Author

H. Geiger

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

Biology Disciplines

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Cancer Biology· 4 Cell Biology· 1 Immunology· 1 Microbiology· 1

Signature Assays, Organisms & Methods

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Approach:experimental assay· 5 Research Focus:cell type annotation· 4 Research Focus:differential expression· 4 Organism:human· 4 Assay:bulk RNA-seq· 3 Organism:mouse· 3 Approach:statistical model· 3 Research Focus:cell signaling & trafficking· 2

Frequent Co-Authors

N. Robine· 3 shared A. Beheshti· 1 shared A. Bercovich· 1 shared A. C. Borczuk· 1 shared A. Corvelo· 1 shared A. Craney· 1 shared A. Hobeika· 1 shared A. J. Kriegel· 1 shared

Activity by Year

2018-2022 · peak 3/yr

Co-Author Collaboration Network

10 top collaborators · 17 mutual co-author links

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Curved chords = mutual co-authorship

3 shared papersCancer Biology

N. Robine

Mutual co-authors in cluster

Author profile →

7 papers

Recent·Most cited

Creating a 'Timeline' of ductal carcinoma in situ to identify processes and biomarkers for progression towards invasive ductal carcinoma

C. A. Rebbeck, J. Xian, S. Bornelov, J. Geradts, A. Hobeika, H. Geiger, J. F. Alvarez, E. Rozhkova, A. Nicholls, N. Robine, H. K. Lyerly, G. J. Hannon

The paper generates a disease progression timeline for DCIS using gene expression data to identify early processes and biomarkers associated with progression to invasive breast cancer.

bioRxiv · Mar 1, 2022Cancer Biology

Inflammatory signals from fatty bone marrow supports the early stages of DNMT3a driven clonal hematopoiesis

N. Zioni, A. Bercovich, N. Chapal-Ilani, A. Solomon, E. Petrovich, M. .Sacma, H. Geiger, M. Scheller, C. Müller-Tidow, D. Lipka, E. Shlush, M. Minden, N. Kaushansky, L. Shlush

This study shows that fatty bone marrow (FBM) promotes DNMT3A-driven clonal hematopoiesis by enhancing inflammatory signals like IL-6, which can be inhibited by blocking the IL-6 receptor.

bioRxiv · Jan 13, 2022Cancer Biology

Occult polyclonality of preclinical pancreatic cancer models drives in vitro evolution.

M. E. Monberg, H. Geiger, R. Sharma, J. J. Lee, A. Semaan, V. Bernard, D. B. Swartzlander, B. M. Stephens, K. Chen, M. H. Katz, N. Robine, P. A. Guerrero, A. Maitra

This study reveals high intratumoral heterogeneity in pancreatic cancer cell lines and highlights issues with reproducibility and validity of preclinical models.

bioRxiv · Apr 13, 2021Cancer Biology

Systemic Tissue and Cellular Disruption from SARS-CoV-2 Infection revealed in COVID-19 Autopsies and Spatial Omics Tissue Maps

J. Park, J. Foox, T. Hether, D. Danko, S. Warren, Y. Kim, J. Reeves, D. J. Butler, C. Mozsary, J. Rosiene, A. Shaiber, E. Afshinnekoo, M. MacKay, Y. Bram, V. Chandar, , Schwar

This study identifies systemic tissue and cellular disruption from SARS-CoV-2 infection using autopsy and spatial omics data, showing tissue-specific damage and transcriptional changes.

bioRxiv · Mar 8, 2021 · PreprintMicrobiology

Systemic inflammation recruits fast-acting anti-inflammatory innate myeloid progenitors from BM into lymphatics

J. Serrano-Lopez, S. Hegde, S. Kumar, J. Serrano, J. Fang, A. Wellendorf, P. Roche, Y. Rangel, L. J. Carrington, H. Geiger, L. Grimes, S. Luther, I. Maillard, J. Sanchez-Garcia, D. Starczynowski, J. Cancelas

The paper shows that systemic inflammation triggers rapid migration of specific myeloid progenitors from bone marrow to lymphatics via Ccl19/Ccr7, promoting anti-inflammatory responses and replenishment of lymph node dendritic cells.

bioRxiv · Jan 20, 2021 · PreprintImmunology

A Wnt5a-Cdc42 axis controls aging and rejuvenation of hair-follicle stem cells

R. L. Tiwari, P. Mishra, N. Martin, N. O. George, V. Sakk, K. Soller, K. Nalapareddy, K. Nattamai, K. S. Kochanek, M. C. Florian, H. Geiger

This study identifies a Wnt5a-Cdc42 signaling axis that regulates hair-follicle stem cell aging and rejuvenation, showing that inhibiting Cdc42 activity restores canonical Wnt signaling and promotes hair regeneration.

bioRxiv · Oct 22, 2020Cell Biology

Genetic mechanisms of primary chemotherapy resistance in pediatric acute myeloid leukemia: A report from the TARGET initiative

N. McNeer, J. Philip, H. Geiger, R. Ries, V.-P. Lavallee, M. Walsh, M. Shah, K. Arora, A.-K. Emde, N. Robine, T. A. Alonzo, E. A. Kolb, A. S. Gamis, M. Smith, D. S. Gerhard, , A. Kentsis

The paper identifies genetic mechanisms of primary chemotherapy resistance in pediatric AML through whole-genome and transcriptome sequencing of treatment-failure cases.

bioRxiv · Nov 26, 2018Cancer Biology