Divide and Conquer: Progress in the Molecular Stratification of Cancer

Tan, Patrick

doi:10.3349/ymj.2009.50.4.464

Cited by 5 publications

(4 citation statements)

References 94 publications

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“…However, in order to achieve a molecular targeted approach in diagnosis, prognosis and therapy, histopathology needs to be complemented with reliable molecular tools. Case in point, histopathology of breast cancer is complemented with molecular tool, and has become valuable in the selection of patients for appropriate therapy and management [24,25]. Taken together, our results lead us to propose that OLP lesions that are in the process of transforming to SCCA present histomorphologically as OLP, but possess a certain molecular signature that represents the specific factors that drive progression to cancer.…”

Section: Discussionmentioning

confidence: 87%

LCK, survivin and PI-3K in the molecular biomarker profiling of oral lichen planus and oral squamous cell carcinoma

Oluwadara¹,

Giacomelli²,

Christensen³

et al. 2009

Bioinformation

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T cell signaling is critical in oral lichen planus (OLP) based on the pathogenesis of this chronic inflammatory autoimmune mucocutaneous lesion. Lck plays a key role in T cell signaling; ultimately this signaling affects other targets such as PI-3K. Excessive activity in PI-3K inhibits apoptosis and promotes uncontrolled cell growth. Molecular biomarker profiling in OLP, Chronic Interface Mucosities (CIM), Epithelial Dysplasia (EpD) and Oral Squamous Cell Carcinoma (SCCA) with application of the principle of biomarker voting may represent a new frontier in the diagnosis, assessment and the arguable debate of OLP transformation to cancer. The presence of Lck, PI-3K and Survivin, a cancer specific anti-apoptotic protein was assessed, using immunohistochemistry and tissue micro-array on patient samples, in OLP, SCCA, CIM and EpD. Lck expression was very high in 78.6 % of OLP patients compared to 3.7% in SCCA; PI-3K was high in 63% of SCCA, 100% of EpD, and 35.7% OLP cases. Survivin was high in 64.3% of OLP cases, 96.3% of SCCA, and 100% of EpD. CIM cases may be slightly different molecularly to OLP. Taken together, our data suggest that biomarker protein voting can be effectively used to isolate high-risk OLP cases. Specifically, we show data with four remarkable cases demonstrating that molecular factors are predictive of histopathology. We conclude that it is safer to treat OLP as premalignant lesions, to adopt aggressive treatment measure in histopathologic described well and moderately differentiated SCCA, and to monitor progress of these diseases molecularly using individualized auto-proteomic approach. The use of Lck inhibitors in OLP management needs to be investigated in the future.

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Section: Discussionmentioning

confidence: 87%

LCK, survivin and PI-3K in the molecular biomarker profiling of oral lichen planus and oral squamous cell carcinoma

Oluwadara¹,

Giacomelli²,

Christensen³

et al. 2009

Bioinformation

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“…All cancers are known to have a genetic basis, and genetic pre-disposition to cancer is well established [5,6]. Although, a number of genetic and epigenetic risk factors associated with cancer pathogenesis have been identified, the underlying molecular mechanisms largely remain to be understood.…”

Section: Introductionmentioning

confidence: 99%

Susceptibility to oral cancers with CD95 and CD95L promoter SNPs may vary with the site and gender

et al. 2015

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We investigated risk association of oral cancers (tongue and buccal mucosa cancers) with FAS (-1377G > A and FAS -670 A > G) and FASL (-844 T > C) SNPs, in males and females. A case-control study of 535 oral cancer and 525 control subjects was performed. SNPs were detected in the genomic DNA isolated from peripheral blood using PCR-RFLP. We report FASL -844 T > C SNPs increased risk for buccal mucosa cancer in females but not in males. On the other hand, FAS genotypes did not alter the risk of the cancers in both females and males. However, co-occurrence of FAS -1377 GA and -670 GG, FAS -1377 AA and -670 GG genotypes, and combined genotypes of FAS and FASL (FAS -1377 AA + FAS -670 GG + FASL -844 CC) alter male susceptibility towards tongue cancer. In females, combined genotypes of FAS (-1377GA and -670 AA) were found to be a risk factor of buccal mucosa cancer (OR = 3.27, CI = 1.28-8.36; P ≤ 0.01). FASL variants (GA and AA) increased tongue cancer risk in females who were tobacco users compared to non-tobacco users. In conclusion, SNPs of the FAS and FASL might alter risk of tongue and buccal mucosa cancers differentially, in a gender-dependent manner.

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“…To solve these essential concerns and limitations of the current treatment, there has been a lot of interest in using the so‐called “cancer research models”. [ 2 ] The scientific community is currently looking at two complementary methodologies: In vitro and in vivo models. [ 3 ] Both these models offer scientists a wide range of experimental options for studying the origins of cancer, detecting cancer etiological agents, characterization of tumor‐biomarkers, elucidating molecular regulation of cancer cells, such as metabolic reactions and cellular signaling pathways, and evaluating therapeutic strategies.…”

Section: Introductionmentioning

confidence: 99%

Emerging In Vitro and In Vivo Models: Hope for the Better Understanding of Cancer Progression and Treatment

Yadav,

Mahajan,

Singh

et al. 2024

Advanced Biology

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Various cancer models have been developed to aid the understanding of the underlying mechanisms of tumor development and evaluate the effectiveness of various anticancer drugs in preclinical studies. These models accurately reproduce the critical stages of tumor initiation and development to mimic the tumor microenvironment better. Using these models for target validation, tumor response evaluation, resistance modeling, and toxicity comprehension can significantly enhance the drug development process. Herein, various in vivo or animal models are presented, typically consisting of several mice and in vitro models ranging in complexity from transwell models to spheroids and CRISPR‐Cas9 technologies. While in vitro models have been used for decades and dominate the early stages of drug development, they are still limited primary to simplistic tests based on testing on a single cell type cultivated in Petri dishes. Recent advancements in developing new cancer therapies necessitate the generation of complicated animal models that accurately mimic the tumor's complexity and microenvironment. Mice make effective tumor models as they are affordable, have a short reproductive cycle, exhibit rapid tumor growth, and are simple to manipulate genetically. Human cancer mouse models are crucial to understanding the neoplastic process and basic and clinical research improvements. The following review summarizes different in vitro and in vivo metastasis models, their advantages and disadvantages, and their ability to serve as a model for cancer research.

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Divide and Conquer: Progress in the Molecular Stratification of Cancer

Cited by 5 publications

References 94 publications

LCK, survivin and PI-3K in the molecular biomarker profiling of oral lichen planus and oral squamous cell carcinoma

LCK, survivin and PI-3K in the molecular biomarker profiling of oral lichen planus and oral squamous cell carcinoma

Susceptibility to oral cancers with CD95 and CD95L promoter SNPs may vary with the site and gender

Emerging In Vitro and In Vivo Models: Hope for the Better Understanding of Cancer Progression and Treatment

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