Author

M. Hitomi

Listed by name: these papers carry no ORCID for this author, so different people with the same name may be mixed together.

Biology Disciplines

Click to filter author papers

Cancer Biology· 5 Cell Biology· 1 Evolutionary Biology· 1

Signature Assays, Organisms & Methods

Click to filter · or open tag

Approach:experimental assay· 5 Organism:human· 5 Research Focus:cancer & tumor microenvironment· 3 Research Focus:cell type annotation· 3 Assay:bulk RNA-seq· 2 Research Focus:cell signaling & trafficking· 1 Approach:deep learning· 1 Research Focus:differential expression· 1

Frequent Co-Authors

J. G. Scott· 4 shared J. D. Lathia· 3 shared A. Dhawan· 2 shared A. Durmaz· 2 shared A. P. Chumakova· 2 shared D. J. Silver· 2 shared E. McClure· 2 shared A. Berezovsky· 1 shared

Activity by Year

2018-2023 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 16 mutual co-author links

Click any collaborator node to inspect or filter shared papers

Focal author (center)Selected co-authorORCID co-authorUnlinked name

Curved chords = mutual co-authorship

4 shared papersCancer Biology

J. G. Scott

Mutual co-authors in cluster

Author profile →

7 papers

Recent·Most cited

Alamar Blue assay optimization to minimize druginterference and inter-assay viability

M. N. Dinh, M. Hitomi, Z. A. Al-Turaihi, J. G. Scott

The paper optimizes the Alamar Blue assay to reduce drug interference and inter-assay viability variability by modifying protocol steps and adding rhodamine B calibration.

bioRxiv · Mar 16, 2023Cell Biology

Measuring competitive exclusion in non-small cell lung cancer

N. Farrokhian, J. Maltas, M. Dinh, A. Durmaz, P. Ellsworth, M. Hitomi, E. McClure, A. Marusyk, A. Kaznatcheev, J. G. Scott

This study measures frequency-dependent interactions between gefitinib-resistant and sensitive NSCLC populations to show that competitive exclusion depends on growth rate data, not just cost of resistance.

bioRxiv · Sep 18, 2020Cancer Biology

Identifying states of collateral sensitivity during the evolution of therapeutic resistance in Ewings sarcoma

J. A. Scarborough, E. McClure, P. Anderson, A. Dhawan, A. Durmaz, S. L. Lessnick, M. Hitomi, J. G. Scott

This study maps the temporal evolution of collateral sensitivity and resistance in Ewings sarcoma, showing unpredictable patterns in drug response and highlighting transcriptomic changes associated with these states.

bioRxiv · Feb 11, 2020Evolutionary Biology

Asymmetric Division Promotes Therapeutic Resistance In Glioblastoma Stem Cells

M. Hitomi, A. P. Chumakova, D. J. Silver, A. M. Knudsen, W. D. Pontius, S. Murphy, N. Anand, B. W. Kristensen, J. D. Lathia

The paper shows that asymmetric division in glioblastoma stem cells generates daughter cells with enhanced therapeutic resistance and co-inherited growth factor receptors.

bioRxiv · Mar 6, 2019Cancer Biology

Recasting the cancer stem cell hypothesis: unification using a continuum model of microenvironmental forces

J. G. Scott, A. Dhawan, A. Hjelmeland, J. Lathia, A. Chumakova, M. Hitomi, A. G. Fletcher, P. K. Maini, A. R. A. Anderson

The paper unifies the cancer stem cell and stochastic models using a continuum model of microenvironmental forces, supported by clonogenic assay results.

Current Stem Cell Reports · Feb 15, 2019Peer-reviewedCancer Biology

High-throughput Automated Single Cell Imaging Analysis Reveals Dynamics Of Glioblastoma Stem Cell Population During State Transition

A. P. Chumakova, M. Hitomi, E. P. Sulman, J. D. Lathia

The paper develops HASCIA, a high-throughput automated single-cell imaging analysis tool, to quantify protein expression and study dynamics of glioblastoma stem cell state transitions.

bioRxiv · Jul 31, 2018Cancer Biology

Development of a Cx46 targeting strategy for cancer stem cells

E. E. Mulkearns-Hubert, L. A. Torre-Healy, D. J. Silver, J. T. Eurich, E. Serbinowski, M. Hitomi, J. Zhou, B. Przychodzen, R. Zhang, S. A. Sprowls, J. S. Hale, T. Alban, A. Berezovsky, B. A. Bell, P. R. Lockman, , J. D. Lathia

This study identifies clofazimine as a Cx46 inhibitor that targets glioblastoma cancer stem cells by disrupting gap junction communication, enhancing the efficacy of temozolomide.

bioRxiv · Mar 26, 2018Cancer Biology