Author

H. Alam

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· 3 Zoology· 1

Signature Assays, Organisms & Methods

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Approach:experimental assay· 3 Research Focus:cancer & tumor microenvironment· 2 Organism:human· 2 Organism:mouse· 2 Assay:bulk RNA-seq· 1 Research Focus:cell type annotation· 1 Research Focus:development & morphogenesis· 1 Research Focus:differential expression· 1

Frequent Co-Authors

F. Muller· 2 shared K. Rai· 2 shared M. Maitituoheti· 2 shared M. Tang· 2 shared S. Amin· 2 shared Y.-H. Lin· 2 shared A. Alvarez-Quilon· 1 shared A. Bonneau Fortin· 1 shared

Activity by Year

2018-2023 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 29 mutual co-author links

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2 shared papersCancer Biology

F. Muller

Mutual co-authors in cluster

Author profile →

4 papers

Recent·Most cited

The extent of regeneration is impacted by the stage of amputation in ladybird beetles: a case study in Cheilomenes sexmaculata

H. Alam, s. rai, p. verma, g. mishra

This study shows that regeneration in ladybird beetles is stage-specific, with earlier larval stages regenerating larger legs and experiencing less developmental delay than later stages.

bioRxiv · Apr 20, 2023Zoology

CCNE1 amplification is synthetic-lethal with PKMYT1 kinase inhibition

D. Gallo, J. T. F. Young, J. Fourtounis, G. Martino, A. Alvarez-Quilon, C. Bernier, N. M. Duffy, R. Papp, A. Roulston, R. Stocco, J. Szychowski, A. Veloso, H. Alam, P. S. Baruah, A. Bonneau Fortin, , D. Durocher

The paper identifies PKMYT1 as a therapeutic target for CCNE1-amplified cancers, showing that its inhibition leads to synthetic lethality and tumor regression in combination with gemcitabine.

bioRxiv · Apr 8, 2021Cancer Biology

Super-enhancer impairment is a link between MLL4 inactivated lung tumors and their vulnerability to glycolysis pathway inhibition

H. Alam, M. Tang, M. Maitituoheti, S. S. Dhar, S. Amin, B. Gu, T.-Y. Chen, Y.-H. Lin, J. Chen, F. Muller, F. J. DeMayo, L. Baseler, K. Rai, M. Lee

The paper shows that MLL4 loss in lung cancer promotes glycolysis and that inhibiting glycolysis selectively targets MLL4-mutant lung tumors.

bioRxiv · Dec 28, 2018 · PreprintCancer Biology

Enhancer Reprogramming Confers Dependence on Glycolysis and IGF signaling in KMT2D Mutant Melanoma

M. Maitituoheti, E. Keung, M. Tang, L. Yan, H. Alam, G. Han, A. Raman, C. Terranova, S. Sarkar, E. Orouji, S. Amin, S. Sharma, M. Williams, N. S. Samant, M. Dhamdhere, , K. Rai

This study identifies KMT2D as a tumor suppressor in melanoma, showing its loss leads to metabolic reprogramming toward glycolysis and dependence on IGF signaling, suggesting therapeutic targeting of these pathways.

bioRxiv · Dec 27, 2018Cancer Biology