…”

Section: Chemotherapy and Radiotherapy Direct Effectmentioning

confidence: 99%

Molecular aspects and clinical methods for preserving ovarian reserves in women receiving cancer treatment

N¹,

Sp²,

Koutroumpa³

et al. 2015

Clin. Exp. Obstet. Gynecol.

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Cancer prevalence is high, and of importance to cancer sufferers is the long term survival and normal activities resumption. Moreover, pregnancy is drawing interest for preserving ovarian reserves in post-chemotherapy affected women, especially of younger ages. The gonadotoxic effect of cancer treatment, involves mechanisms that are not fully understood, mainly due to the variety of molecular pathways triggered once therapeutic agents applied. Reported rates of premature ovarian failure after the treatment effect and the application of various treatment protocols, differ extensively due to the protocol itself but also due to the age of treated patients. Several options for preserving ovarian reserves are currently employed in the clinique, such as ovarian transposition, embryos cryopreservation and the use of gonadotropin-releasing hormone (GnRH) and its agonists/antagonists, but most of them are still under investigation. This paper reviews these methods and the molecular mechanisms that are possibly involved in the action of agents such as GnRH.

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Section: Chemotherapy and Radiotherapy Direct Effectmentioning

confidence: 99%

Molecular aspects and clinical methods for preserving ovarian reserves in women receiving cancer treatment

N¹,

Sp²,

Koutroumpa³

et al. 2015

Clin. Exp. Obstet. Gynecol.

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“…MMR deficient human cancer cell lines tolerate cytotoxic drugs, suggesting that loss of MMR could cause platinum resistance [51]. Most MMR-deficient cancers have mutations in MLH1 or MSH2.…”

Section: Dna Mismatch Repairmentioning

confidence: 99%

Molecular Mechanisms of Platinum Resistance in Ovarian Cancer

Tapia¹,

Díaz-Padilla²

2013

Ovarian Cancer - A Clinical and Translational Update

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regards to biological pathways implicated in the development of platinum resistance, focusing on ovarian cancer therapeutics. 2. Cisplatin: Mechanism of action Once introduced actively into the cell mediated by a copper transporter (CTR1), the molecule is activated through a series of aquation reactions, in which one of the chloride ligands is slowly displaced by water. Aquated cisplatin avidly binds DNA, with a predilection for nucleophilic N7-sites on purine bases [10]. The first step of the reaction involves the formation of monoadducts. These monoadducts may then react further to form intra-strand and inter-strand crosslinks. The cytotoxic activity of platinum compounds has been related to binding with DNA and the production of intra-strand and inter-strand crosslinks, as well as the formation of adducts that cause conformational DNA changes, impeding the separation of both DNA strands, which subsequently impairs replication and inhibits DNA synthesis [11]. Intra-strand cross-links are the most abundant products of the interaction with DNA (around 70% of all platinum-DNA linking products). These lesions cause significant distortions in the DNA that can be recognized by one or more DNA binding proteins. These proteins can either initiate DNA damage repair or signal for apoptosis. Platinum-mediated programmed cell death is caused by cell cycle arrest in the G2-phase, although the pathways from platinum-DNA binding to apoptosis are not completely understood [12].

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Models for Drug Development and Drug Resistance

Chou

Chang

2005

The Cancer Handbook

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Drug Resistance: The Clinical Perspective

Cited by 4 publications

References 38 publications

Molecular aspects and clinical methods for preserving ovarian reserves in women receiving cancer treatment

Molecular aspects and clinical methods for preserving ovarian reserves in women receiving cancer treatment

Molecular Mechanisms of Platinum Resistance in Ovarian Cancer

Models for Drug Development and Drug Resistance

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