Готові списки джерел за темами / Luminal lineage

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Добірка наукової літератури з теми "Luminal lineage"

Автор: Grafiati

Опубліковано: 11 березня 2023

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Статті в журналах з теми "Luminal lineage"

Matsuo, Junichi, Naing Naing Mon, Daisuke Douchi, Akihiro Yamamura, Madhura Kulkarni, Dede Liana Heng, Sabirah Chen, et al. "A Runx1-enhancer Element eR1 Identified Lineage Restricted Mammary Luminal Stem Cells." Stem Cells 40, no. 1 (January 1, 2022): 112–22. http://dx.doi.org/10.1093/stmcls/sxab009.

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Abstract Mammary gland homeostasis is maintained by adult tissue stem-progenitor cells residing within the luminal and basal epithelia. Dysregulation of mammary stem cells is a key mechanism for cancer development. However, stem cell characterization is challenging because reporter models using cell-specific promoters do not fully recapitulate the mammary stem cell populations. We previously found that a 270-basepair Runx1 enhancer element, named eR1, marked stem cells in the blood and stomach. Here, we identified eR1 activity in a rare subpopulation of the ERα-negative luminal epithelium in mouse mammary glands. Lineage-tracing using an eR1-CreERT2 mouse model revealed that eR1+ luminal cells generated the entire luminal lineage and milk-secreting alveoli—eR1 therefore specifically marks lineage-restricted luminal stem cells. eR1-targeted-conditional knockout of Runx1 led to the expansion of luminal epithelial cells, accompanied by elevated ERα expression. Our findings demonstrate a definitive role for Runx1 in the regulation of the eR1-positive luminal stem cell proliferation during mammary homeostasis. Our findings identify a mechanistic link for Runx1 in stem cell proliferation and its dysregulation in breast cancer. Runx1 inactivation is therefore likely to be an early hit in the cell-of-origin of ERα+ luminal type breast cancer.

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Miyano, Masaru, Rosalyn W. Sayaman, Parijat Senapati, Stefan Hinz, Victoria E. Seewaldt, Dustin Schones, and Mark A. LaBarge. "Abstract PR006: Integrating noise into a signal: Luminal epithelial cells integrate variable responses to aging into stereotypical changes that underlie breast cancer susceptibility." Cancer Research 83, no. 2_Supplement_1 (January 15, 2023): PR006. http://dx.doi.org/10.1158/1538-7445.agca22-pr006.

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Abstract Effects from aging in any single cell are unpredictable, whereas aging phenotypes at the organ and tissue levels tend to appear as stereotypical changes. The mammary epithelium, the origin of breast carcinomas, is a bilayer of two major phenotypically and functionally distinct cell lineages, the luminal epithelial and myoepithelial cells. We have shown that luminal epithelia exhibit substantial stereotypical changes with age, which merits attention as they are putative breast cancer cells of origin. Hallmark aging changes in mammary gland are loss of lineage specificity in luminal epithelia exemplified by acquiring expression of proteins normally reserved for myoepithelial cells, and progenitor cells that accumulate and attain a basal differentiation bias. We hypothesize that effects from aging that impinge upon maintenance of lineage specificity increases susceptibility to cancer initiation. Indeed, histologically normal breast tissue from young women, who were known to be highly susceptible to breast cancer because they harbor a germline mutation in BRCA1, BRCA2, or PALB2 genes, exhibited hallmarks of accelerated aging. These included increased proportions of luminal epithelial cells with acquired myoepithelial proteins, acceleration of a breast specific biological clock by 10 to 40 years compared to chronological age, and a basal differentiation bias or failure of differentiation of cKit+ progenitors. To gain insight into the underlying molecular changes we interrogated transcriptomes, proteomes, and methylomes of mammary epithelia at lineage resolution. Strikingly, age-dependent differential gene expression and DNA methylation occurred almost exclusively in luminal epithelia, whereas changes due to increased variance of gene and protein expression occurs in both luminal and myoepithelial lineages. Most gene changes that were previously associated with early breast cancer are detectable as age-driven changes in normal luminal epithelia. The genes with age-dependent differential and variant changes in expression distinguish normal tissue from breast cancers and are predictive of PAM50 breast cancer subtypes. Heterochronus, multilineage, co-cultures demonstrated that the age-dependent phenotype of luminal cells is at least partly dependent on the microenvironment created on the apical surfaces of neighboring myoepithelial cells. We show that increased variance is a substantial outcome of aging and is likely central to understanding increased susceptibility to breast cancer with age. We speculate that the luminal epithelium is a site of integration of the variant responses to aging in their surrounding tissue, and that their emergent phenotype of aging both endows cells with the ability to become a cancer cell of origin and embodies a biosensor that presages one’s cancer susceptibility. Citation Format: Masaru Miyano, Rosalyn W. Sayaman, Parijat Senapati, Stefan Hinz, Victoria E. Seewaldt, Dustin Schones, Mark A. LaBarge. Integrating noise into a signal: Luminal epithelial cells integrate variable responses to aging into stereotypical changes that underlie breast cancer susceptibility [abstract]. In: Proceedings of the AACR Special Conference: Aging and Cancer; 2022 Nov 17-20; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2022;83(2 Suppl_1):Abstract nr PR006.

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Feng, Felix Yi-Chung, Shuang Zhao, Seiwon Laura Chang, Nicholas Erho, Jonathan Lehrer, Mohammed Alshalalfa, Matthew R. Cooperberg, et al. "Luminal and basal subtyping of prostate cancer." Journal of Clinical Oncology 35, no. 6_suppl (February 20, 2017): 3. http://dx.doi.org/10.1200/jco.2017.35.6_suppl.3.

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3 Background: There is a clear need to develop a clinically relevant molecular subtyping approach for prostate cancer. We hypothesized that prostate cancer can be subtyped based on luminal versus basal lineage. Methods: We applied the PAM50 classifier, which is used clinically to identify luminal and basal cancers in breast cancer, to subtype a total of 3,782 prostate cancer samples using a high-density microarray platform run in a CLIA-certified laboratory. We examined the associations of these subtypes and clinical outcomes. Results: We demonstrate that PAM50 segregates prostate cancer into three reproducible subtypes in both retrospective cohorts and on prospective validation: luminal A (33.3%-34.3%), luminal B (28.5%-32.6%), and basal (34.1%-37.1%). Luminal B prostate cancers exhibited the worst clinical prognoses, followed by basal and luminal A subtypes (10-year biochemical recurrence-free survival: 29/39/41%; distant metastasis-free survival: 53/73/73%; prostate cancer-specific survival: 78/86/89%; overall survival: 69/80/82% respectively) on both univariable and multivariable analyses accounting for standard clinicopathologic prognostic factors. Known luminal lineage markers, such as NKX3.1 and KRT18, and the basal lineage CD49f signature, were enriched in luminal- and basal-like cancers respectively, demonstrating the connection between these subtypes and established prostate cancer biology. While both luminal-like subtypes were associated with increased AR expression and signaling, only luminal B prostate cancers were significantly associated with post-operative response to androgen deprivation therapy (ADT) in a subset analysis matching patients based on clinicopathologic variables (interaction p = 0.006, luminal B 10-year metastasis: 33% (treated) vs. 55% (untreated), non-luminal B: 37% (treated) vs. 21% (untreated)). Conclusions: These findings contribute novel insight into the biology of prostate cancer, and provide translatable clinical tools for personalizing post-operative ADT for patients with prostate cancer. Similar to breast cancer, these findings suggest that luminal/basal subtyping may be useful in treatment selection in prostate cancer.

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Wang, Chunhui, John R. Christin, Maja H. Oktay, and Wenjun Guo. "Lineage-Biased Stem Cells Maintain Estrogen-Receptor-Positive and -Negative Mouse Mammary Luminal Lineages." Cell Reports 18, no. 12 (March 2017): 2825–35. http://dx.doi.org/10.1016/j.celrep.2017.02.071.

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Yoo, Kyung Hyun, Sumin Oh, Keunsoo Kang, Chaochen Wang, Gertraud W. Robinson, Kai Ge, and Lothar Hennighausen. "Histone Demethylase KDM6A Controls the Mammary Luminal Lineage through Enzyme-Independent Mechanisms." Molecular and Cellular Biology 36, no. 16 (May 23, 2016): 2108–20. http://dx.doi.org/10.1128/mcb.00089-16.

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Establishment of the mammary luminal cell lineage is controlled primarily by hormones and through specific transcription factors (TFs). Previous studies have linked histone methyltransferases to the differentiation of mammary epithelium, thus opening the possibility of biological significance of counteracting demethylases. We have now demonstrated an essential role for the H3K27me3 demethylase KDM6A in generating a balanced alveolar compartment. Deletion ofKdm6ain the mammary luminal cell lineage led to a paucity of luminal cells and an excessive expansion of basal cells, bothin vivoandin vitro. The inability to form structurally normal ducts and alveoli during pregnancy resulted in lactation failure. Mutant luminal cells did not exhibit their distinctive transcription factor pattern and displayed basal characteristics. The genomic H3K27me3 landscape was unaltered in mutant tissue, and support for a demethylase-independent mechanism came from mice expressing a catalytically inactive KDM6A. Mammary tissue developed normally in these mice. Chromatin immunoprecipitation sequencing (ChIP-seq) experiments demonstrated KDM6A binding to putative enhancers enriched for key mammary TFs and H3K27ac. This study demonstrated for the first time that the mammary luminal lineage relies on KDM6A to ensure a transcription program leading to differentiated alveoli. Failure to fully implement this program results in structurally and functionally impaired mammary tissue.

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Shalabi, Sundus F., Masaru Miyano, Rosalyn W. Sayaman, Jennifer C. Lopez, Tiina A. Jokela, Michael E. Todhunter, Stefan Hinz, et al. "Evidence for accelerated aging in mammary epithelia of women carrying germline BRCA1 or BRCA2 mutations." Nature Aging 1, no. 9 (September 2021): 838–49. http://dx.doi.org/10.1038/s43587-021-00104-9.

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Miyano, Masaru, Sundus Shalabi, Rosalyn W. Sayaman, Martha Stampfer, Victoria E. Seewaldt, and Mark A. LaBarge. "Abstract 5682: Accelerated biological age is a driver of cancer susceptibility in genetic high risk breast tissue." Cancer Research 82, no. 12_Supplement (June 15, 2022): 5682. http://dx.doi.org/10.1158/1538-7445.am2022-5682.

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Abstract During aging in the human mammary gland, luminal epithelial cells lose lineage fidelity by expressing markers normally expressed in myoepithelial cells. We hypothesize that loss of lineage fidelity is a general manifestation of epithelia that are susceptible to cancer initiation. We show that histologically normal breast tissue from younger women who are susceptible to breast cancer because they harbor a germline mutation in BRCA1, BRCA2, or PALB2 genes, exhibit hallmarks of accelerated aging. These include proportionately increased luminal epithelial cells that acquired myoepithelial markers, decreased proportions of myoepithelial cells, and a basal differentiation bias or failure of differentiation of cKit+ progenitors. High-risk luminal and myoepithelial cells are transcriptionally enriched for genes of the opposite lineage, inflammatory, and cancer-related pathways. Genetically high risk luminal epithelial cells also show evidence of accelerated age, by as much as four decades compared to their chronological age, using a breast specific biological clock comprised of measurements of methylation and expression of the luminal-specific ELF5 transcription factor. We have identified breast aging hallmarks that reflect a convergent biology of cancer susceptibility, regardless of the specific underlying genetic or age-dependent risk, or the associated breast cancer subtype. Citation Format: Masaru Miyano, Sundus Shalabi, Rosalyn W. Sayaman, Martha Stampfer, Victoria E. Seewaldt, Mark A. LaBarge. Accelerated biological age is a driver of cancer susceptibility in genetic high risk breast tissue [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2022; 2022 Apr 8-13. Philadelphia (PA): AACR; Cancer Res 2022;82(12_Suppl):Abstract nr 5682.

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Rodilla, Veronica, Alessandro Dasti, Mathilde Huyghe, Daniel Lafkas, Cécile Laurent, Fabien Reyal, and Silvia Fre. "Luminal Progenitors Restrict Their Lineage Potential during Mammary Gland Development." PLOS Biology 13, no. 2 (February 17, 2015): e1002069. http://dx.doi.org/10.1371/journal.pbio.1002069.

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Yamamoto, Shoji, Zhenhua Wu, Hege G. Russnes, Shinji Takagi, Guillermo Peluffo, Charles Vaske, Xi Zhao, et al. "JARID1B Is a Luminal Lineage-Driving Oncogene in Breast Cancer." Cancer Cell 25, no. 6 (June 2014): 762–77. http://dx.doi.org/10.1016/j.ccr.2014.04.024.

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Mohamed, Gadisti Aisha Nurulhijjah Binti, Nevena B. Ognjenovic, Sundis Mahmood, Sarah Min Kyung Lee, Brock C. Christensen, Kristen E. Muller, and Diwakar R. Pattabiraman. "Abstract 1602: Lineage plasticity enables low ER luminal tumors to evolve and gain basal-like traits." Cancer Research 82, no. 12_Supplement (June 15, 2022): 1602. http://dx.doi.org/10.1158/1538-7445.am2022-1602.

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Abstract Stratifying breast cancer into specific molecular or histological subtypes aids in therapeutic decision-making and predicting outcomes, however, these subtypes may not be as distinct as previously thought. Patients with luminal-like, Estrogen Receptor (ER)-expressing tumors have better prognosis than patients with more aggressive, triple-negative or basal-like tumors. There is, however, a subset of luminal-like tumors that express lower levels of ER, which exhibit more basal-like features. Previous studies have suggested that triple negative, basal-like tumors may arise from a luminal cell-of-origin, but there are no definitive studies that identify the cell-of-origin of these low ER tumors. Analysis of 2208 invasive breast carcinomas from 2012-2020 revealed that 2% of tumors have low ER expression (less than 10% ER positive cells), which are mostly high-grade carcinomas and exhibit basal-like features. TCGA analysis revealed that tumors with lower ER expression (lowest quartile of ER expression) expressed higher basal signature genes as compared to tumors with higher levels of ER expression. This variation within the ER+ subtype and the emergence of basal-like characteristics within low ER tumors suggest that some luminal tumors may evolve into a more basal-like or triple-negative subtype. The luminal mouse mammary tumor, MMTV-PyMT, was used to model low ER human tumors and, similar to the patient tumor samples, basal-like tumor cells were also found within these tumors. Lineage tracing using tissue-specific and inducible Cre recombinase-based labelling was performed to elucidate the lineage-of-origin of these basal-like cells, revealing that these basal-like cells were derived from normal luminal epithelial cells, not basal cells. Our study uncovers the existence of luminal-basal plasticity within tumors of a low ER subtype that enables these cells to transition into a more basal-like state. Understanding the factors that enable this plasticity to occur may reveal opportunities to curb the evolution of more aggressive traits, potentially improving the way breast cancer is currently managed and treated. Citation Format: Gadisti Aisha Nurulhijjah Binti Mohamed, Nevena B. Ognjenovic, Sundis Mahmood, Sarah Min Kyung Lee, Brock C. Christensen, Kristen E. Muller, Diwakar R. Pattabiraman. Lineage plasticity enables low ER luminal tumors to evolve and gain basal-like traits [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2022; 2022 Apr 8-13. Philadelphia (PA): AACR; Cancer Res 2022;82(12_Suppl):Abstract nr 1602.

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Більше джерел

Дисертації з теми "Luminal lineage"

De, Felice Dario. "Retinoic acid is required for prostate luminal lineage differentiation and epithelial integrity via Foxa1 expression." Doctoral thesis, Università degli studi di Trento, 2021. http://hdl.handle.net/11572/324422.

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Retinoids are a class of compounds derived from the metabolism of vitamin A and β-carotene. Retinoid signaling has vital functions in both vertebrate and invertebrate embryogenesis such as the formation of body axes and the control of organogenesis. Genetic evidence suggests a role of retinoids in cell fate decision, maturation and homeostasis of the prostate epithelium. Knockout (KO) of the retinoic acid receptor gamma (RARG) gene in mice leads to growth deficits and male sterility due to squamous metaplasia and keratinization of the seminal vesicles and prostate. Noteworthy, synergistic antitumor effects of retinoids and vitamin D have been described in prostate cancer cell lines, although a mechanistic link between retinoic acid (RA) signaling and prostate epithelium differentiation and tumorigenesis has not yet been elucidated. Here, taking advantage of mouse prostate organoids (mPrOs), we report an essential role for RA in the differentiation and integrity of the periurethral and proximal luminal compartments of the prostate epithelium. Mechanistically, RA, through the activation of RARγ, promotes the expression of Foxa1, a pioneer transcription factor that cooperates with androgen receptor (AR) in directing progenitor cells towards the luminal lineage. Reduced RA signaling in organoids leads to downregulation of key structural and polarity proteins along with a loss of luminal identity, a phenotype that is fully rescued by constitutive expression of exogenous Foxa1. Overall, our study demonstrates the importance of RA signaling in prostate epithelium differentiation and homeostasis. In addition to the tumorigenic role of Foxa1 mutations recently described in several human cancers, alteration in RA pathway due to altered uptake/absorption/metabolism of vitamin A and β-carotene, or depending on specific molecular dysfunctions (e.g., epigenetic RARB silencing), could represent a critical rheostat for prostate tumorigenesis.

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Книги з теми "Luminal lineage"

Lobont, Florin, Marian Vasile, and Valeriu Sofronie. Ultimul Blaga. Editura Universitara, 2021. http://dx.doi.org/10.5682/9786062812669.

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Este uimitor in cate feluri poate fi lecturat si inteles Lucian Blaga! Au trecut mai bine de o suta de ani de la aparitia primelor sale lucrari, iar elogiile care l-au intampinat atunci continua sa o faca si astazi. In loc sa-si piarda intensitatea, acestea si-au deschis si adancit continuu semnificatiile, transformandu-se treptat in bunuri universale. An dupa an apar carti si articole menite a pune in lumina un aspect nou sau altul al operei sale, care reuseste, aproape paradoxal, sa desfasoare o complexitate baroca uimitoare, fara a cadea in neinteligibilitate. In parte, secretul fecunditatii si seductiei gandului blagian sta in plasticitatea poetica a scriiturii filosofice si in armonia conceptual-filosofica a poeziei si prozei sale. An dupa an, un mare numar de absolventi de facultate (filosofie, litere, sociologie, antropologie, teologie, arte) isi aleg lucrari de licenta sau doctorat cu tematica blagiana. De asemenea, filosofii, istoricii si criticii literari, esteticienii, teoreticienii stiintei, sociologii, teologii etc. nu contenesc sa se alature in idee si emotie celui care le devine, tot mai profund, Maestru, ascutindu-si cugetul si simtirea, rafinandu-le. E un omagiu care creste continuu, in pofida (sau poate ca tocmai ca afirmare a permanentei non-lineare a Timpului marelui filosof-artist) faptului ca Blaga nu si-a dorit nici discipoli si nici nu s-a imaginat intemeietor de scoala. Lucrarea de fata, reunind nume din tara si din afara ei, specialisti in opera lui Blaga, dar si admiratori inflacarati, este un omagiu adus puterii sale creatoare.

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Частини книг з теми "Luminal lineage"

Hannezo, Edouard, and Colinda L. G. J. Scheele. "A Guide Toward Multi-scale and Quantitative Branching Analysis in the Mammary Gland." In Cell Migration in Three Dimensions, 183–205. New York, NY: Springer US, 2023. http://dx.doi.org/10.1007/978-1-0716-2887-4_12.

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AbstractThe mammary gland consists of a bilayered epithelial structure with an extensively branched morphology. The majority of this epithelial tree is laid down during puberty, during which actively proliferating terminal end buds repeatedly elongate and bifurcate to form the basic structure of the ductal tree. Mammary ducts consist of a basal and luminal cell layer with a multitude of identified sub-lineages within both layers. The understanding of how these different cell lineages are cooperatively driving branching morphogenesis is a problem of crossing multiple scales, as this requires information on the macroscopic branched structure of the gland, as well as data on single-cell dynamics driving the morphogenic program. Here we describe a method to combine genetic lineage tracing with whole-gland branching analysis. Quantitative data on the global organ structure can be used to derive a model for mammary gland branching morphogenesis and provide a backbone on which the dynamics of individual cell lineages can be simulated and compared to lineage-tracing approaches. Eventually, these quantitative models and experiments allow to understand the couplings between the macroscopic shape of the mammary gland and the underlying single-cell dynamics driving branching morphogenesis.

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Gorvine, William M. "Situating Bön and the Life of Shardza." In Envisioning a Tibetan Luminary, 19–36. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780199362349.003.0002.

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The opening chapter locates Bön within a broader Tibetan cultural landscape, with a view to how historical developments have contributed to modern Bönpo identity in the nineteenth and early twentieth centuries. Beginning with a general orientation to what it has meant to be an adherent of Bön, the chapter introduces key historical developments that have shaped Bön in ways significant to our understanding of Shardza’s life. These include complex and sometimes contentious relations with nascent Buddhist lineages in Tibet, internal divisions within Bön itself, and the climate of nonsectarianism that emerged in eastern Tibet in the nineteenth century. This presentation concludes with a look at some of the particular dynamics that fueled a dispute erupting late in Shardza’s career, in which his commitment to time-honored Bön tradition came to be questioned by critics from within the lineage.

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Guo, Qitao. "A Land of Prominent Lineages." In Huizhou: Local Identity and Mercantile Lineage Culture in Ming China, 50–79. University of California Press, 2022. http://dx.doi.org/10.1525/luminos.119.c.

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Guo, Qitao. "Wang Daokun and the Promotion of Mercantile Lineage Culture." In Huizhou: Local Identity and Mercantile Lineage Culture in Ming China, 83–110. University of California Press, 2022. http://dx.doi.org/10.1525/luminos.119.d.

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Guo, Qitao. "Cheng Minzheng and the Rise of Huizhou Consciousness." In Huizhou: Local Identity and Mercantile Lineage Culture in Ming China, 13–49. University of California Press, 2022. http://dx.doi.org/10.1525/luminos.119.b.

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Guo, Qitao. "Introduction." In Huizhou: Local Identity and Mercantile Lineage Culture in Ming China, 1–10. University of California Press, 2022. http://dx.doi.org/10.1525/luminos.119.a.

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Guo, Qitao. "Conclusion." In Huizhou: Local Identity and Mercantile Lineage Culture in Ming China, 160–62. University of California Press, 2022. http://dx.doi.org/10.1525/luminos.119.g.

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Guo, Qitao. "The Local Religious Order." In Huizhou: Local Identity and Mercantile Lineage Culture in Ming China, 134–59. University of California Press, 2022. http://dx.doi.org/10.1525/luminos.119.f.

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Guo, Qitao. "“A Confucian Heartland of Women”." In Huizhou: Local Identity and Mercantile Lineage Culture in Ming China, 111–33. University of California Press, 2022. http://dx.doi.org/10.1525/luminos.119.e.

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"State and Revolution: Nations, Tribes, and Lineages." In Anthropologies of Revolution: Forging Time, People, and Worlds, 41–66. University of California Press, 2020. http://dx.doi.org/10.1525/luminos.89.c.

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Тези доповідей конференцій з теми "Luminal lineage"

Sale, Sanja, Daniel Lafkas, and Spyros Artavanis-Tsakonas. "Abstract LB-208: Notch2in vivogenetic labeling reveals novel epithelial subtypes within mammary luminal lineage." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-lb-208.

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Bragt, Maaike van, Luwei Tao, and Zhe Li. "Abstract 3033: An alveolar-restricted stem cell population in the mammary luminal lineage revealed by lineage tracing serves as cells of origin of heterogeneous mammary tumors." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-3033.

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Omene, Coral O., Manan Patel, Kasthuri Kannan, Adriana Heguy, and Mary Helen Barcellos-Hoff. "Abstract 4232: CAPE (caffeic acid phenethyl ester) induces a mammary stem cell lineage restriction to a luminal phenotype via chromatin remodeling." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-4232.

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Zhdankin, Olga, Melanie Bomier, Donna Parke, Jon Holy, and Teresa Rose-Hellekant. "Abstract B004: Expansion of lineage negative, CD24high, CD61+ mammary cells is an early step in mammary tumorigenesis in NRL-TGFalpha and MMTV-c-neu but not MMTV-c-myc models of luminal breast cancer." In Abstracts: AACR Special Conference on Advances in Breast Cancer Research: Genetics, Biology, and Clinical Applications - October 3-6, 2013; San Diego, CA. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1557-3125.advbc-b004.

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Suo, Jin, Michael McDaniel, Parham Eshtehardi, Saurabh S. Dhawan, Lucas H. Timmins, Hanjoong Jo, Robert W. Taylor, Habib Samady, and Don Giddens. "Intimal Thickening Sourced From Low Wall Shear Stress in Human Left Coronary Artery Was Observed by Optical Coherence Tomography." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53017.

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The high resolution of optical coherence tomography (OCT) may offer improved description of luminal surfaces and intimal thickening in human coronary arteries by comparison to other imaging modalities, such as intravascular ultrasound (IVUS). We investigated the left anterior descending (LAD) coronary artery of a patient using both OCT and IVUS methods and found an asymmetrical distribution of intimal thickness (IT) around the lumen circumference in the OCT images, whereas the IVUS images showed a lumen with no asymmetry in IT. We reconstructed a 3D coronary artery model from the OCT slices that represented the morphological details of local luminal surfaces accurately and used this to simulate the pulsatile flow field in the model employing computational fluid dynamics (CFD). The pulsatile wall shear stress (WSS) distribution on the LAD surface was derived, and time-averaged WSS was computed. The data for IT and WSS distributions in the LAD segment were compared, and a linear inverse relationship between IT and WSS was found; higher WSS (> 25±5 dynes per square centimeter) favors thinner intima (< 0.12±0.05 millimeters) and lower WSS (< 12±5 dynes per square centimeter) favors thicker intima (> 0.33±0.05 millimeters). The enhanced spatial resolution of OCT offers an improved imaging technique for developing CFD models and assessing early atherosclerosis in patients with coronary artery disease.

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Borysova, Maryna. "Development and performance of a compact LumiCal prototype calorimeter for future linear collider experiments." In 40th International Conference on High Energy physics. Trieste, Italy: Sissa Medialab, 2021. http://dx.doi.org/10.22323/1.390.0822.

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Souza, Priscila M., Filomena M. Carvalho, Fernando N. Aguiar, Débora Gagliato, and Alfredo C. S. D. Barros. "ASSOCIATION BETWEEN GATA3 AND PATHOLOGIAL AND IMMUNOHISTOCHEMICAL PREDICTIVE AND PROGNOSTIC PARAMETERS IN EARLY BREAST CANCER." In Scientifc papers of XXIII Brazilian Breast Congress - 2021. Mastology, 2021. http://dx.doi.org/10.29289/259453942021v31s1046.

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Introduction: GATA3 gene, at 10p14, a member of the GATA family with two GATA-type zinc-fingers, encodes the transcription factors GATA - binding protein 3 (GATA3), critical for the luminal breast epithelium development and maintenance. The GATA3 protein is a linear one, with more than 400 aminoacids, that can be recognized by immunohistochemical analysis. Mutations of the GATA3 and loss of the expression of its related protein are implicated in breast cancer development and aggressiveness. As the most frequent transcription factor in luminal tumor cells, GATA3 became an important marker of mammary differentiation in neoplasias of unknown origin, better than mammaglobin and gross cystic disease fluid protein (GCDFP). Objectives: In this study, we aimed at assessing pathological and immunohistochemical variables and their association with GATA3 expression, adding bases for breast carcinogenesis comprehension and BC (Breast Cancer) precision therapy. Methods: GATA3 was analyzed by immunohistochemistry in whole histological sections of tumors from 105 female patients with histological diagnosis of invasive breast carcinoma and at clinical stages I, II and IIIA, who underwent primary surgical treatment (protocol approval number: 1,604,792). GATA3 nuclear expression was determined in percentage of tumor cells and categorized as preserved (positive expression in more than 95% of cells) or reduced (negative or expression in up to 95% of tumor cells). GATA3 expression was analyzed according to patient’s age, tumor and node pathological stage, histological type, histological and nuclear grade, lymphovascular invasion, estrogen receptor, progesterone receptor, androgen receptor, HER2 status, and Ki-67. Results: GATA3 expression was detected in 103/105 (98.1%) cases. Reduced expression was associated with higher histological and nuclear grade, negative hormonal receptors, HER2-positive and higher proliferative activity according to Ki-67 expression. Triple negative breast carcinomas (TNBC) and ER-negative/HER2-positive presented the highest frequency of GATA3 reduction (75%) compared to ER-positive/HER2-negative (4.1%) and ER-positive/HER2-positive (20%). Proliferative activity in TNBC tended to be higher among tumors with GATA3 reduced, irrespective of androgen receptor expression. In the group of ER-positive/ HER2-negative tumors only 3 cases presented GATA3 reduction, all of them with high proliferative activity. Conclusions: GATA3 expression is present in almost all cases of early breast cancer. Reduction in its expression is associated with adverse prognostic factors and higher proliferative activity in all subtypes, including ER-positive/HER2-negative tumors.

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Swanson, William H., Vivianne C. Smith, Joel Pokorny, and Ram L. P. Vimal. "Phase shifts for heterochromatic flicker at intermediate frequencies." In OSA Annual Meeting. Washington, D.C.: Optica Publishing Group, 1985. http://dx.doi.org/10.1364/oam.1985.wj50.

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We measured sensitivity to sinusoidal modulation of two equally luminant chromatic sources as a function of physical phase difference. The stimuli were presented in a two-channel Maxwellian view system employing red (625-nm) and green (564-nm) LEDs. Radiance was controlled by voltage-to-frequency converters fed by computer-controlled analog multipliers designed to give a linear response up to 1800 cd. The 2.0° stimulus field with a mean luminance of 900 cd was viewed in a dark surround. Using a method of adjustment, threshold modulation was determined for up to forty phases from 0° to 356°, at thirteen frequencies ranging from 1 to 40 Hz. In any given block of trials, frequency was held constant and phase varied from trial to trial. At high (>13-Hz) and low (<2.8-Hz) frequencies the modulation vs phase functions were symmetric ~0°. At intermediate frequencies the point of symmetry occurred at 10-40°, the exact amount differing among the three subjects.

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Chen, Kuangxu, Bin Zhang, and Chunlei Liang. "A 3D Parallel High-Order Solver With Curved Local Mesh Refinement for Predicting Arterial Flow Through Varied Degrees of Stenoses." In ASME 2020 Pressure Vessels & Piping Conference. American Society of Mechanical Engineers, 2020. http://dx.doi.org/10.1115/pvp2020-21667.

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Abstract A 3D parallel high-order spectral difference (SD) solver with curved local mesh refinement is developed in this research to simulate flow through stenoses of varied degrees (50%, 60%, 65%, 70% and 75%) of radius constriction at inlet Reynolds number of 500. This solver employs high-order curved mesh in the vicinity of arterial wall and the local mesh refinement technique reduces the overall computational cost by distributing more elements in critical regions. In simulation of flow through stenosis of 50% radius constriction, velocity profiles predicted from the SD solver agree well with previous DNS results and experimental data. Mesh independency study shows that numerical results from a conforming and a non-conforming mesh agree well with each other. When the constriction degree is larger than 50%, visualizations through iso-surfaces of Q-criterion show that vortex rings are ejected from the stenosis throat, advecting downstream before they hit the vessel walls and they finally break down and merge into a large bulk region of small-scale turbulence. The observation is consistent with the vorticity contour which is characterized by development of the Kelvin-Helmholtz instability when shear layers are formed, rolled up and advected downstream between the central jet and the recirculation region. When the constriction degree turns to 75%, the flow transitions rapidly downstream of stenosis throat and dramatic pressure drop is witnessed. This provides a fluid-dynamic explanation for clinical definition of critical stenosis (i.e. over 75% luminal radius narrowing). Furthermore, pressure drop across a stenosis is found to be proportional to square of ratio of non-stenosed area to minimum area at the stenosis throat with a linear correlation coefficient equal to 0.9998. Finally, this solver is proven to have excellent scalability on massively parallel computers when multi-level refinement of meshes is performed to capture small-scale structures in the turbulence region.

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Swanson, William H., Joel Pokorny, and Vivianne C. Smith. "Phase-dependent sensitivity to heterochromatic flicker: subject differences in color-normal males." In OSA Annual Meeting. Washington, D.C.: Optica Publishing Group, 1986. http://dx.doi.org/10.1364/oam.1986.my6.

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We measured sensitivity to sinusoidal temporal modulation as a function of the relative phase of two equally luminant chromatic sources. We previously reported data for three observers at a range of temporal frequencies (OSA 1985); now we report data for a range of observers at a single temporal frequency. The stimuli were presented in a two-channel Maxwellian view system employing red (625-nm) and green (564-nm) light-emitting diodes (LEDs). The two sources were matched by heterochromatic flicker photometry, and their mixture was metameric to ~600 nm. The radiance of the LEDs was controlled by computer-driven electronic circuitry that provided a linear response up to 900 td/LED. A 350 td, 2° test field was superimposed on 8°, 600-nm adapting fields of 100 and 1000 td. We measured modulation sensitivity to 6-Hz flicker for eighteen phases from 0° to 340° and computed an axis of symmetry. Color-normal males had phase axes in the range of 123–173° and 112–156° for adapting fields of 100 and 1000 td (that is, stimulus condition red-leads-green gives minimum sensitivity). In comparison, color-defective males had phase axes of 176–184°. We discuss the data in terms of cone density ratios.

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