bluuebunny/crossref_metadata_2025_split huggingface dataset:
Abstract LB-449: The relationship between CHRNA5 gene polymorphism and the strength of nicotine addiction in lung cancer, COPD and healthy smokers
Authors: Wojas-Krawczyk Kamila , Krawczyk Pawel A. , Biernacka Beata , Kucharczyk Tomasz , Mlak Radosław , Kowalski Dariusz M. , Andrzejuk Jolanta , Milanowski Janusz 
Published: July 2012

Abstract
Introduction. A rare variant of chromosomal region 15q25.1, marked by rs16969968 (substitution 1354G&gt;A or D398N in CHRNA5 gene), was found to be associated with increased lung cancer risk and nicotine dependence appearance. We attempted to confirm the relationship between polymorphism of gene for nicotine acetylocholine receptor A subunit 5 (CHRNA5) and stage of nicotine dependence measured by the result of Fagerström test and cotinine level in serum in lung cancer, COPD and healthy smokers.
Methods. Polymorphism of CHRNA5 gene was analised using PCR-RFLP method in the group of 97 lung cancer patients, 99 COPD patients and 98 healthy volunteers. The Fagerström Test for Nicotine Dependence was used as a standard instrument for assessing the intensity of this physical addiction. Cotinine serum level was measured using ELISA method.
Results. In all analyzed subjects, the frequency of AA, AG and GG genotypes were 11%, 47% and 42%, respectively. The polymorphism of CHRNA5 gene does not have a significant influence on the elevated risk of lung cancer and COPD. The presence of GG genotype decreased the risk of strength of nicotine addiction (HR=0.238, 95%CI:[0.066–0.857], p&lt;0.05). We observed that allele A was presented more frequently in the subjects with high level of nicotine dependence and in the subjects with early (&lt;25 years) onset of addiction (p&lt;0.05). Moreover, cotinine serum level significantly correlated with results of Fagerström test (p&lt;0.001). The carriers of allele A expressed significantly higher level of serum cotinine when compared with the carriers of GG genotype (p=0.05).
Conclusion. In the presented abstract we report for the first time the relationship between the polymorphism of CHRNA5 gene and the strength of nicotine addiction.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr LB-449. doi:10.1158/1538-7445.AM2011-LB-449
Abstract LB-61: Trends in Kidney Cancer.
Authors: Bitkower Jay 
Published: July 2012

Abstract
Kidney cancer_one of only four cancer types that have experienced greater than a 2 percent increase in incidence per year_has not had a significant decline in the mortality rate. According to the National Cancer Institute, kidney cancer incidence has been steadily increasing for the last 65 years. Meanwhile, although Federal funding for the disease has increased, it still lags behind the major cancers, especially when analysed with respect to research dollars per mortality.
A group of kidney cancer survivors and caregivers formed the organization Action to Cure Kidney Cancer (ACKC) out of concerns about the inadequate government and private funding for kidney cancer research. ACKC's primary mission is to advocate specifically for kidney cancer research, and through our advocacy efforts, ACKC has reached out to thousands of kidney cancer survivors throughout the country. With their support, ACKC has met with members of Congress and local political leaders, has mounted letter writing campaigns, conducted briefings on kidney cancer for both the U.S. Senate and House health aides, and initiated a request by the House Labor, Health and Human Services and Education (LHHSE) sub-committee asking the National Cancer Institute to develop a strategic plan to combat kidney cancer. A another major focus of ACKC's efforts is to convince the U.S. Congress to appropriate kidney cancer research money for the Congressionally Directed Medical Research Programs (CDMRP) at the Department of Defense.
In addition to the organization's efforts at the federal level, ACKC raises funds in order to grant awards to researchers developing innovative studies in the field of kidney cancer. ACKC has enabled grants supporting the work to develop an early screening test for kidney cancer based on methylated genes, to investigate the effects of the activation of a human endogenous retrovirus in the pathogenesis of kidney cancer, and to develop a therapy using a cytotoxic agent that destroys cancer cells based on the principle of synthetic lethality, to name a few.
ACKC communicates with its constituency via its website www.ackc.org, Facebook (actiontocurekidneycancer), listservs like ACOR (Association of On-line Cancer Resources), and personal emails. Mr. Bitkower's poster will describe his organization's efforts and accomplishments in increasing research funding for this deadly disease.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr LB-61. doi:10.1158/1538-7445.AM2011-LB-61
Abstract LB-63: From the Golf Course to Education: Outreach & Support for Prostate Cancer
Authors: Brown Egbert 
Published: July 2012

Abstract
Central Ohio Men Against Prostate Cancer provides access to education, outreach and support for diagnosed or at-risk prostate cancer patients, their families, and friends. There is extensive medical information available online and through healthcare providers. The organization's goal is to help people connect with resources that can help them become more aware of prostate cancer, better informed about treatment options, and lead men to seek early screening for prostate cancer.
Prostate cancer is the second leading cause of deaths in African American men. It was estimated that 3,690 deaths from prostate cancer would occur in African American men in 2009. African American men have the highest mortality rate for prostate cancer of any racial or ethnic group in the U.S. An estimated 27,130 cases of prostate cancer were expected to occur among African American men in 2009, accounting for 34 percent of all cancers diagnosed in African American men. Between 2001–2005, the average annual prostate cancer incidence rate was 59 percent higher in African American men than in white men.
Numerous studies have shown that education and support have an impact on the decision of individuals to be screened for prostate cancer, resulting in early detection and diagnosis.
The Central Ohio Men Against Prostate Cancer organization was founded in 2004 by a group of African American gentlemen who were golfing buddies. Since its inception, the group has raised awareness of prostate cancer among all men living in Central Ohio through education, outreach and fundraising. An annual golf tournament has donated funds to the Columbus Cancer Clinic to help cover costs of digital rectal examinations and prostate specific antigen tests for underserved men. The advocacy efforts of the group have extended to participation in national initiatives for prostate cancer, including memberships in the US Too National Prostate Cancer Education and Support Team, memberships in the National Association of Prostate Cancer Advocates, and service as an ad- hoc member of the U. S. Army Research and Materials Command Prostate Cancer Research Program.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr LB-63. doi:10.1158/1538-7445.AM2011-LB-63
Abstract LB-78: A New Paradigm: the Inflammatory Breast Cancer Research Foundation BioBank
Authors: McWilliams Carol 
Published: July 2012

Abstract
The Inflammatory Breast Cancer Research Foundation is a non-profit 501(c) (3) incorporated in 1994, whose mission is to assist scientists and researchers in indentifying the definitive causes of inflammatory breast cancer, and in finding more effective treatments for this highly aggressive form of breast cancer. The organization aims to support research in order to reach an unambiguous definition of inflammatory breast cancer (IBC) and assure that all cases of IBC will be correctly diagnosed, possible sub-types more easily identified, and better treatment outcomes as a result. Research has been hampered by the lack of an easily accessible, well-documented IBC cohort, and IBC cell lines are limited. However, the Inflammatory Breast Cancer Research Foundation has established a BioBank and Clinical Database. The BioBank contains non-tumor DNA, blocks and slides from diagnostic pathology, and medical records describing clinical and pathologic findings at diagnosis providing an invaluable resource. A unique characteristic of this BioBank is the inclusion of specimens and records from deceased patients who had rapid disease progression and resistance to treatment. This data provides valuable comparison for future study.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr LB-78. doi:10.1158/1538-7445.AM2011-LB-78
Abstract LB-80: Building Bridges for Pancreatic Cancer Research
Authors: Peckenpaugh Jason 
Published: July 2012

Abstract
Almost 40 years after President Nixon signed into law the National Cancer Act, the survival rate for pancreatic cancer has not substantially improved. Today, 75 percent of patients diagnosed with pancreatic cancer die within one year of diagnosis, and 94 percent of pancreatic cancer patients will die within five years of diagnosis.
Although pancreatic cancer is the fourth leading cause of cancer death in the U.S., causing 36,800 deaths in 2010, only two percent of the National Cancer Institute's budget is spent on researching the disease ($89.4 million in 2009). Early detection tools for pancreatic cancer do not exist, and thus, patients are typically diagnosed after the disease has metastasized and surgery is no longer a possibility.
Jason Peckenpaugh became an independent advocate for pancreatic cancer patients and research after seeing his father, Jon, bravely battle pancreatic cancer for 18 months until his passing in October 2009. Mr. Peckenpaugh's fight illustrates the statistics above, including his seven month quest to simply discover his diagnosis.
The focus of his advocacy work is communicating scientific information with caregivers, patients, and the public, while sharing the perspective of patients and caregivers with oncologists and researchers. He is participating in the AACR Scientist&lt;–&gt;Survivor Program to improve my knowledge of cancer science and research so that he may become a patient advocate on GI cancer grant committees and/or research control boards. Despite the poor prognosis for patients with pancreatic cancer, this is a promising time for pancreatic cancer research, in part due to grants from the Stand Up 2 Cancer organization, advances in molecular profiling of tumors, and recent research showing the progression of pancreatic cancer. Pancreatic cancer needs a patient advocate at the table wherever gastrointestinal cancers and other cancers are being discussed. Patient advocates serve on grant review boards of the Food and Drug Administration, the Gastrointestinal Specialized Program of Research Excellence (GI SPORE), and other government research consortia.
Mr. Peckenpaugh is a volunteer with the Pancreatic Cancer Action Network (PanCAN) and a volunteer fundraiser for the Lustgarten Foundation and Johns Hopkins University's pancreatic cancer research program. He has raised more than $14,000 for pancreatic cancer research since 2008.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr LB-80. doi:10.1158/1538-7445.AM2011-LB-80
Abstract LB-82: Basal Cell Carcinoma Nevus Syndrome: Networking for Good
Authors: Burr Kristi Schmitt 
Published: July 2012

Abstract
Basal Cell Carcinoma Nevus Syndrome (BCCNS) Life Support Network set out on its journey in 2000 and have since provided support to over 1200 families, stimulated new drug development, and connected with diverse medical specialties – including dermatology, plastic surgery, genetics, cardiology, radiology, oral surgery and dentistry – to increase medical professionals' awareness of the needs of the BCCNS patient community.
The organization's success means a better future for everyone vulnerable to this potentially disabling and life-threatening disease. While BCCNS affects a small portion of the American public (1 in 19,000 or about 16,500 American adults and children annually), the disease comes with significant cost and burdens. As there is no cure and few effective treatments, people suffering with this disease face a lifetime challenge in managing the disease. The numerous skin cancers and jaw cysts_the most common symptoms of the disease_generally require numerous surgeries throughout one's life. In addition, patients' experiences are afflicted by brain tumors, cognitive delays, physical disabilities including auditory, vision and speech impairments. Early diagnosis is important in order for children with BCCNS to survive life-threatening brain tumors and to overcome potential future disability. The financial burden for all patients is significant.
A major hurdle in coping with BCCNS is finding a doctor knowledgeable about the disorder. Securing a prompt diagnosis and appropriate treatment is complicated by the fact that the disease affects so many different parts of the body, thereby crossing over diverse medical specialties. Working with inadequate knowledge, caregivers may use inappropriate therapies which can cause deformities and increased morbidity and mortality. Common treatments, such as radiation and x-rays, can result in the formation of thousands of basal cell carcinomas (BCCs or skin cancers), which are particularly perilous for undiagnosed children exhibiting brain tumors.
To minimize the occurrence of death, widespread networking and education is essential. This is the cornerstone of the organization as it is only through communicating directly with individuals that advocates are made aware of new practices and current concerns. BCCNS is able to connect members with medical professionals in their region, or offer advice on preventative screenings, and serve as a knowledgeable resource. As the only national organization in the United States serving BCCNS patients, the organization has extensive experience in providing educational support to patients and doctors, national credibility and recognition among patients and stakeholders, and well-established communication links with many medical specialties.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr LB-82. doi:10.1158/1538-7445.AM2011-LB-82
Abstract LB-85: Advocacy in Indian Country
Authors: Whitewolf Celeste 
Published: July 2012

Abstract
Native People's Circle of Hope (NPCOH) aims to help cancer survivors, their family members and caregivers understand they are not alone. Advocating for quality health care for native people is NPCOH's primary goal. NPCOH projects include the Medicine Bag Project, which gifts newly diagnosed cancer survivors items they may need during treatment; the Native Hope Project, which promotes wearing yellow (the color of hope) in traditional regalia to show solidarity with cancer survivors; the Roots of Strength Annual Conference; the Speaker's Bureau; and the educational training session titled, “How to Start Your Own Cancer Support Group.” Local chapters are the basis of community support and advocacy. NPCOH's AACR poster features the activities of the local chapters and provides examples of their personalized projects.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr LB-85. doi:10.1158/1538-7445.AM2011-LB-85
Abstract LB-9: Intersection of Notch and ERBB signalling in melanoma
Authors: Bedogni Barbara 
Published: July 2012

Abstract
Malignant melanoma is an aggressive malignancy of the melanocytes. The incidence rates for melanoma are steadily increasing and melanoma has now become the most common form of cancer among young adults between the ages of 25 and 29 years old. Because melanomas are highly resistant to the majority of therapies, the survival rate for patients with metastatic disease is less than 15%. There is a clear need for novel more effective therapies.
Identification of the signaling pathways that are altered in melanoma provides opportunities for the development of novel targeted therapies. The Notch pathway is an evolutionary conserved signaling cascade that has an essential role in embryonic development but is inappropriately active in various types of cancers. Studies from our group and others have shown that hyper activation of Notch1 is an early event in melanocyte transformation and modulates both growth and metastasis in melanoma.
We have found a new interaction between Notch1 and neuregulin1 (NRG1) signaling that plays a role in melanoma. Neuregulin1 is the ligand for ERBB3, a member of the Epidermal Growth Factor family of receptors that are involved in the genesis and progression of a number of cancers. Notch1 binds to the NRG1 promoter thereby modulating NRG1 expression and consequently the activation of the ERBB3 pathway. Inhibition of either NRG1 or ERBB3 activity in melanoma cells lead to cell growth inhibition and tumor growth delay similar to Notch1 inhibition. Mechanistically, these effects are dependent on the accumulation of p27 following either NRG1 or Notch1 down regulation. In addition, we find that NRG1/ERBB3 signaling influences Notch1 activation likely through the modulation of the Notch ligands Jaggged-1 (JAG-1) and Delta like 3 (Dll3), thus providing a feed forward regulatory loop linking the two pathways.
Taken together, our findings underline a new, previously undescribed interaction between Notch1 and NRG1/ERBB3 in melanoma. Our goal is to investigate the mechanisms by which these two oncogenic signaling pathways intersect to promote a highly aggressive disease phenotype and to provide experimental evidence that the targeting of Notch and ERBB signaling is a tractable and effective approach to treat forms of melanoma that may be resistant to current available therapies.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr LB-9. doi:10.1158/1538-7445.AM2011-LB-9
Abstract LB-99: Bif-1 promotes EGFR endocytic degradation and contributes to suppression of metastatic potential in breast and colon cancers
Authors: Runkle Kristin B. , Takahashi Yoshinori , Wang Hong-Gang 
Published: July 2012

Abstract
Bif-1, a member of the endophilin B protein family, is involved in apoptosis and autophagy induction and in regulating membrane dynamics of organelles such as the Golgi and mitochondria. While endophilin A family members are involved in the formation and fission of endocytic vesicles at the plasma membrane, recent data suggest a role for Bif-1 in promoting epidermal growth factor receptor (EGFR) endocytic degradation. Increased EGFR expression is seen in a variety of tumors including breast and colorectal cancers and has been correlated with disease progression, poor survival, poor response to therapy, and resistance to cytotoxic agents. Activation of EGFR promotes cell growth, differentiation, survival, and migration through MAPK, PI3K, STAT, and Src signaling pathways; whereas signal termination and receptor down-regulation occur primarily through clathrin-mediated endocytosis and lysosomal degradation. However, the mechanism through which Bif-1 regulates EGFR endocytic trafficking and degradation has not been thoroughly investigated. Here we report that suppression of Bif-1 expression in breast and colon cancer cells delays EGFR degradation. While Bif-1 depletion does not disrupt EGFR internalization or trafficking to the vicinity of LAMP-1 positive late endosomes/lysosomes, endosome maturation and endosome/lysosome fusion seem to be suppressed in cells lacking Bif-1. Moreover, knockdown of Bif-1 enhances breast cancer cell migration and invasion. These findings, together with previous data showing that loss of Bif-1 promotes tumorigenesis in mice and that decreased expression of Bif-1 is seen in many types of human cancers including breast and colorectal cancers, further suggest that Bif-1 functions as a tumor suppressor. In addition to its roles in apoptosis and autophagy induction, this study supports a new role for Bif-1 in regulating the late stages of EGFR lysosomal degradation and identifies Bif-1 as a suppressor of metastatic potential in breast cancer.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr LB-99. doi:10.1158/1538-7445.AM2011-LB-99
Abstract PL02-01: A systems biology approach to integrative cancer genomics
Authors: Califano Andrea 
Published: July 2012

Abstract
The recent onslaught of molecular data across multiple human malignancies is producing an unprecedented repertoire of genetic and epigenetic alterations contributing to tumorigenesis and progression. Yet, the direct impact of this knowledge on tumor treatment and prevention is still largely unproven. Loss of tumor suppressor function is difficult to target pharmacologically and, with a handful of exceptions, alterations providing potential drug targets are relatively infrequent in cancer patients and are thus unlikely to support clinical development.
By reconstructing and interrogating the regulatory logic of the cancer cell, which is responsible for integrating multiple aberrant signals in vivo, systems biology is starting to elucidate broad addiction mechanisms, both oncogene and non-oncogene based that are exquisitely specific to the cancer subtype. In this presentation, we will discuss recent result in the discovery of synergistic, non-oncogene addiction mechanisms in high-grade glioma, of the upstream genetic alterations causally related to their functional activation, and of candidate targets for combination therapy. This approach has been generalized to a number of additional tumor subtypes and provides a novel framework for cancer target discovery and development in patient-centric fashion.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr PL02-01. doi:10.1158/1538-7445.AM2011-PL02-01