Individualizing breast cancer treatment—The dawn of personalized medicine

Nandy, Argha; Gangopadhyay, Sudeshna; Mukhopadhyay, Ashis

doi:10.1016/j.yexcr.2013.09.002

Cited by 28 publications

(17 citation statements)

References 98 publications

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“…There is now significant interest in the discovery of such biomarkers by pharmaceutical companies and the regulatory authorities as biomarker-based tests can improve stratification of patients prior to clinical trials (Izmailov et al, 2011). This approach could help to revolutionize treatment of psychiatric disorders by leading to a similar personalized medicine strategy as have already begun to emerge in other areas of medicine, such as oncology (Nandy et al, 2014). Recent studies have shown that patients with anxiety disorders (Salim et al, 2012), major depressive disorder (Zunszain et al, 2013), schizophrenia (Suvisaari and Mantere, 2013), bipolar disorder (Munkholm et al, 2013) and autism spectrum disorders (Gesundheit et al, 2013) have altered serum concentrations of cytokines and other molecules associated with inflammation or immune function and dysfunction.…”

Section: Introductionmentioning

confidence: 99%

Applications of blood-based protein biomarker strategies in the study of psychiatric disorders

Chan

Gottschalk

Haenisch

et al. 2014

Progress in Neurobiology

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Section: Introductionmentioning

confidence: 99%

Applications of blood-based protein biomarker strategies in the study of psychiatric disorders

Chan

Gottschalk

Haenisch

et al. 2014

Progress in Neurobiology

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“…Mediators of chronic inflammation inevitably contribute to tumour initiation and development, as well as progression. Hence there is also a recent shift of focus towards personalized medicine, where the patient genomic profile is assessed before administration of a treatment regimen in order to optimize the therapeutic outcome [183][184][185]. For instance, as discussed above, increased levels of CXC chemokines are not only associated with chemoresistance, but also may contribute to poor prognosis in patients.…”

Section: Discussionmentioning

confidence: 99%

Analysis of the intricate relationship between chronic inflammation and cancer

Chai

Siveen

Shanmugam

et al. 2015

Biochemical Journal

171

124

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Deregulated inflammatory response plays a pivotal role in the initiation, development and progression of tumours. Potential molecular mechanism(s) that drive the establishment of an inflammatory-tumour microenvironment is not entirely understood owing to the complex cross-talk between pro-inflammatory and tumorigenic mediators such as cytokines, chemokines, oncogenes, enzymes, transcription factors and immune cells. These molecular mediators are critical linchpins between inflammation and cancer, and their activation and/or deactivation are influenced by both extrinsic (i.e. environmental and lifestyle) and intrinsic (i.e. hereditary) factors. At present, the research pertaining to inflammation-associated cancers is accumulating at an exponential rate. Interest stems from hope that new therapeutic strategies against molecular mediators can be identified to assist in cancer treatment and patient management. The present review outlines the various molecular and cellular inflammatory mediators responsible for tumour initiation, progression and development, and discusses the critical role of chronic inflammation in tumorigenesis.

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“…5 The efficacy of such a personalized approach has already been demonstrated in medical conditions ranging from breast cancer 107 to cystic fibrosis, 108 and identification of individual etiological routes may inform psychiatric treatment as well. 109,110 For example, drugs that target CCK basket cell functioning may be uniquely effective in individuals with schizophrenia who have a particular genotype and had heavy use of cannabis during adolescence.…”

Section: Discussionmentioning

confidence: 99%

Different Paths to Core Pathology: The Equifinal Model of the Schizophrenia Syndrome

Green

Glausier

2015

SCHBUL

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Schizophrenia is a clinically heterogeneous disorder that is perhaps more accurately characterized as "the schizophrenia syndrome." This clinical heterogeneity is reflected in the heterogeneous neurobiological presentations associated with the illness. Moreover, even highly specific neural aberrations that are associated with distinct symptoms of schizophrenia are linked to a wide range of risk factors. As such, any individual with schizophrenia likely has a particular set of risk factors that interact and converge to cross the disease threshold, forming a particular etiology that ultimately generates a core pathophysiology. This core pathophysiology may then produce 1 or more symptoms of schizophrenia, leading to common symptoms across individuals in spite of disparate etiologies. As such, the schizophrenia syndrome can be considered as an equifinal entity: a state of dysfunction that can arise from different upstream etiologies. Moreover, schizophrenia etiologies are multifactorial and can involve the interactive effects of a broad range of genetic, environmental, and developmental risk factors. Through a consideration of how disparate etiologies, caused by different sets of risk factors, converge on the same net dysfunction, this paper aims to model the equifinal nature of schizophrenia symptoms. To demonstrate the equifinal model, we discuss how maternal infection and adolescent cannabis use, 2 recognized schizophrenia risk factors, may interact with other genetic, environmental, and/or developmental risk factors to cause the conserved clinical presentation of impaired working memory.

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Individualizing breast cancer treatment—The dawn of personalized medicine

Cited by 28 publications

References 98 publications

Applications of blood-based protein biomarker strategies in the study of psychiatric disorders

Applications of blood-based protein biomarker strategies in the study of psychiatric disorders

Analysis of the intricate relationship between chronic inflammation and cancer

Different Paths to Core Pathology: The Equifinal Model of the Schizophrenia Syndrome

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