Radioresistance in carcinoma of the breast

Jameel, Jainudeen K.A.; Rao, Vittal; Cawkwell, Lynn; Drew, PJ

doi:10.1016/j.breast.2004.08.004

Cited by 102 publications

(100 citation statements)

References 37 publications

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“…The specific nature of those interactions is an important target of future research. Cellular immune changes induced by cancer therapy could potentially persist in the aftermath of treatment due to for example alterations in T-cell homeostasis, replicative potential, and senescence (43,44), and these changes might potentially underlie long-term alterations in constitutive inflammatory activity. Alternatively, treatment-induced reactivation of latent infections (45) could potentially induce long-term changes in immune system homeostasis.…”

Section: Discussionmentioning

confidence: 99%

Inflammatory Biomarkers for Persistent Fatigue in Breast Cancer Survivors

Collado-Hidalgo¹,

Bower

Ganz

et al. 2006

Clinical Cancer Research

347

263

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Purpose: This study seeks to define immunologic and inflammatory variables associated with persistent post-treatment fatigue in breast cancer survivors. Experimental Design: Leukocyte subsets, plasma inflammatory markers, and ex vivo proinflammatory cytokine production were assessed in 50 fatigued and nonfatigued breast cancer survivors recruited z2 years after successful primary therapy. Multivariate statistical analyses were used to define a composite immunologic biomarker of fatigue risk. Results: Fatigued breast cancer survivors were distinguished from nonfatigued survivors by increased ex vivo monocyte production of interleukin (IL)-6 and tumor necrosis factor-a following lipopolysaccharide stimulation, elevated plasma IL-1ra and soluble IL-6 receptor (sIL-6R/CD126), decreased monocyte cell-surface IL-6R, and decreased frequencies of activated T lymphocytes and myeloid dendritic cells in peripheral blood (all P < 0.05). An inverse correlation between sIL-6R and cell-surface IL-6R was consistent with inflammation-mediated shedding of IL-6R, and in vitro studies confirmed that proinflammatory cytokines induced such shedding. Multivariate linear discriminant function analysis identified two immunologic markers, the ratio of sIL-6R to monocyte-associated IL-6R and decreased circulating CD69 + T lymphocytes, as highly diagnostic of fatigue (P = 0.0005), with cross-validation estimates indicating 87% classification accuracy (sensitivity = 0.83; specificity = 0.83). Conclusion: These results extend links between fatigue and inflammatory markers to show a functional alteration in proinflammatory cytokine response to lipopolysaccharide and define a prognostic biomarker of behavioral fatigue.

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Section: Discussionmentioning

confidence: 99%

Inflammatory Biomarkers for Persistent Fatigue in Breast Cancer Survivors

Collado-Hidalgo¹,

Bower

Ganz

et al. 2006

Clinical Cancer Research

347

263

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“…In particular, radiotherapy plays a crucial role in achieving local control following surgery. Accordingly, development of radioresistance in breast cancer cells presents a difficult problem in the course of treatment (18). Therefore, a breast cancer cell model is an important and useful model when studying radiosensitization and cancer cell survival pathways.…”

Section: Introductionmentioning

confidence: 99%

Targeting the Akt/mammalian target of rapamycin pathway for radiosensitization of breast cancer

Albert

Kim²,

Cao

et al. 2006

Molecular Cancer Therapeutics

165

141

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The phosphatidylinositol 3-kinase (PI3K)/Akt pathway is known to be activated by radiation. The mammalian target of rapamycin (mTOR) is downstream of Akt, and we investigated the effects of radiation on Akt/mTOR signaling in breast cancer cell models. RAD001 (everolimus), a potent derivative of the mTOR inhibitor rapamycin, was used to study the effects of mTOR inhibition, as the role of mTOR inhibition in enhancing radiation remains unexplored. RAD001 decreased clonogenic cell survival in both breast cancer cell lines MDA-MB-231 and MCF-7, although the effect is greater in MDA-MB-231 cells.

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“…The phosphatase PTEN, which is often mutated or underexpressed in many cancer cells, negatively regulates this pathway via inhibiting PI-3K (Carnero et al, 2008). Importantly, hyperactivation of the PI-3K/AKT/mTOR pathway was found to be associated with resistance to radiation and chemotherapy (Jameel et al, 2004). Therefore it presents a promising therapeutic target for tumor sensitization.…”

Section: Pi-3k/akt/mtormentioning

confidence: 99%

DNA Repair, Cancer and Cancer Therapy

Wang¹

2011

DNA Repair and Human Health

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Radioresistance in carcinoma of the breast

Cited by 102 publications

References 37 publications

Inflammatory Biomarkers for Persistent Fatigue in Breast Cancer Survivors

Inflammatory Biomarkers for Persistent Fatigue in Breast Cancer Survivors

Targeting the Akt/mammalian target of rapamycin pathway for radiosensitization of breast cancer

DNA Repair, Cancer and Cancer Therapy

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