Capecitabine use in geriatric oncology: An analysis of current safety, efficacy, and quality of life data

Ershler, William B.

doi:10.1016/j.critrevonc.2005.08.006

Cited by 17 publications

(7 citation statements)

References 49 publications

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“…The fluoropyrimidine 5-fluorouracil (5-FU) is widely used in cancer treatment including colorectal and breast cancer treatments [53, 54], but resistance to that drug remains a major clinical obstacle; 5- is part of its antitumor activity and FU targets the tumor suppressor p53 and subsequently triggers the cell cycle. 5-FU-induced apoptosis is p53-dependent; however, apoptosis can also occur in p53 mutant cell lines by a mechanism still unknown [55–57].…”

Section: Apoptosis Defect and Cancermentioning

confidence: 99%

Apoptosis and Molecular Targeting Therapy in Cancer

Hassan

Watari

Abu-Almaaty

et al. 2014

BioMed Research International

943

720

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Apoptosis is the programmed cell death which maintains the healthy survival/death balance in metazoan cells. Defect in apoptosis can cause cancer or autoimmunity, while enhanced apoptosis may cause degenerative diseases. The apoptotic signals contribute into safeguarding the genomic integrity while defective apoptosis may promote carcinogenesis. The apoptotic signals are complicated and they are regulated at several levels. The signals of carcinogenesis modulate the central control points of the apoptotic pathways, including inhibitor of apoptosis (IAP) proteins and FLICE-inhibitory protein (c-FLIP). The tumor cells may use some of several molecular mechanisms to suppress apoptosis and acquire resistance to apoptotic agents, for example, by the expression of antiapoptotic proteins such as Bcl-2 or by the downregulation or mutation of proapoptotic proteins such as BAX. In this review, we provide the main regulatory molecules that govern the main basic mechanisms, extrinsic and intrinsic, of apoptosis in normal cells. We discuss how carcinogenesis could be developed via defective apoptotic pathways or their convergence. We listed some molecules which could be targeted to stimulate apoptosis in different cancers. Together, we briefly discuss the development of some promising cancer treatment strategies which target apoptotic inhibitors including Bcl-2 family proteins, IAPs, and c-FLIP for apoptosis induction.

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Section: Apoptosis Defect and Cancermentioning

confidence: 99%

Apoptosis and Molecular Targeting Therapy in Cancer

Hassan

Watari

Abu-Almaaty

et al. 2014

BioMed Research International

943

720

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show abstract

“…The fluoropyrimidine 5-fluorouracil (5-FU) is widely used in the treatment of a range of cancers including colorectal cancer and breast tumors [1], [2], but resistance to the drug remains a major clinical problem. The antimetabolite 5-FU is an analogue of uracil with a fluorine atom at the C5 position of the pyrimidine ring.…”

Section: Introductionmentioning

confidence: 99%

The Chemotherapeutic Drug 5-Fluorouracil Promotes PKR-Mediated Apoptosis in a p53- Independent Manner in Colon and Breast Cancer Cells

et al. 2011

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The chemotherapeutic drug 5-FU is widely used in the treatment of a range of cancers, but resistance to the drug remains a major clinical problem. Since defects in the mediators of apoptosis may account for chemo-resistance, the identification of new targets involved in 5-FU-induced apoptosis is of main clinical interest. We have identified the ds-RNA-dependent protein kinase (PKR) as a key molecular target of 5-FU involved in apoptosis induction in human colon and breast cancer cell lines. PKR distribution and activation, apoptosis induction and cytotoxic effects were analyzed during 5-FU and 5-FU/IFNα treatment in several colon and breast cancer cell lines with different p53 status. PKR protein was activated by 5-FU treatment in a p53-independent manner, inducing phosphorylation of the protein synthesis translation initiation factor eIF-2α and cell death by apoptosis. Furthermore, PKR interference promoted a decreased response to 5-FU treatment and those cells were not affected by the synergistic antitumor activity of 5-FU/IFNα combination. These results, taken together, provide evidence that PKR is a key molecular target of 5-FU with potential relevance in the clinical use of this drug.

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“…In parallel with this, it would appear that elderly colorectal cancer patients over the age of 70 continue to be under‐treated, and are also under‐represented in clinical drug trials in spite of the fact that their exclusion from such research is unwarranted (Rougier et al., 2004). Similar attitudes have been demonstrated by medical oncologists and radiotherapists in respect of elderly breast cancer patients (Protière et al., 2009; Hershman et al., 2008) so that their management is sometimes sub‐optimal and predicated on clinical trials carried out on younger patients whose responses to specific treatment dosages may be very different (Ershler, 2006; Porock et al., 2009).…”

mentioning

confidence: 63%

“…Oral chemotherapy drugs do have proven efficacy in the elderly however, and are undoubtedly beneficial since they spare them the inconvenience, discomfort and iatrogenic risks associated with hospitalisation or repeated visits to the outpatient clinic for parenteral therapy (Rousseau et al., 2010; Kotsori et al., 2010; Yap et al., 2007; Ershler, 2006). However, as Brearley et al.…”

mentioning

confidence: 99%

Continuing disparities in survival rates between younger and older cancer patients in Europe. Might oral chemotherapy provide one solution to the problem?

OʼConnor

2009

European Journal of Cancer Care

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Capecitabine use in geriatric oncology: An analysis of current safety, efficacy, and quality of life data

Cited by 17 publications

References 49 publications

Apoptosis and Molecular Targeting Therapy in Cancer

Apoptosis and Molecular Targeting Therapy in Cancer

The Chemotherapeutic Drug 5-Fluorouracil Promotes PKR-Mediated Apoptosis in a p53- Independent Manner in Colon and Breast Cancer Cells

Continuing disparities in survival rates between younger and older cancer patients in Europe. Might oral chemotherapy provide one solution to the problem?

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