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Bowman-Colin, Christian

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Bowman-Colin

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Christian

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Bowman-Colin, Christian
Author's Publications: search.filters.isAuthorOfPublication.4962c6ac-48e7-4e20-a025-c1698086de69

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Now showing 1 - 5 of 5
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    BRCA1 haploinsufficiency for replication stress suppression in primary cells
    (Nature Pub. Group, 2014) Pathania, Shailja; Bade, Sangeeta; Le Guillou, Morwenna; Burke, Karly; Reed, Rachel; Bowman-Colin, Christian; Su, Ying; Ting, David; Polyak, Kornelia; Richardson, Andrea; Feunteun, Jean; Garber, Judy; Livingston, David
    BRCA1—a breast and ovarian cancer suppressor gene—promotes genome integrity. To study the functionality of BRCA1 in the heterozygous state, we established a collection of primary human BRCA1+/+ and BRCA1mut/+ mammary epithelial cells and fibroblasts. Here we report that all BRCA1mut/+ cells exhibited multiple normal BRCA1 functions, including the support of homologous recombination- type double-strand break repair (HR-DSBR), checkpoint functions, centrosome number control, spindle pole formation, Slug expression and satellite RNA suppression. In contrast, the same cells were defective in stalled replication fork repair and/or suppression of fork collapse, that is, replication stress. These defects were rescued by reconstituting BRCA1mut/+ cells with wt BRCA1. In addition, we observed ‘conditional’ haploinsufficiency for HR-DSBR in BRCA1mut/+ cells in the face of replication stress. Given the importance of replication stress in epithelial cancer development and of an HR defect in breast cancer pathogenesis, both defects are candidate contributors to tumorigenesis in BRCA1-deficient mammary tissue.
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    Palb2 synergizes with Trp53 to suppress mammary tumor formation in a model of inherited breast cancer
    (Proceedings of the National Academy of Sciences, 2013) Bowman-Colin, Christian; Xia, B.; Bunting, S.; Klijn, C.; Drost, R.; Bouwman, P.; Fineman, L.; Chen, X.; Culhane, Aedin; Cai, H.; Rodig, Scott; Bronson, Roderick; Jonkers, J.; Nussenzweig, A.; Kanellopoulou, C.; Livingston, David
    Germ-line mutations in PALB2 lead to a familial predisposition to breast and pancreatic cancer or to Fanconi Anemia subtype N. PALB2 performs its tumor suppressor role, at least in part, by supporting homologous recombination-type double strand break repair (HRDSBR) through physical interactions with BRCA1, BRCA2, and RAD51. To further understand the mechanisms underlying PALB2mediated DNA repair and tumor suppression functions, we targeted Palb2 in the mouse. Palb2-deficient murine ES cells recapitulated DNA damage defects caused by PALB2 depletion in human cells, and germline deletion of Palb2 led to early embryonic lethality. Somatic deletion of Palb2 driven by K14-Cre led to mammary tumor formation with long latency. Codeletion of both Palb2 and Tumor protein 53 (Trp53) accelerated mammary tumor formation. Like BRCA1 and BRCA2 mutant breast cancers, these tumors were defective in RAD51 focus formation, reflecting a defect in Palb2 HR-DSBR function, a strongly suspected contributor to Brca1, Brca2, and Palb2 mammary tumor development. However, unlike the case of Brca1mutant cells, Trp53bp1 deletion failed to rescue the genomic instability of Palb2- or Brca2-mutant primary lymphocytes. Therefore, Palb2-driven DNA damage control is, in part, distinct from that executed by Brca1 and more similar to that of Brca2. The mechanisms underlying Palb2 mammary tumor suppression functions can now be explored genetically in vivo.
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    Isolation and characterization of novel RECK tumor suppressor gene splice variants
    (Impact Journals LLC, 2015) Trombetta-Lima, Marina; Winnischofer, Sheila Maria Brochado; Demasi, Marcos Angelo Almeida; Filho, Renato Astorino; Carreira, Ana Claudia Oliveira; Wei, Beiyang; de Assis Ribas, Thais; Konig, Michelle Silberspitz; Bowman-Colin, Christian; Oba-Shinjo, Sueli Mieko; Marie, Suely Kazue Nagahashi; Stetler-Stevenson, William; Sogayar, Mari Cleide
    Glioblastoma multiforme is the most common and lethal of the central nervous system glial-derived tumors. RECK suppresses tumor invasion by negatively regulating at least three members of the matrix metalloproteinase family: MMP-9, MMP-2, and MT1-MMP. A positive correlation has been observed between the abundance of RECK expression in tumor samples and a more favorable prognosis for patients with several types of tumors. In the present study, novel alternatively spliced variants of the RECK gene: RECK-B and RECK-I were isolated by RT-PCR and sequenced. The expression levels and profiles of these alternative RECK transcripts, as well as canonical RECK were determined in tissue samples of malignant astrocytomas of different grades and in a normal tissue RNA panel by qRT-PCR. Our results show that higher canonical RECK expression, accompanied by a higher canonical to alternative transcript expression ratio, positively correlates with higher overall survival rate after chemotherapeutic treatment of GBM patients. U87MG and T98G cells over-expressing the RECK-B alternative variant display higher anchorage-independent clonal growth and do not display modulation of, respectively, MMP-2 and MMP-9 expression. Our findings suggest that RECK transcript variants might have opposite roles in GBM biology and the ratio of their expression levels may be informative for the prognostic outcome of GBM patients.
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    The Role of Endocrine System in the Inflammatory Process
    (Hindawi Publishing Corporation, 2016) Bowman-Colin, Christian; Salazar, Luis A.; Martins, Joilson O.
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    A Reference Map of the Human Binary Protein Interactome
    (Nature Research, 2020-04-08) Luck, Katja; Kim, Dae-Kyum; Lambourne, Luke; Spirohn, Kerstin; Begg, Bridget E; Bian, Wenting; Brignall, Ruth; Cafarelli, Tiziana; Campos-Laborie, Francisco J.; Charloteaux, Benoit; Choi, Dongsic; Coté, Atina; Daley, Meaghan; Deimling, Steven; Desbuleux, Alice; Dricot, Amélie; Gebbia, Marinella; Hardy, Madeleine; Kishore, Nishka; Knapp, Jennifer; Kovács, István A.; Lemmens, Irma; Mee, Miles W.; Mellor, Joseph C.; Pollis, Carl; Pons, Carles; Richardson, Aaron; Schlabach, Sadie; Teeking, Bridget; Yadav, Anupama; Babor, Mariana; Balcha, Dawit; Basha, Omer; Bowman-Colin, Christian; Chin, Suet-Feung; Choi, Soon Gang; Colabella, Claudia; Coppin, Georges; D'Amata, Cassandra; De Ridder, David; De Rouck, Steffi; Duran-Frigola, Miquel; Ennajdaoui, Hanane; Goebels, Florian; Goehring, Liana; Gopal, Anjali; Haddad, Ghazal; Hatchi, Elodie; Helmy, Mohamed; Jacob, Yves; Kassa, Yoseph; Landini, Serena; Li, Roujia; van Lieshout, Natascha; MacWilliams, Andrew; Markey, Dylan; Paulson, Joseph; Rangarajan, Sudharshan; Rasla, John; Rayhan, Ashyad; Rolland, Thomas; San Miguel Delgadillo, Adriana; Shen, Yun; Sheykhkarimli, Dayag; Sheynkman, Gloria; Simonovsky, Eyal; Taşan, Murat; Tejeda, Alexander; Tropepe, Vincent; Twizere, Jean-Claude; Wang, Yang; Weatheritt, Robert; Weile, Jochen; Xia, Yu; Yang, Xinping; Yeger-Lotem, Esti; Zhong, Quan; Aloy, Patrick; Bader, Gary D.; De Las Rivas, Javier; Gaudet, Suzanne; Hao, Tong; Rak, Janusz; Tavernier, Jan; Hill, David; Vidal, Marc; Roth, Frederick P.; Calderwood, Michael
    Global insights into cellular organization and genome function require comprehensive understanding of the interactome networks that mediate genotype-phenotype relationships. Here, we present a human “all-by-all” reference interactome map of human binary protein interactions, or “HuRI”. With ~53,000 high-quality protein-protein interactions (PPIs), HuRI has approximately four times more such interactions than high-quality curated interactions from small-scale studies. Integrating HuRI with genome, transcriptome, and proteome data enables the study of cellular function within most physiological or pathological cellular contexts. We demonstrate the utility of HuRI in identifying specific subcellular roles of PPIs. Inferred tissue-specific networks reveal general principles for the formation of cellular context-specific functions and elucidate potential molecular mechanisms underlying tissue-specific phenotypes of Mendelian diseases. HuRI represents a systematic proteome-wide reference linking genomic variation to phenotypic outcomes.