Publications

 

The high correlation of CANscript predictions to actual clinical outcomes has been demonstrated and documented in peer reviewed publications and major conference presentations. Mitra Biotech is continuously developing clinical utility and outcomes data to support the use of CANscript.

Scroll down for a list of peer-review publications.

For a list of presentations and abstracts, click here.

Predicting clinical response to anticancer drugs using an ex vivo platform that captures tumour heterogeneity

Nature Communications (February 2015)

Predicting clinical response to anticancer drugs remains a major challenge in cancer treatment. Emerging reports indicate that the tumour microenvironment and heterogeneity can limit the predictive power of current biomarker-guided strategies for chemotherapy. Here we report the engineering of personalized tumour ecosystems that contextually conserve the tumour heterogeneity, and phenocopy the tumour microenvironment using tumour explants maintained in defined tumour grade-matched matrix support and autologous patient serum.

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Rationally co-targeting divergent pathways in KRAS wild-type colorectal cancers by CANscript technology reveals tumor dependence on Notch and Erbb2

Scientific Reports (February 2015)

KRAS mutation status can distinguish between metastatic colorectal carcinoma (mCRC) patients who may benefit from therapies that target the epidermal growth factor receptor (EGFR), such as cetuximab. These findings highlight the importance of integrating molecular profile and functional testing tools for optimization of alternate strategies in resistant population.

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Temporally sequenced anticancer drugs overcome adaptive resistance by targeting a vulnerable chemotherapy-induced phenotypic transition

Nature Communications (February 2015)

Using human breast cancer explants, in vitro cell lines, mouse in vivo studies and mathematical modelling, here we show that exposure to a taxane induces phenotypic cell state transition towards a favoured transient CD44HiCD24Hi chemotherapytolerant state.

 

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Cancer immunotherapy and personalized medicine: Emerging technologies and biomarker-based approaches

Journal of Molecular Biomarkers & Diagnosis (September 2017)

We introduce new techniques that seek to tailor immunotherapy by re-programming patient-autologous T-cells, and new technologies that are emerging to predict clinical efficacy by mapping infiltration of lymphocytes, and harnessing fully humanized platforms that reconstruct and interrogate immune checkpoint blockade, ex vivo.

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Preclinical cancer models and biomarkers for drug development: New technologies and emerging tools

Journal of Molecular Biomarkers & Diagnosis (September 2017)

Predicting the efficacy of anticancer therapy is the holy grail of drug development and treatment selection in the clinic. We present a focused, brief perspective on emerging preclinical models for anticancer therapy that attempt to address the challenge posed by tumor heterogeneity, highlighting biomarkers of response and resistance.

 

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Integrating biological and mathematical models to explain and overcome drug resistance in cancer. Part 1: Biological facts and studies in drug resistance

Current Stem Cell Reports (August 2017)

Cancer stem cells (CSC) comprise (typically) a rare tumor subpopulation that contributes both intrinsic drug resistance and tumor re-initiation after therapy. Successful, durable cancer treatment is limited by drug resistance. Harnessing biology and math to simulate, study, and explain the mechanisms of resistance, by considering the whole tumor population, is providing new clues to overcome it.

 

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Integrating biological and mathematical models to explain and overcome drug resistance in cancer. Part 2: From theoretical biology to mathematical models

Current Stem Cell Reports (August 2017)

In this second part of our review, that can be taken independently of Part I, we focus on the level of cell populations, the only one amenable to completely take into account phenotype plasticity in its observable consequences on the evolution of proliferative diseases, and on heterogeneity, that makes sense only in the context of cell populations, together with the fundamental evolutionary potential of cancer cell populations (and not only of single cancer cells).

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Inhibition of rapamycin-induced AKT activation elicits differntial antitumor response in head and neck cancers

Cancer Research (January 2013)

The PI3K/AKT/mTOR pathway is an important signaling axis that is perturbed in majority of cancers. Biomarkers such as pS6RP, GLUT1, and tumor FDG uptake are being evaluated in patient stratification for mTOR pathway inhibitors. Collectively, our results suggest that, in addition to biomarker-based segregation, functional assessment of a patient’s tumor before treatment with mTOR/AKT inhibitors may be useful for patient stratification.

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