“First do no harm” and the importance of prediction in oncology

Characiejus, Dainius; Hodzic, Jasmina; Jacobs, John J. L.

doi:10.1007/s13167-010-0042-1

Cited by 15 publications

(11 citation statements)

References 48 publications

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“…Hence, IFN‐α seems to induce the opposite changes in peripheral blood CD8 + CD57 + T‐cell levels (i.e. increase versus decrease) depending on their pre‐treatment values 129 . Collectively our data suggest that in melanoma patients the cytotoxic subsets of the CD8 + CD57 + T‐cell population may predominate while in patients with renal cell carcinoma the expansion of its immunosuppressive subsets may prevail.…”

Section: Cd8+ Cd28− (Cd8+ Cd57+) T Cells In Health and Diseasementioning

confidence: 74%

CD8+ CD28− and CD8+ CD57+ T cells and their role in health and disease

2011

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Summary Chronic antigenic stimulation leads to gradual accumulation of late‐differentiated, antigen‐specific, oligoclonal T cells, particularly within the CD8+ T‐cell compartment. They are characterized by critically shortened telomeres, loss of CD28 and/or gain of CD57 expression and are defined as either CD8+CD28− or CD8+CD57+ T lymphocytes. There is growing evidence that the CD8+CD28− (CD8+CD57+) T‐cell population plays a significant role in various diseases or conditions, associated with chronic immune activation such as cancer, chronic intracellular infections, chronic alcoholism, some chronic pulmonary diseases, autoimmune diseases, allogeneic transplantation, as well as has a great influence on age‐related changes in the immune system status. CD8+CD28− (CD8+CD57+) T‐cell population is heterogeneous and composed of various functionally competing (cytotoxic and immunosuppressive) subsets thus the overall effect of CD8+CD28− (CD8+CD57+) T‐cell‐mediated immunity depends on the predominance of a particular subset. Many articles claim that CD8+CD28− (CD8+CD57+) T cells have lost their proliferative capacity during process of replicative senescence triggered by repeated antigenic stimulation. However recent data indicate that CD8+CD28− (CD8+CD57+) T cells can transiently up‐regulate telomerase activity and proliferate under certain stimulation conditions. Similarly, conflicting data is provided regarding CD8+CD28− (CD8+CD57+) T‐cell sensitivity to apoptosis, finally leading to the conclusion that this T‐cell population is also heterogeneous in terms of its apoptotic potential. This review provides a comprehensive approach to the CD8+CD28− (CD8+CD57+) T‐cell population: we describe in detail its origins, molecular and functional characteristics, subsets, role in various diseases or conditions, associated with persistent antigenic stimulation.

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Section: Cd8+ Cd28− (Cd8+ Cd57+) T Cells In Health and Diseasementioning

confidence: 74%

CD8+ CD28− and CD8+ CD57+ T cells and their role in health and disease

2011

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“…As new technologies emerge allowing the identification of CRC gene mutation status, this information will inform clinicians as to the most appropriate and efficacious form of treatment. This individualised approach to managing mCRC fits in well with the PPPM model put forward by EPMA [144,145]. However, in order to gain most benefit from these novel technologies, targeted therapy must be informed by well-designed studies, large cohort sizes and internationally standardised detection protocols.…”

Section: Discussionmentioning

confidence: 74%

Targeted therapies in colorectal cancer—an integrative view by PPPM

2013

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In developed countries, colorectal cancer (CRC) is the third most common malignancy, but it is the second most frequent cause of cancer-related death. Clinicians are still faced with numerous challenges in the treatment of this disease, and future approaches which target the molecular features of the disorder will be critical for success in this disease setting. Genetic analyses of many solid tumours have shown that up to 100 protein-encoding genes are mutated. Within CRC, numerous genetic alterations have been identified in a number of pathways. Therefore, understanding the molecular pathology of CRC may present information on potential routes for treatment and may also provide valuable prognostic information. This will be particularly pertinent for molecularly targeted treatments, such as anti-vascular endothelial growth factor therapies and anti-epidermal growth factor receptor (EGFR) monoclonal antibody therapy. KRAS and BRAF mutations have been shown to predict response to anti-EGFR therapy. As EGFR can also signal via the phosphatidylinositol 3-kinase (PI3K) kinase pathway, there is considerable interest in the potential roles of members of this pathway (such as PI3K and PTEN) in predicting treatment response. Therefore, a combined approach of new techniques that allow identification of these biomarkers alongside interdisciplinary approaches to the treatment of advanced CRC will aid in the treatment decision-making process and may also serve to guide future therapeutic approaches.

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“…No Harm" and "Prediction in Oncology" is discussed [1]. The authors review data on cancer-treatment modalities that could have either cancer-promoting or cancer-inhibiting effects.…”

Section: The Connection Between the Two Concepts "First Domentioning

confidence: 99%

Cancer diagnostics and treatment: are we ready to implement PPPM?

Desiderio

2010

EPMA Journal

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The scientific community is always excited whenever a new journal appears in the open scientific literature. Such was the case when the first issue of the EPMA Journal of International Reviews in Predictive, Preventive and Personalized Medicine (PPPM) appeared in 2010.This present issue focuses on PPPM in Cancer, and it contains a spectrum of topics that covers the range from basic research, via clinical research, to potential implementation. Each review focuses on one or a reasonable combination of the three main topics embodied in the EPMA journal, and highlights the predictive, preventive, and personalized aspects of cancer treatment. It is clear from the scientific literature, in general, and in each one of the reviews in this issue, in particular, that the next quantum leap in clinical science now derives explicitly from one or more of those three features of medicine: accurate prediction, efficacious prevention, and detailed personalized treatment. The objective of this journal and of this issue on cancer is to present state-of-the-art results from researchers from around the world, and to provide timely reviews of cutting-edge basic research, clinical research, and clinical results. The reviews will range from the molecular level (DNA, RNA, proteins, metabolites), the cellular level, clinical research, and clinical practice.A brief overview follows of each topic that appears in this current issue of PPPM in Cancer. These reviews cover the following areas of research: the "First Do No Harm" concept; the shift from correlative to predictive oncology; selenium and oxidative stress in cancer; BRCA1 and BRCA2 gene mutations; a proposal for non-invasive proteomics in breast cancer; gene-expression profiling in breast cancer; proteomics and nitroproteomics of pituitary adenomas; epidemiological analysis of gastric adenocarcinomas; endoscopic diagnosis for the early detection of gastrointestinal cancer; fluoropyrimidine toxicity and polymorphisms of the dihydropyrimidine dehydrogenase gene; and circulating DNA and RNA.

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“First do no harm” and the importance of prediction in oncology

Cited by 15 publications

References 48 publications

CD8+ CD28− and CD8+ CD57+ T cells and their role in health and disease

CD8+ CD28− and CD8+ CD57+ T cells and their role in health and disease

Targeted therapies in colorectal cancer—an integrative view by PPPM

Cancer diagnostics and treatment: are we ready to implement PPPM?

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