A5037817316- Cancer Cells and Metastasis
- Cancer-related Molecular Pathways
- Wnt/β-catenin signaling in development and cancer
- Genetic factors in colorectal cancer
- Cancer-related gene regulation
- RNA Research and Splicing
- RNA modifications and cancer
- Inflammatory mediators and NSAID effects
- Cancer Genomics and Diagnostics
- Estrogen and related hormone effects
- Immunotherapy and Immune Responses
- Cancer Immunotherapy and Biomarkers
- Advanced Breast Cancer Therapies
- Drug Transport and Resistance Mechanisms
- Ubiquitin and proteasome pathways
- Cancer therapeutics and mechanisms
- Cytokine Signaling Pathways and Interactions
- Genomics and Chromatin Dynamics
- Hippo pathway signaling and YAP/TAZ
- DNA Repair Mechanisms
- HER2/EGFR in Cancer Research
- Microtubule and mitosis dynamics
- PARP inhibition in cancer therapy
- Cancer-related molecular mechanisms research
- Advanced Biosensing Techniques and Applications
University of Notre Dame
2015-2024
Indiana University School of Medicine
2015-2024
Mike and Josie Harper Cancer Research Institute
2017-2024
Indiana University South Bend
2015-2024
Indiana University
2014-2023
Indiana University – Purdue University Indianapolis
2014-2019
Cancer Research Institute
2014-2017
University of Chicago
2009-2015
South Bend Museum of Art
2015
University of Indianapolis
2014
Our previous data illustrated that activation of the canonical Wnt signaling pathway was enriched in triple-negative breast cancer and associated with reduced overall survival all patients. To determine whether may be a promising therapeutic target for cancer, we investigated β-catenin necessary tumorigenic behaviors vivo vitro. expression level significantly two human cell lines, MDA-MB-231 HCC38, using lentiviral delivery β-catenin-specific small hairpin RNAs (shRNAs). Upon implantation...
Chemoresistance is one of the leading causes cancer-related deaths in United States. Triple negative breast cancer (TNBC), a subtype lacking known receptors used for targeted therapy, reliant on chemotherapy as standard care. The Adenomatous Polyposis Coli (APC) tumor suppressor mutated or hypermethylated 70% sporadic cancers with APC-deficient tumors resembling TNBC subtype. Using mammary cells from Apc
The Adenomatous Polyposis Coli (APC) tumor suppressor is most commonly mutated in colorectal cancers such as familial adenomatous polyposis (FAP); well many other epithelial like breast, pancreatic, and lung cancer. APC mutations usually result a truncated form of the protein lacking carboxy-terminal region resulting loss function. Mutations have been identified early stages cancer development making it gatekeeper progression therefore an ideal therapeutic target. best known for its role...
Breast cancer incidence and mortality vary significantly among different nations racial groups. African have the highest breast rates in world, even though are below those of many nations. Differences disease progression suggest that aggressive tumors may harbor a unique molecular signature to promote progression. However, few studies investigated pathology clinical markers expressed tissue from regional patient populations. We collected 68 malignant 89 non-cancerous samples Kenyan tissue....
The Adenomatous Polyposis Coli (APC) tumor suppressor is mutated or hypermethylated in up to 70 % of sporadic breast cancers depending on subtype; however, the effects APC mutation tumorigenic properties remain unexplored. Using Apc Min/+ mouse crossed Polyoma middle T antigen (PyMT) transgenic model, we identified enhanced tumorigenesis and alterations genes critical therapeutic resistance independent Wnt/β-catenin signaling. changed histopathology from solid squamous adenocarcinomas,...
Abstract Background The APC tumor suppressor is mutated or downregulated in many types, and prominently localized to punctate clusters at protrusion tips migratory cells, such as astrocytes where it has been implicated directed cell motility. Although loss considered an initiating event colorectal cancer, for example, less clear what role plays motility whether of might be important promoter progression addition initiation. Methods localization β-catenin was analyzed multiple lines,...
The Adenomatous Polyposis Coli (APC) tumor suppressor gene is silenced by hypermethylation or mutated in up to 70% of human breast cancers. In mouse models, Apc mutation disrupts normal mammary development and predisposes formation; however, the cooperation between APC other mutations tumorigenesis has not been studied. To test hypothesis that loss one copy promotes oncogene-mediated tumorigenesis, Apc(Min/+) mice were crossed with virus (MMTV)-Polyoma middle T antigen (PyMT) MMTV-c-Neu...
Resistance to chemotherapy is one of the leading causes death from breast cancer. We recently established that loss Adenomatous Polyposis Coli (APC) in Mouse Mammary Tumor Virus - Polyoma middle T (MMTV-PyMT) transgenic mouse model results resistance cisplatin or doxorubicin-induced apoptosis. Herein, we aim establish mechanism responsible for APC-mediated chemotherapeutic resistance. Our data demonstrate MMTV-PyMT;ApcMin/+ cells have increased signal transducer and activator transcription 3...
Abstract Inactivation of the adenomatous polyposis coli (APC) tumor suppressor has been associated with mammary tumorigenesis in mouse models and through epidemiological studies human breast cancers, but normal role for APC development not thoroughly characterized. We report here that Apc Min/+ mice containing one functional allele have severely disrupted lobuloalveolar during pregnancy lactation, time points at which gene expression is its highest levels mice. This phenotype was accompanied...
Physicochemically modified silicon substrates can provide a high quality alternative to nitrocellulose-coated glass slides for use in reverse-phase protein microarrays. Enhancement of microarray sensitivities is an important goal, especially because molecular targets within patient tissues exist low abundance. The ideal array substrate has binding affinity and intrinsic background signal. Silicon, which autofluorescence, being explored as potential surface. In previous paper ( Nijdam , A. J....
Adenomatous Polyposis Coli (APC) is lost in approximately 70% of sporadic breast cancers, with an inclination towards triple negative cancer (TNBC). TNBC treated traditional chemotherapy, such as paclitaxel (PTX); however, tumors often develop drug resistance. We previously created APC knockdown cells (APC shRNA1) using the human cells, MDA-MB-157, and showed that loss induces PTX To understand mechanisms behind APC-mediated response, we performed cell cycle analysis analyzed related...
Triple-negative breast cancer (TNBC) patients are treated with traditional chemotherapy, such as the taxane class of drugs. One drug, paclitaxel (PTX), can be effective in treating TNBC; however, many tumors will develop drug resistance, which lead to recurrence. In order improve patient outcomes and survival, there lies a critical need understand mechanism behind resistance. Our lab made novel observation that decreased expression Adenomatous Polyposis Coli (APC) tumor suppressor using...
Loss of the Adenomatous Polyposis Coli (APC) tumor suppressor in colorectal cancer elicits rapid signaling through Wnt/β-catenin pathway. In contrast to this well-established role APC, recent studies from our laboratory demonstrated that APC functions Wnt-independent pathways mediate vitro and vivo models breast tumorigenesis. Pancreatic ductal adenocarcinoma (PDAC) has an overall median survival less than one year with a 5-year rate 7.2%. is lost subset pancreatic cancers, but impact on Wnt...
Tumors commonly are infiltrated by leukocytes, or tumor infiltrating leukocytes (TILs). It remains unclear, however, if the density and type of individual TILs has a direct simply correlative role in promoting poor prognosis breast cancer patients. Breast Kenyan women is aggressive with presentation at young age, advanced grade (grade III), large size (>2.0 cm), prognosis. We previously observed that tumors were predominantly estrogen receptor positive (ER+) but also included both high...