ArticlePLoS computational biology2014
Lattice-based model of ductal carcinoma in situ suggests rules for breast cancer progression to an invasive state.
Article in PLoS computational biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
13 citing papers in PubMed, 31 citations in OpenAlex.
- Data-driven spatio-temporal modelling of glioblastoma.Royal Society open science · 2023Review
- Bayesian calibration of a stochastic, multiscale agent-based model for predicting in vitro tumor growth.PLoS computational biology · 2021Article
- RORα Suppresses Cancer-Associated Inflammation by Repressing Respiratory Complex I-Dependent ROS Generation.International journal of molecular sciences · 2021Article
- A Multiscale Agent-Based Model of Ductal Carcinoma In Situ.IEEE transactions on bio-medical engineering · 2020Article
- Involvement of Annexin A2 Expression and Apoptosis in Reverse Polarization of Invasive Micropapillary Carcinoma of the Breast.Case reports in pathology · 2020Article
- A checkpoint-oriented cell cycle simulation model.Cell cycle (Georgetown, Tex.) · 2019Article
- Multicompartment cell-based modeling of confined migration: regulation by cell intrinsic and extrinsic factors.Molecular biology of the cell · 2018Article
- Comparative histopathology and immunohistochemistry of human and canine mammary tumors.Open veterinary journal · 2018Article
- Towards personalized computational oncology: from spatial models of tumour spheroids, to organoids, to tissues.Journal of the Royal Society, Interface · 2018Review
- An agent-based model of triple-negative breast cancer: the interplay between chemokine receptor CCR5 expression, cancer stem cells, and hypoxia.BMC systems biology · 2017Article
- Increased ROS production in non-polarized mammary epithelial cells induces monocyte infiltration in 3D culture.Journal of cell science · 2017Article
- A hybrid agent-based model of the developing mammary terminal end bud.Journal of theoretical biology · 2016Article
- Multiscale mechanobiology: computational models for integrating molecules to multicellular systems.Integrative biology : quantitative biosciences from nano to macro · 2015Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Ductal carcinoma in situ (DCIS) is a heterogeneous group of non-invasive lesions of the breast that result from abnormal proliferation of mammary epithelial cells. Pathologists characterize DCIS by four tissue morphologies (micropapillary, cribriform, solid, and comedo), but the underlying mechanisms that distinguish the development and progression of these morphologies are not well understood. Here we explored the conditions leading to the emergence of the different morphologies of DCIS using a two-dimensional multi-cell lattice-based model that incorporates cell proliferation, apoptosis, necrosis, adhesion, and contractility. We found that the relative rates of cell proliferation and apoptosis governed which of the four morphologies emerged. High proliferation and low apoptosis favored the emergence of solid and comedo morphologies. In contrast, low proliferation and high apoptosis led to the micropapillary morphology, whereas high proliferation and high apoptosis led to the cribriform morphology. The natural progression between morphologies cannot be investigated in vivo since lesions are usually surgically removed upon detection; however, our model suggests probable transitions between these morphologies during breast cancer progression. Importantly, cribriform and comedo appear to be the ultimate morphologies of DCIS. Motivated by previous experimental studies demonstrating that tumor cells behave differently depending on where they are located within the mammary duct in vivo or in engineered tissues, we examined the effects of tissue geometry on the progression of DCIS. In agreement with our previous experimental work, we found that cells are more likely to invade from the end of ducts and that this preferential invasion is regulated by cell adhesion and contractility. This model provides additional insight into tumor cell behavior and allows the exploration of phenotypic transitions not easily monitored in vivo.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.