Hijacking the Hematopoietic System and Other Dirty Tricks that Breast Cancers Play
NCI’s Center for Cancer Research (CCR) Grand Rounds Dr. McAllister is an Associate Scientist in the Hematology Division at Brigham &Women’s Hospital and an Assistant Professor of Medicine at Harvard Medical School in Boston. She received her undergraduate degree at the University of Michigan in Ann Arbor and completed her Ph.D. studies in molecular and cellular biology at Washington University School of Medicine in St. Louis. She joined Robert Weinberg’s laboratory at the Whitehead Institute for Biomedical Research as a postdoctoral fellow where she established new pre-clinical models to study breast cancer pathophysiology. She joined the faculty of Brigham &Women’s Hospital and Harvard Medical School in 2009, and is also an affiliate member of the Harvard Stem Cell Institute, an associate member of the Broad Institute, and a member of the Dana Farber/Harvard Cancer Center. Dr. McAllister studies cancer as a systemic disease and focuses her research efforts on identifying physiological processes that contribute to tumor progression and finding ways to interdict their function. Dr. McAllister is an American Cancer Society Scholar, the 2013 recipient of the AACR Gertrude B. Elion Cancer Research Award, and was presented with the Presidential Early Career Award for Scientists and Engineers by President Obama in 2014.Air date: 5/13/2016 12:00:00 PM
Authors: Yan Y, Yin Y, Feng X, Chen Y, Shi J, Weng H, Wang D Abstract There is existing evidence that elevated homocysteine (Hcy) levels are risk factors for some neurodegenerative disorders. The pathogenesis of neurological diseases could be contributed to excessive cell dysfunction and death caused by defective DNA damage response (DDR) and accumulated DNA damage. Hcy is a neurotoxic amino acid and acts as a DNA damage inducer. However, it is not clear whether Hcy participates in the DDR. To investigate the effects of Hcy on DNA damage and the DDR, we employed mitomycin C (MMC) to cause DNA damage in NE4C murine ...
Contributors : Carol E Lange ; Julie H OstranderSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensTrascriptome analysis of mcf7 cell lines were performed
AbstractCockle shell-derived aragonite calcium carbonate nanoparticles (CACNP) have demonstrated prospect as nano-sized drug carriers for targeting cancer cells. CACNP is biocompatible, biodegradable and its biomaterial is readily available and is of low cost. In addition, CACNP is highly porous, has a large surface area which confer a high loading capacity. The pH-dependent release properties as well as its potential for surface functionalization with targeting agents make CACNP useful in passive and active targeting of cancer cells and cancer stem cells. In this article, we reviewed the current state of CACNP as nano-siz...
Stem Cells and Development, Ahead of Print.
Conclusion: Natural compound emodin suppresses EMT and CSC formation of breast cancer cells by blocking TGF-β1-mediated crosstalk between TAMs and breast cancer cells. Our study provides evidence suggesting that emodin harbors the potential for clinical development as a new effective and safe agent to halt metastatic recurrence of breast cancer.
Conclusions: These results demonstrate that SIRT4 exerts its tumor-suppressive activity via modulating SIRT1 expression in breast cancer and provide a novel cross-talk between mitochondrial and nuclear sirtuins.
Abstract Radiation therapy is frequently a critical component of breast cancer care but carries with it side effects that are particularly damaging to reconstructive efforts. Autologous lipotransfer has the ability to improve radiated skin throughout the body due to the pluripotent stem cells and multiple growth factors transferred therein. The oncologic safety of lipotransfer to the breasts is demonstrated in the literature and is frequently considered an adjunctive procedure for improving the aesthetic outcomes of breast reconstruction. Using lipotransfer as an integral rather than adjunctive step in the reconst...
Epithelial-mesenchymal transition (EMT) is implicated in breast-cancer invasion/metastasis. Cancer cells acquire stem cell properties to self-renew/form new tumors through EMT. PTEN converts PIP3 to PIP2, antagonizes the PI3K-Akt pathway to inhibit proliferation, migration, apoptosis, and this contributes to PTEN ’s tumor suppressor function. PTEN also processes protein phosphatase activities. Substrates of its protein phosphatase and their importance in cancer development/metastasis are largely unexplored.
Conclusions: The significance of the most prominent cell type in normal breast stroma, the fibroblast, in directingepithelial differentiation is largely unknown. Through establishment of lobular and interlobular fibroblast cell lines,we here demonstrate that epithelial progenitors are submitted to stromal cues for site-specific differentiation. Ourfindings lend credence to considering stromal subtleties of crucial importance in the development of normal breastand, in turn, breast cancer.
CONCLUSION: YM155 treatment could be used to overcome BCSCs resistance to oxidative stress-based anticancer therapies. PMID: 32986362 [PubMed - as supplied by publisher]