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Relevant bibliographies by topics / George (Philadelphia, Pa.)

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Academic literature on the topic 'George (Philadelphia, Pa.)'

Author: Grafiati

Published: 4 June 2021

Last updated: 31 January 2023

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Journal articles on the topic "George (Philadelphia, Pa.)"

1

Wheeler, Nicholas J. "Book Review: George J. Andreopoulos, Genocide: Conceptual and Historical Dimensions (Philadelphia, PA: University of Pennsylvania Press, 1994, 265 pp., no price given)." Millennium: Journal of International Studies 25, no. 1 (March 1996): 154–56. http://dx.doi.org/10.1177/03058298960250010903.

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2

Kien, C. Lawrence. "Book Reviews: NUTRITIONAL CARE FOR HIGH RISK NEW-BORNS, Ohio Neonatal Nutritionists. George F. Stickley Company, Philadelphia, PA, 1985, 214 pp, $17.50." Journal of Parenteral and Enteral Nutrition 11, no. 4 (July 1987): 428–29. http://dx.doi.org/10.1177/014860718701100420.

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3

Drell, Joanna H. "Florence and Its Church in the Age of Dante. By George W. Dameron. (Philadelphia, Pa.: University of Pennsylvania Press, 2005. Pp.x, 374. $65.00.)." Historian 70, no. 4 (December 1, 2008): 828–29. http://dx.doi.org/10.1111/j.1540-6563.2008.00227_52.x.

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4

Yang, Li, Jae Young So, Nicolas Skrypek, Anand Merchant, George Nelson, Howard Yang, and Maxwell Lee. "Abstract P1-05-08: Targeting tumor heterogeneity and breast cancer metastasis through the metastatic microenvironment mediated epigenetic reprogramming." Cancer Research 82, no. 4_Supplement (February 15, 2022): P1–05–08—P1–05–08. http://dx.doi.org/10.1158/1538-7445.sabcs21-p1-05-08.

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Abstract Targeting tumor heterogeneity and breast cancer metastasis through the metastaticmicroenvironment mediated epigenetic reprogrammingLi Yang and Jae Young So, Nicolas Skrypek, Anand Merchant, George Nelson, Howard H.Yang, Maxwell P. LeeNational Cancer Institute, National Institutes of Health, Bethesda, MD 20892Current cancer treatments are largely based on the genetic characterization of primarytumors and are ineffective for metastatic disease. There is lack of mechanistic understanding ashow cancer cells are selected and evolved to establish distant metastatic colonies. In addition,tumor heterogeneity and biomarker identification remain to be some of the most difficultchallenges in cancer treatment. In the current study, we discovered an increased DNAmethyltransferase 3B (DNMT3B) in metastatic nodules and in tumor cells with epithelia tomesenchymal (EMT) phenotype. Of great interest, high levels of DNMT3B were correlated withpoor clinical outcomes in multiple human breast cancer datasets. Mechanistically, DNMT3Balters multiple pathways including STAT3, NFkappaB, PI3K/Akt, beta-catenin, Notch signalingas well as EMT, which are critical for cancer cell survival, apoptosis, proliferation, invasion, andcolonization. We further identified PGE2 and IL6 as critical inflammatory mediators inDNMT3B induction. Importantly, targeting IL6 or PGE2 production reduced DNMT3Bexpression and improved chemo treatment or PD1 immune therapy. Furthermore, perioperative(surgical removal of primary tumors) targeting DNMT3B in combination with chemotherapymarkedly suppressed tumor recurrence and metastasis in preclinical mouse models for triplenegative breast cancer. Our studies identify DNMT3B as an important mechanism fortranscription regulation in tumor heterogeneity that is critical for tumor invasion and metastasis,thus suggesting a validated target for treating metastatic disease. Citation Format: Li Yang, Jae Young So, Nicolas Skrypek, Anand Merchant, George Nelson, Howard Yang, Maxwell Lee. Targeting tumor heterogeneity and breast cancer metastasis through the metastatic microenvironment mediated epigenetic reprogramming [abstract]. In: Proceedings of the 2021 San Antonio Breast Cancer Symposium; 2021 Dec 7-10; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2022;82(4 Suppl):Abstract nr P1-05-08.

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5

Eksi, Ece Sebnem, Zeynep Sayar, Alex Chitsazan, George T. Thomas, Andrew Adey, Paul T. Spellman, and Ryan Kopp. "Abstract 999: Epigenetic loss of heterogeneity from low to high grade localized prostate tumors." Cancer Research 82, no. 12_Supplement (June 15, 2022): 999. http://dx.doi.org/10.1158/1538-7445.am2022-999.

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Abstract Identifying precise molecular subtypes attributable to specific stages of localized prostate cancer has proven difficult due to high levels of heterogeneity. Bulk assays represent a population-average, which mask the heterogeneity that exists at the single-cell level. In this work, we sequenced the accessible chromatin regions of 14,424 single-cells from 18 flash-frozen prostate tumors. We observe shared chromatin features among low-grade prostate cancer cells are lost in high-grade tumors. Despite this loss, high-grade tumors exhibit an enrichment for FOXA1, HOXB13 and CDX2 transcription factor binding sites, indicating a shared trans-regulatory program. We identify two unique genes encoding neuronal adhesion molecules that are highly accessible in high-grade prostate tumors. We show NRXN1 and NLGN1 expression in epithelial, endothelial, immune and neuronal cells in prostate cancer using cyclic immunofluorescence. Our results provide a deeper understanding of the active gene regulatory networks in primary prostate tumors, critical for molecular stratification of the disease. Citation Format: Ece Sebnem Eksi, Zeynep Sayar, Alex Chitsazan, George T. Thomas, Andrew Adey, Paul T. Spellman, Ryan Kopp. Epigenetic loss of heterogeneity from low to high grade localized prostate tumors [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 999.

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6

Doucet, Brian. "Driving Detroit: The Quest for Respect in the Motor City. by George Galster 2012. Philadelphia, PA: University of Pennsylvania Press. 328 pp. ISBN 978-0-8122-4429-8." Tijdschrift voor economische en sociale geografie 105, no. 3 (June 6, 2014): 368–69. http://dx.doi.org/10.1111/tesg.12089.

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7

D'Rozario, Joshua, Julie George, and Roman Thomas. "Abstract 6028: Patient derived organoids demonstrate hallmark characteristics of small cell lung cancer." Cancer Research 82, no. 12_Supplement (June 15, 2022): 6028. http://dx.doi.org/10.1158/1538-7445.am2022-6028.

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Abstract Small cell lung cancer (SCLC) accounts for approximately 15% of all lung cancers with an overall 5-year survival rate of 5-10%. Although transgenic mouse models and patient derived xenograft models have been shown to capture the heterogeneity and complexity of SCLC, the costs involved and timeframe of generating these models can be extensive. Furthermore, these models lack the ability to study the patients’ immune components and tumor microenvironment. Alternatively, in other cancer types in vitro methods to generate organoids have been successful in the hope to develop personalized patient derived organoids for screening and further downstream analyses. Here, we have generated and characterized small cell lung cancer patient-derived tumor organoids and confirmed that the organoids possess similar molecular characteristics, genetic profiles and morphological architectures to the corresponding patient tumor tissue. Organoids were shown to express hallmark features for SCLC, which included expression of neuroendocrine markers CD56, CHGA, INSM1 and SYP shown by immunohistochemistry. We suggest utilizing these organoids as SCLC patient models would be ideal for investigating the tumor microenvironment in SCLC, mechanisms between tumor immune cell interactions as well as assessing patients’ responses to therapy. Citation Format: Joshua D'Rozario, Julie George, Roman Thomas. Patient derived organoids demonstrate hallmark characteristics of small cell lung cancer [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 6028.

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8

Ku, Amy T., Adelaide Young, Ahmed A. Ibrahim, Wen Bu, Weiyu Jiang, Meng Lin, Laterrica C. Williams, et al. "Abstract P007: Short-term PI3K inhibition prevents breast cancer in preclinical models." Cancer Prevention Research 16, no. 1_Supplement (January 1, 2023): P007. http://dx.doi.org/10.1158/1940-6215.precprev22-p007.

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Abstract Antiestrogen medication is the only chemoprevention currently available for women at a high risk of developing breast cancer; however, antiestrogen therapy requires years to achieve efficacy and has adverse side effects. Therefore, it is important to develop an efficacious chemoprevention strategy that requires only a short course of treatment. PIK3CA is commonly activated in breast atypical hyperplasia, the known precancerous precursor of breast cancer. Targeting PI3K signaling in these precancerous lesions may offer a new strategy for chemoprevention. Here, we first established a mouse model that mimics the progression from precancerous lesions to breast cancer. Next, we demonstrated that a short course prophylactic treatment with the clinically approved PI3K inhibitor alpelisib slowed early lesion expansion and prevented cancer formation in this model. Furthermore, we showed that alpelisib suppressed ex vivo expansion of patient-derived atypical hyperplasia. Together, these data indicate that the progression of breast precancerous lesions heavily depends on the PI3K signaling, and that prophylactic targeting of PI3K activity can prevent breast cancer. Citation Format: Amy T. Ku, Adelaide Young, Ahmed A. Ibrahim, Wen Bu, Weiyu Jiang, Meng Lin, Laterrica C. Williams, Bryant McCue, George Miles, Chandandeep Nagi, Fariba Behbod, Yi Li. Short-term PI3K inhibition prevents breast cancer in preclinical models. [abstract]. In: Proceedings of the AACR Special Conference: Precision Prevention, Early Detection, and Interception of Cancer; 2022 Nov 17-19; Austin, TX. Philadelphia (PA): AACR; Can Prev Res 2023;16(1 Suppl): Abstract nr P007.

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9

Calin, George A. "Abstract IA025: About motifs, non-codingRNAs and metastases." Cancer Research 83, no. 2_Supplement_2 (January 15, 2023): IA025. http://dx.doi.org/10.1158/1538-7445.metastasis22-ia025.

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Abstract MicroRNA and other short or long non-codingRNAs alterations are involved in the initiation, progression and metastases of human cancer. The main molecular alterations are represented by variations in gene expression, usually mild and with consequences for a vast number of target protein coding genes. The causes of the widespread differential expression of non-codingRNAs in malignant compared with normal cells can be explained by the location of these genes in cancer-associated genomic regions, by epigenetic mechanisms and by alterations in the processing machinery. MicroRNA and other short or long non-codingRNAs expression profiling of human tumors has identified signatures associated with diagnosis, staging, progression, prognosis and response to treatment. In addition, profiling has been exploited to identify non-codingRNAs that may represent downstream targets of activated oncogenic pathways or that are targeting protein coding genes involved in cancer. Recent studies proved that miRNAs and non-coding ultraconserved genes are main candidates for the elusive class of cancer predisposing genes and that other types of non-codingRNAs participate in the genetic puzzle giving rise to the malignant phenotype. These discoveries could be exploited for the development of useful markers for diagnosis and prognosis, as well as for the development of new RNA-based cancer therapies. Citation Format: George A. Calin. About motifs, non-codingRNAs and metastases [abstract]. In: Proceedings of the AACR Special Conference: Cancer Metastasis; 2022 Nov 14-17; Portland, OR. Philadelphia (PA): AACR; Cancer Res 2022;83(2 Suppl_2):Abstract nr IA025.

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10

Sanchez-Covarrubias, Alex P., Ramlogan Sowamber, Leah Dodds, Andre Pinto, Sophia George, and Matthew Schlumbrecht. "Abstract C052: Endometrial cancer genomics varies by race." Cancer Epidemiology, Biomarkers & Prevention 32, no. 1_Supplement (January 1, 2023): C052. http://dx.doi.org/10.1158/1538-7755.disp22-c052.

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Abstract Introduction Variability in endometrial cancer (EC) risk and outcomes exist, with Black women disproportionately negatively affected related to White women. The biologic etiologies of these observations are poorly understood. Our objective was to describe the somatic mutations of the tumor genome and compare them to RNA expression in self-identified Black and White women diagnosed with EC. Methods Women with newly diagnosed EC and undergoing hysterectomy were recruited prospectively. Fresh tumors obtained at the time of surgery were flash-frozen, underwent DNA and RNA extraction and were submitted for whole exome sequencing (WES) analysis (DNA) or bulk RNA sequencing analysis. Differentially expressed genes between racial groups and tumor grade were calculated using Deseq2. Genomic ancestry was determined using ADMIXTURE. Chi-square and Mann Whitney U tests were used for analyses, with a threshold for significance of p<0.05. Results A total of 49 patients with EC were included. Thirty (61.2%) women were diagnosed with low-grade EC and 19 (38.8%) with high grade EC. Twenty (40.8%) women self-identified as Black, 27 (55.1%) as White and 2 (4.1%) as Asian/other. Admixture analysis showed that 36 (73.4%) had >14% African ancestry. The remaining 13 (26.5%) patients had admixed European and Native American ancestry, with <1% African ancestry. In the RNA-seq, we found significant DEGs by tumor grade; with 2132 DEG in High grade compared to Low grade tumors with a false discovery rate of <0.05 and a fold change (FC) of ≤-1.5 or ≥1.5. Top 10 DEG included MT4, TAF15, SLFN5 and PLEKHS1 (upregulated) and MCRIP1, MAZ, MYOM3, PRPH, BCL7C, AC016700.5 (downregulated). In the WES analysis, 8 Black women had mutations in GON4L compared to 1 in the White woman (44.4% vs 3.7%, padj=0.04); and 7 Black women had a mutation in PRAMEF14 compared to 1 White woman (38.8% vs 3.7%, padj= 0.06). Conclusion GON4L, which is a transcription factor associated with decreased apoptosis and promotion of tumor growth through CD24 regulation, was significantly more mutated in the EC genome of Black women relative to White women. Somatic mutation and transcriptional changes are seen between tumor grade and self-identified race and require further exploration for its relationship to aggressive disease. Citation Format: Alex P. Sanchez-Covarrubias, Ramlogan Sowamber, Leah Dodds, Andre Pinto, Sophia George, Matthew Schlumbrecht. Endometrial cancer genomics varies by race [abstract]. In: Proceedings of the 15th AACR Conference on the Science of Cancer Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; 2022 Sep 16-19; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2022;31(1 Suppl):Abstract nr C052.

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Books on the topic "George (Philadelphia, Pa.)"

1

Fisher, Sidney George. A Philadelphia perspective: The Civil War diary of Sidney George Fisher. New York, NY: Fordham University Press, 2007.

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2

General Howe's dog: George Washington, the Battle of Germantown, and the dog who crossed enemy lines. New York: Chamberlain Bros., 2005.

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3

Pa.) Republican National Convention (37th 2000 Philadelphia. Official report of the proceedings of the Thirty-seventh Republican National Convention, held in Philadelphia, Pennsylvania, July 31, 2000, August 1, 2, 3, 2000: Resulting in the nomination of George W. Bush, of Texas, for president, and the nomination of Dick Cheney, of Wyoming, for vice president. United States]: Republican National Committee, 2000.

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Pickett's charge: The untold story. Fort Lee, NJ: Barricade Books, 2013.

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Jennifer, Fox, and Juarez Fernando ill, eds. A feast of freedom: Tasty tidbits from the City Tavern. Philadelphia: Running Press Kids, 2010.

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Grindle, Lucretia W. The nightspinners: A novel. New York: Random House, 2003.

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Romero, George A. Dawn of the Dead. George Romero, Susanna Sparrow. Sphere, 2012.

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Fisher, Sidney George. A Philadelphia Perspective: The Civil War Diary of Sidney George Fisher (North's Civil War). Fordham University Press, 2007.

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Fisher, Sidney George. A Philadelphia Perspective: The Civil War Diary of Sidney George Fisher (North's Civil War). Fordham University Press, 2007.

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Jones, Russ. Death of George Arthur Palmer. America Star Books, 2009.

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Conference papers on the topic "George (Philadelphia, Pa.)"

1

Beggs, Robert. "Preserve, Educate and Inspire - Founding the American Helicopter Museum and Education Center." In Vertical Flight Society 77th Annual Forum & Technology Display. The Vertical Flight Society, 2021. http://dx.doi.org/10.4050/f-0077-2021-16813.

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The American Helicopter Museum and Education Center opened to the public at the Brandywine Airport on October 18, 1996. This milestone was the realization of a vision adopted at a luncheon meeting hosted by the Philadelphia Chapter of the American Helicopter Society on July 30, 1993. Chapter leaders had previously brainstormed potential ideas for commemorating the upcoming 50th Anniversary of the American Helicopter Society in 1994, but recognized the need to engage a broader constituency to do something significant. With the goal of establishing a 50th Anniversary Committee, a luncheon was scheduled at Boeing Helicopters in Ridley Park, PA. Participants included the author, several Chapter officers and an invitation list that included Philadelphia area rotary-wing business leaders, industry pioneers and influencers. Attendees at that first meeting included Lee Douglas, Frank Duke, Vincent Genovese, Euan Hooper, Warren Jacobs, Wes Moore, Ren Pierpoint, John Schneider, George Townson, Edward B. Wilford III and Peter Wright, Sr. After debating multiple options for the commemoration, the idea of a museum was embraced when Peter Wright, then President of Keystone Helicopters, offered to donate several vintage helicopters if a museum was established. Two weeks later, the nascent 50th Anniversary Committee met again with a mission to: “Lay the foundation for a permanent rotary-wing restoration, conservation and exhibition facility in the Delaware Valley.” Referencing the documented minutes of the aforementioned meeting and that of subsequent meetings of the 50th Anniversary Committee, other documents and the recollections of the author, this paper will trace the formative years of the museum from July 1993 to October 1996. It will address the many challenges of founding an aviation museum including incorporation, location identification, building the collection and creating the exhibits and programs. It will recall the people involved and their significant contributions. This paper is particularly compelling to publish this year, recognizing the 25th anniversary of the American Helicopter Museum and Education Center on 18 October 2021.

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