The biology and mathematical modelling of glioma invasion: a review

Abstract

Adult gliomas are aggressive brain tumours associated with low patient survival rates and limited life expectancy. The most important hallmark of this type of tumour is its invasive behaviour, characterized by a markedly phenotypic plasticity, infiltrative tumour morphologies and the ability of malignant progression from low-to high-grade tumour types. Indeed, the widespread infiltration of healthy brain tissue by glioma cells is largely responsible for poor prognosis and the difficulty of finding curative therapies. Meanwhile, mathematical models have been established to analyse potential mechanisms of glioma invasion. In this review, we start with a brief introduction to current biological knowledge about glioma invasion, and then critically review and highlight future challenges for mathematical models of glioma invasion.

Impact of four lncRNA polymorphisms (rs2151280, rs7763881, rs1136410, and rs3787016) on glioma risk and prognosis: A case‐control study

“…In China, 1 016 000 people were diagnosed with brain and CNS cancer . Despite advances in surgical resection, chemotherapy, and radiotherapy, the prognosis of patients with glioma remains unfavorable, even with 15 months median survival in high‐grade glioma . Therefore, a better understanding of tumor characteristics and biology and further refinement of tumor classification and patient stratification are necessary for individualized treatment.…”

“…3 Despite advances in surgical resection, chemotherapy, and radiotherapy, the prognosis of patients with glioma remains unfavorable, even with 15 months median survival in highgrade glioma. 4,5 Therefore, a better understanding of tumor characteristics and biology and further refinement of tumor classification and patient stratification are necessary for individualized treatment. Genetic syndromes, familial aggregation, telomere maintenance, and genetic polymorphisms are reported to be related to the susceptibility and prognosis of glioma.…”

Temporally feathered intensity‐modulated radiation therapy: A planning technique to reduce normal tissue toxicity

“…Furthermore, we assume that both the delivery of each treatment fraction and response to radiation are instantaneous. We notice that similar dynamical models have been previously proposed to simulate the effect of radiation on brain and lung tumors, as well as to define an organ‐specific NTCP model …”

“…The dynamical NTCP model considered in this work parallels prior similar models which have been proposed to simulate radiation effects on different tumor types, as well as in healthy tissues . The current BED formulation is limited by the lack of a temporal recovery term of radiation‐induced damage, and therefore are not suitable models to compare radiation schema with various fractionations over time.…”

Mitigating Temozolomide Resistance in Glioblastoma via DNA Damage-Repair Inhibition

“…Our approach offers the key advantage of consistent comparison across strategies since a virtual patient may be treated with as many strategies as needed, allowing us to compare results without the confounding factor of inter-patient variability. Mathematical models have been employed extensively to describe the growth and treatment of gliomas (for instance, see [16,17,18,19]; see [20] for a recent review). However, to the best of our knowledge, ours is the first to explicitly incorporate DNA methylation and repair pathways, and to consider DNA repair inhibition in combination with chemotherapy.…”