Search

Your search keyword '"Siegel, Marni B."' showing total 35 results
Start Over Author "Siegel, Marni B."
35 results on '"Siegel, Marni B."'

1. Integrated RNA and DNA sequencing reveals early drivers of metastatic breast cancer

Author

Siegel, Marni B., He, Xiaping, Hoadley, Katherine A., Hoyle, Alan, Pearce, Julia B., Garrett, Amy L., Kumar, Sunil, Moylan, Vincent J., Brady, Claudia M., Van Swearingen, Amanda E.D., Marron, David, Gupta, Gaorav P., Thorne, Leigh B., Kieran, Niamh, Livasy, Chad, Mardis, Elaine R., Parker, Joel S., Chen, Mengjie, Anders, Carey K., Carey, Lisa A., and Perou, Charles M.

Subjects
Cancer genetics -- Research, DNA sequencing -- Usage -- Health aspects, RNA sequencing -- Usage -- Health aspects, Breast cancer -- Genetic aspects -- Development and progression, Cancer metastasis -- Genetic aspects -- Development and progression, Health care industry
Abstract

Breast cancer metastasis remains a clinical challenge, even within a single patient across multiple sites of the disease. Genome-wide comparisons of both the DNA and gene expression of primary tumors and metastases in multiple patients could help elucidate the underlying mechanisms that cause breast cancer metastasis. To address this issue, we performed DNA exome and RNA sequencing of matched primary tumors and multiple metastases from 16 patients, totaling 83 distinct specimens. We identified tumor-specific drivers by integrating known protein-protein network information with RNA expression and somatic DNA alterations and found that genetic drivers were predominantly established in the primary tumor and maintained through metastatic spreading. In addition, our analyses revealed that most genetic drivers were DNA copy number changes, the TP53 mutation was a recurrent founding mutation regardless of subtype, and that multiclonal seeding of metastases was frequent and occurred in multiple subtypes. Genetic drivers unique to metastasis were identified as somatic mutations in the estrogen and androgen receptor genes. These results highlight the complexity of metastatic spreading, be it monoclonal or multiclonal, and suggest that most metastatic drivers are established in the primary tumor, despite the substantial heterogeneity seen in the metastases., Introduction Breast cancer remains the second leading cause of cancer-related death in women in the United States and is typically caused by metastasis. Significant genetic heterogeneity exists both within a [...]

Published
2018
Full Text
View/download PDF

2. Supplemental Methods from Efficacy of Carboplatin Alone and in Combination with ABT888 in Intracranial Murine Models of BRCA-Mutated and BRCA–Wild-Type Triple-Negative Breast Cancer

Author

Karginova, Olga, primary, Siegel, Marni B., primary, Van Swearingen, Amanda E.D., primary, Deal, Allison M., primary, Adamo, Barbara, primary, Sambade, Maria J., primary, Bazyar, Soha, primary, Nikolaishvili-Feinberg, Nana, primary, Bash, Ryan, primary, O'Neal, Sara, primary, Sandison, Katie, primary, Parker, Joel S., primary, Santos, Charlene, primary, Darr, David, primary, Zamboni, William, primary, Lee, Yueh Z., primary, Miller, C. Ryan, primary, and Anders, Carey K., primary

Published
2023
Full Text
View/download PDF

3. Supplemental Table from Efficacy of Carboplatin Alone and in Combination with ABT888 in Intracranial Murine Models of BRCA-Mutated and BRCA–Wild-Type Triple-Negative Breast Cancer

Author

Karginova, Olga, primary, Siegel, Marni B., primary, Van Swearingen, Amanda E.D., primary, Deal, Allison M., primary, Adamo, Barbara, primary, Sambade, Maria J., primary, Bazyar, Soha, primary, Nikolaishvili-Feinberg, Nana, primary, Bash, Ryan, primary, O'Neal, Sara, primary, Sandison, Katie, primary, Parker, Joel S., primary, Santos, Charlene, primary, Darr, David, primary, Zamboni, William, primary, Lee, Yueh Z., primary, Miller, C. Ryan, primary, and Anders, Carey K., primary

Published
2023
Full Text
View/download PDF

4. Supplemental Figure Legends from Efficacy of Carboplatin Alone and in Combination with ABT888 in Intracranial Murine Models of BRCA-Mutated and BRCA–Wild-Type Triple-Negative Breast Cancer

Author

Karginova, Olga, primary, Siegel, Marni B., primary, Van Swearingen, Amanda E.D., primary, Deal, Allison M., primary, Adamo, Barbara, primary, Sambade, Maria J., primary, Bazyar, Soha, primary, Nikolaishvili-Feinberg, Nana, primary, Bash, Ryan, primary, O'Neal, Sara, primary, Sandison, Katie, primary, Parker, Joel S., primary, Santos, Charlene, primary, Darr, David, primary, Zamboni, William, primary, Lee, Yueh Z., primary, Miller, C. Ryan, primary, and Anders, Carey K., primary

Published
2023
Full Text
View/download PDF

5. Data from Efficacy of Carboplatin Alone and in Combination with ABT888 in Intracranial Murine Models of BRCA-Mutated and BRCA–Wild-Type Triple-Negative Breast Cancer

Author

Karginova, Olga, primary, Siegel, Marni B., primary, Van Swearingen, Amanda E.D., primary, Deal, Allison M., primary, Adamo, Barbara, primary, Sambade, Maria J., primary, Bazyar, Soha, primary, Nikolaishvili-Feinberg, Nana, primary, Bash, Ryan, primary, O'Neal, Sara, primary, Sandison, Katie, primary, Parker, Joel S., primary, Santos, Charlene, primary, Darr, David, primary, Zamboni, William, primary, Lee, Yueh Z., primary, Miller, C. Ryan, primary, and Anders, Carey K., primary

Published
2023
Full Text
View/download PDF

6. Supplemental Figures S1-S9 from Efficacy of Carboplatin Alone and in Combination with ABT888 in Intracranial Murine Models of BRCA-Mutated and BRCA–Wild-Type Triple-Negative Breast Cancer

Author

Karginova, Olga, primary, Siegel, Marni B., primary, Van Swearingen, Amanda E.D., primary, Deal, Allison M., primary, Adamo, Barbara, primary, Sambade, Maria J., primary, Bazyar, Soha, primary, Nikolaishvili-Feinberg, Nana, primary, Bash, Ryan, primary, O'Neal, Sara, primary, Sandison, Katie, primary, Parker, Joel S., primary, Santos, Charlene, primary, Darr, David, primary, Zamboni, William, primary, Lee, Yueh Z., primary, Miller, C. Ryan, primary, and Anders, Carey K., primary

Published
2023
Full Text
View/download PDF

7. Orphan Gpr182 suppresses ERK-mediated intestinal proliferation during regeneration and adenoma formation

Author

Kechele, Daniel O., Blue, R. Eric, Zwarycz, Bailey, Espenschied, Scott T., Mah, Amanda T., Siegel, Marni B., Perou, Charles M., Ding, Shengli, Magness, Scott T., Lund, P. Kay, and Caron, Kathleen M.

Subjects
Adenoma -- Genetic aspects -- Development and progression, Gene expression -- Health aspects, Phosphotransferases -- Health aspects, Cellular signal transduction -- Genetic aspects -- Health aspects, Cell receptors -- Health aspects, Health care industry
Abstract

Orphan GPCRs provide an opportunity to identify potential pharmacological targets, yet their expression patterns and physiological functions remain challenging to elucidate. Here, we have used a genetically engineered knockin reporter mouse to map the expression pattern of the Gpr182 during development and adulthood. We observed that Gpr182 is expressed at the crypt base throughout the small intestine, where it is enriched in crypt base columnar stem cells, one of the most active stem cell populations in the body. Gpr182 knockdown had no effect on homeostatic intestinal proliferation in vivo, but led to marked increases in proliferation during intestinal regeneration following irradiation-induced injury. In the [Apc.sup.Min] mouse model, which forms spontaneous intestinal adenomas, reductions in Gpr182 led to more adenomas and decreased survival. Loss of Gpr182 enhanced organoid growth efficiency ex vivo in an EGF-dependent manner. Gpr182 reduction led to increased activation of ERK1/2 in basal and challenge models, demonstrating a potential role for this orphan GPCR in regulating the proliferative capacity of the intestine. Importantly, GPR182 expression was profoundly reduced in numerous human carcinomas, including colon adenocarcinoma. Together, these results implicate Gpr182 as a negative regulator of intestinal MAPK signaling-induced proliferation, particularly during regeneration and adenoma formation., Introduction Deorphanization of GPCRs remains an active area of research, especially considering that approximately 40% of all approved drugs for humans target only a small fraction of the GPCRome (1, [...]

Published
2017
Full Text
View/download PDF

9. HIF1α and HIF2α independently activate SRC to promote melanoma metastases

Author

Hanna, Sara C., Krishnan, Bhavani, Bailey, Sean T., Moschos, Stergios J., Kuan, Pei-Fen, Shimamura, Takeshi, Osborne, Lukas D., Siegel, Marni B., Duncan, Lyn M., O'Brien, III, E. Tim, Superfine, Richard, Miller, C. Ryan, Simon, M. Celeste, Wong, Kwok-Kin, and Kim, William Y.

Subjects
Metastasis -- Genetic aspects, Cancer -- Genetic aspects, Melanoma -- Genetic aspects -- Development and progression, Health care industry
Abstract

Malignant melanoma is characterized by a propensity for early lymphatic and hematogenous spread. The hypoxia-inducible factor (HIF) family of transcription factors is upregulated in melanoma by key oncogenic drivers. HIFs [...]

Published
2013
Full Text
View/download PDF

10. Tumor Evolution in Two Patients with Basal-like Breast Cancer: A Retrospective Genomics Study of Multiple Metastases

Author

Hoadley, Katherine A., Siegel, Marni B., Kanchi, Krishna L., Miller, Christopher A., Ding, Li, Zhao, Wei, He, Xiaping, Parker, Joel S., Wendl, Michael C., Fulton, Robert S., Demeter, Ryan T., Wilson, Richard K., Carey, Lisa A., Perou, Charles M., and Mardis, Elaine R.

Subjects
Breast cancer -- Genetic aspects -- Development and progression -- Care and treatment, Gene expression -- Health aspects, Cancer metastasis -- Genetic aspects -- Development and progression -- Care and treatment, Biological sciences
Abstract

Background Metastasis is the main cause of cancer patient deaths and remains a poorly characterized process. It is still unclear when in tumor progression the ability to metastasize arises and whether this ability is inherent to the primary tumor or is acquired well after primary tumor formation. Next-generation sequencing and analytical methods to define clonal heterogeneity provide a means for identifying genetic events and the temporal relationships between these events in the primary and metastatic tumors within an individual. Methods and Findings We performed DNA whole genome and mRNA sequencing on two primary tumors, each with either four or five distinct tissue site-specific metastases, from two individuals with triple-negative/basal-like breast cancers. As evidenced by their case histories, each patient had an aggressive disease course with abbreviated survival. In each patient, the overall gene expression signatures, DNA copy number patterns, and somatic mutation patterns were highly similar across each primary tumor and its associated metastases. Almost every mutation found in the primary was found in a metastasis (for the two patients, 52/54 and 75/75). Many of these mutations were found in every tumor (11/54 and 65/75, respectively). In addition, each metastasis had fewer metastatic-specific events and shared at least 50% of its somatic mutation repertoire with the primary tumor, and all samples from each patient grouped together by gene expression clustering analysis. TP53 was the only mutated gene in common between both patients and was present in every tumor in this study. Strikingly, each metastasis resulted from multiclonal seeding instead of from a single cell of origin, and few of the new mutations, present only in the metastases, were expressed in mRNAs. Because of the clinical differences between these two patients and the small sample size of our study, the generalizability of these findings will need to be further examined in larger cohorts of patients. Conclusions Our findings suggest that multiclonal seeding may be common amongst basal-like breast cancers. In these two patients, mutations and DNA copy number changes in the primary tumors appear to have had a biologic impact on metastatic potential, whereas mutations arising in the metastases were much more likely to be passengers., Author(s): Katherine A. Hoadley 1,2, Marni B. Siegel 1,2, Krishna L. Kanchi 3, Christopher A. Miller 3, Li Ding 3, Wei Zhao 1,2, Xiaping He 2, Joel S. Parker 1,2, [...]

Published
2016
Full Text
View/download PDF

11. Cross-species transcriptional analysis reveals conserved and host-specific neoplastic processes in mammalian glioma

Author

Connolly, Nina P., Shetty, Amol C., Stokum, Jesse A., Hoeschele, Ina, Siegel, Marni B., Miller, C. Ryan, Kim, Anthony J., Ho, Cheng-Ying, Davila, Eduardo, Simard, J. Marc, Devine, Scott E., Rossmeisl, John H. Jr., Holland, Eric C., Winkles, Jeffrey A., Woodworth, Graeme F., Connolly, Nina P., Shetty, Amol C., Stokum, Jesse A., Hoeschele, Ina, Siegel, Marni B., Miller, C. Ryan, Kim, Anthony J., Ho, Cheng-Ying, Davila, Eduardo, Simard, J. Marc, Devine, Scott E., Rossmeisl, John H. Jr., Holland, Eric C., Winkles, Jeffrey A., and Woodworth, Graeme F.

Abstract

Glioma is a unique neoplastic disease that develops exclusively in the central nervous system (CNS) and rarely metastasizes to other tissues. This feature strongly implicates the tumor-host CNS microenvironment in gliomagenesis and tumor progression. We investigated the differences and similarities in glioma biology as conveyed by transcriptomic patterns across four mammalian hosts: rats, mice, dogs, and humans. Given the inherent intra-tumoral molecular heterogeneity of human glioma, we focused this study on tumors with upregulation of the platelet-derived growth factor signaling axis, a common and early alteration in human gliomagenesis. The results reveal core neoplastic alterations in mammalian glioma, as well as unique contributions of the tumor host to neoplastic processes. Notable differences were observed in gene expression patterns as well as related biological pathways and cell populations known to mediate key elements of glioma biology, including angiogenesis, immune evasion, and brain invasion. These data provide new insights regarding mammalian models of human glioma, and how these insights and models relate to our current understanding of the human disease.

Published
2018
Full Text
View/download PDF

12. Cross-species transcriptional analysis reveals conserved and host-specific neoplastic processes in mammalian glioma

Author

Small Animal Clinical Sciences, Statistics, Fralin Life Sciences Institute, Connolly, Nina P., Shetty, Amol C., Stokum, Jesse A., Hoeschele, Ina, Siegel, Marni B., Miller, C. Ryan, Kim, Anthony J., Ho, Cheng-Ying, Davila, Eduardo, Simard, J. Marc, Devine, Scott E., Rossmeisl, John H. Jr., Holland, Eric C., Winkles, Jeffrey A., Woodworth, Graeme F., Small Animal Clinical Sciences, Statistics, Fralin Life Sciences Institute, Connolly, Nina P., Shetty, Amol C., Stokum, Jesse A., Hoeschele, Ina, Siegel, Marni B., Miller, C. Ryan, Kim, Anthony J., Ho, Cheng-Ying, Davila, Eduardo, Simard, J. Marc, Devine, Scott E., Rossmeisl, John H. Jr., Holland, Eric C., Winkles, Jeffrey A., and Woodworth, Graeme F.

Abstract

Glioma is a unique neoplastic disease that develops exclusively in the central nervous system (CNS) and rarely metastasizes to other tissues. This feature strongly implicates the tumor-host CNS microenvironment in gliomagenesis and tumor progression. We investigated the differences and similarities in glioma biology as conveyed by transcriptomic patterns across four mammalian hosts: rats, mice, dogs, and humans. Given the inherent intra-tumoral molecular heterogeneity of human glioma, we focused this study on tumors with upregulation of the platelet-derived growth factor signaling axis, a common and early alteration in human gliomagenesis. The results reveal core neoplastic alterations in mammalian glioma, as well as unique contributions of the tumor host to neoplastic processes. Notable differences were observed in gene expression patterns as well as related biological pathways and cell populations known to mediate key elements of glioma biology, including angiogenesis, immune evasion, and brain invasion. These data provide new insights regarding mammalian models of human glioma, and how these insights and models relate to our current understanding of the human disease.

Published
2018

15. LCCC 1025: a phase II study of everolimus, trastuzumab, and vinorelbine to treat progressive HER2-positive breast cancer brain metastases

Author

Van Swearingen, Amanda E. D., primary, Siegel, Marni B., additional, Deal, Allison M., additional, Sambade, Maria J., additional, Hoyle, Alan, additional, Hayes, D. Neil, additional, Jo, Heejoon, additional, Little, Paul, additional, Dees, Elizabeth Claire, additional, Muss, Hyman, additional, Jolly, Trevor, additional, Zagar, Timothy M., additional, Patel, Nirali, additional, Miller, C. Ryan, additional, Parker, Joel S., additional, Smith, J. Keith, additional, Fisher, Julie, additional, Shah, Nikita, additional, Nabell, Lisle, additional, Nanda, Rita, additional, Dillon, Patrick, additional, Abramson, Vandana, additional, Carey, Lisa A., additional, and Anders, Carey K., additional

Published
2018
Full Text
View/download PDF

16. Cross-species transcriptional analysis reveals conserved and host-specific neoplastic processes in mammalian glioma

Author

Connolly, Nina P., primary, Shetty, Amol C., additional, Stokum, Jesse A., additional, Hoeschele, Ina, additional, Siegel, Marni B., additional, Miller, C. Ryan, additional, Kim, Anthony J., additional, Ho, Cheng-Ying, additional, Davila, Eduardo, additional, Simard, J. Marc, additional, Devine, Scott E., additional, Rossmeisl, John H., additional, Holland, Eric C., additional, Winkles, Jeffrey A., additional, and Woodworth, Graeme F., additional

Published
2018
Full Text
View/download PDF

17. Approaches for optimal drug development and clinical trial design for breast cancer brain metastasis

Author

Siegel, Marni B., Van Swearingen, Amanda E.D., and Anders, Carey K.

Subjects
Metastasis -- Research -- Drug therapy -- Patient outcomes, Antineoplastic agents -- Product development, Brain cancer -- Development and progression -- Drug therapy, Breast cancer -- Research -- Drug therapy -- Patient outcomes, Antimitotic agents -- Product development, Health
Abstract

Brain metastases arising from breast cancer constitute a clinically unmet need and a situation that portends a poor prognosis with few therapeutic options. Current treatment options are limited to local [...]

Published
2014

18. Abstract A03: Several rational combination kinase inhibitor treatments identified by synthetic lethality screens are efficacious in intracranial triple negative breast cancer models

Author

Swearingen, Amanda E.D. Van, primary, Sambade, Maria J., additional, Siegel, Marni B., additional, Sud, Shivani, additional, Bevill, Samantha M., additional, Golitz, Brian T., additional, Bash, Ryan E., additional, Santos, Charlene M., additional, Darr, David B., additional, Parker, Joel S., additional, Miller, C. Ryan, additional, Johnson, Gary L., additional, and Anders, Carey K., additional

Published
2017
Full Text
View/download PDF

19. Abstract 5008: The brain microenvironment mediates resistance in luminal breast cancer to PI3K inhibition through HER3 activation

Author

Ferraro, Gino B., primary, Kodack, David P., additional, Askoxylakis, Vasileios, additional, Sheng, Qing, additional, Badeaux, Mark, additional, Goel, Shom, additional, Qi, Xiaolong, additional, Shankaraiah, Ram, additional, Cao, Alexander Z., additional, Ramjiawan, Rakesh R., additional, Bezwada, Divya, additional, Patel, Bhushankumar, additional, Song, Youngchul, additional, Costa, Carlotta, additional, Naxerova, Kamila, additional, Wong, Christina, additional, Kloepper, Jonas, additional, Das, Rita, additional, Tam, Angela, additional, Tanboon, Jantima, additional, Duda, Dan G., additional, Miller, Ryan C., additional, Siegel, Marni B., additional, Anders, Carey K., additional, Sanders, Melinda, additional, Estrada, Valeria M., additional, Schlegel, Robert, additional, Arteaga, Carlos L., additional, Brachtel, Elena, additional, Huang, Alan, additional, Fukumura, Dai, additional, Engelman, Jeffrey A., additional, and Jain, Rakesh K., additional

Published
2017
Full Text
View/download PDF

20. The brain microenvironment mediates resistance in luminal breast cancer to PI3K inhibition through HER3 activation

Author

Kodack, David P., primary, Askoxylakis, Vasileios, additional, Ferraro, Gino B., additional, Sheng, Qing, additional, Badeaux, Mark, additional, Goel, Shom, additional, Qi, Xiaolong, additional, Shankaraiah, Ram, additional, Cao, Z. Alexander, additional, Ramjiawan, Rakesh R., additional, Bezwada, Divya, additional, Patel, Bhushankumar, additional, Song, Yongchul, additional, Costa, Carlotta, additional, Naxerova, Kamila, additional, Wong, Christina S. F., additional, Kloepper, Jonas, additional, Das, Rita, additional, Tam, Angela, additional, Tanboon, Jantima, additional, Duda, Dan G., additional, Miller, C. Ryan, additional, Siegel, Marni B., additional, Anders, Carey K., additional, Sanders, Melinda, additional, Estrada, Monica V., additional, Schlegel, Robert, additional, Arteaga, Carlos L., additional, Brachtel, Elena, additional, Huang, Alan, additional, Fukumura, Dai, additional, Engelman, Jeffrey A., additional, and Jain, Rakesh K., additional

Published
2017
Full Text
View/download PDF

21. Combined kinase inhibitors of MEK1/2 and either PI3K or PDGFR are efficacious in intracranial triple-negative breast cancer

Author

Van Swearingen, Amanda E D, primary, Sambade, Maria J, additional, Siegel, Marni B, additional, Sud, Shivani, additional, McNeill, Robert S, additional, Bevill, Samantha M, additional, Chen, Xin, additional, Bash, Ryan E, additional, Mounsey, Louisa, additional, Golitz, Brian T, additional, Santos, Charlene, additional, Deal, Allison, additional, Parker, Joel S, additional, Rashid, Naim, additional, Miller, C Ryan, additional, Johnson, Gary L, additional, and Anders, Carey K, additional

Published
2017
Full Text
View/download PDF

24. Combination therapy with potent PI3K and MAPK inhibitors overcomes adaptive kinome resistance to single agents in preclinical models of glioblastoma

Author

McNeill, Robert S, primary, Canoutas, Demitra A, additional, Stuhlmiller, Timothy J, additional, Dhruv, Harshil D, additional, Irvin, David M, additional, Bash, Ryan E, additional, Angus, Steven P, additional, Herring, Laura E, additional, Simon, Jeremy M, additional, Skinner, Kasey R, additional, Limas, Juanita C, additional, Chen, Xin, additional, Schmid, Ralf S, additional, Siegel, Marni B, additional, Van Swearingen, Amanda E D, additional, Hadler, Michael J, additional, Sulman, Erik P, additional, Sarkaria, Jann N, additional, Anders, Carey K, additional, Graves, Lee M, additional, Berens, Michael E, additional, Johnson, Gary L, additional, and Miller, C Ryan, additional

Published
2017
Full Text
View/download PDF

25. Correction: Tumor Evolution in Two Patients with Basal-like Breast Cancer: A Retrospective Genomics Study of Multiple Metastases

Author

Hoadley, Katherine A., primary, Siegel, Marni B., additional, Kanchi, Krishna L., additional, Miller, Christopher A., additional, Ding, Li, additional, Zhao, Wei, additional, He, Xiaping, additional, Parker, Joel S., additional, Wendl, Michael C., additional, Fulton, Robert S., additional, Demeter, Ryan T., additional, Wilson, Richard K., additional, Carey, Lisa A., additional, Perou, Charles M., additional, and Mardis, Elaine R., additional

Published
2017
Full Text
View/download PDF

27. Abstract 2579: Combination therapy with MEK inhibition is efficacious in intracranial triple negative breast cancer models

Author

Van Swearingen, Amanda E.D., primary, Siegel, Marni B., additional, Sambade, Maria J., additional, Sud, Shivani, additional, Miller, Samantha M., additional, Silva, Grace, additional, Bash, Ryan E., additional, Santos, Charlene M., additional, Darr, David B., additional, Golitz, Brian, additional, Parker, Joel S., additional, Miller, C. Ryan, additional, Johnson, Gary L., additional, and Anders, Carey K., additional

Published
2015
Full Text
View/download PDF

28. Combined Targeted DNA Sequencing in Non-Small Cell Lung Cancer (NSCLC) Using UNCseq and NGScopy, and RNA Sequencing Using UNCqeR for the Detection of Genetic Aberrations in NSCLC

Author

Zhao, Xiaobei, primary, Wang, Anyou, additional, Walter, Vonn, additional, Patel, Nirali M., additional, Eberhard, David A., additional, Hayward, Michele C., additional, Salazar, Ashley H., additional, Jo, Heejoon, additional, Soloway, Matthew G., additional, Wilkerson, Matthew D., additional, Parker, Joel S., additional, Yin, Xiaoying, additional, Zhang, Guosheng, additional, Siegel, Marni B., additional, Rosson, Gary B., additional, Earp, H. Shelton, additional, Sharpless, Norman E., additional, Gulley, Margaret L., additional, Weck, Karen E., additional, Hayes, D. Neil, additional, and Moschos, Stergios J., additional

Published
2015
Full Text
View/download PDF

29. Efficacy of Carboplatin Alone and in Combination with ABT888 in Intracranial Murine Models of BRCA-Mutated and BRCA–Wild-Type Triple-Negative Breast Cancer

Author

Karginova, Olga, primary, Siegel, Marni B., additional, Van Swearingen, Amanda E.D., additional, Deal, Allison M., additional, Adamo, Barbara, additional, Sambade, Maria J., additional, Bazyar, Soha, additional, Nikolaishvili-Feinberg, Nana, additional, Bash, Ryan, additional, O'Neal, Sara, additional, Sandison, Katie, additional, Parker, Joel S., additional, Santos, Charlene, additional, Darr, David, additional, Zamboni, William, additional, Lee, Yueh Z., additional, Miller, C. Ryan, additional, and Anders, Carey K., additional

Published
2015
Full Text
View/download PDF

34. Tumor Evolution in Two Patients with Basal-like Breast Cancer: A Retrospective Genomics Study of Multiple Metastases

Author

Perou, Charles M., Wilson, Richard K., Siegel, Marni B., Hoadley, Katherine A., Kanchi, Krishna L., He, Xiaping, Fulton, Robert S., Wendl, Michael C., Carey, Lisa A., Mardis, Elaine R., Ding, Li, Zhao, Wei, Parker, Joel S., Demeter, Ryan T., and Miller, Christopher A.

Subjects
3. Good health
Abstract

Metastasis is the main cause of cancer patient deaths and remains a poorly characterized process. It is still unclear when in tumor progression the ability to metastasize arises and whether this ability is inherent to the primary tumor or is acquired well after primary tumor formation. Next-generation sequencing and analytical methods to define clonal heterogeneity provide a means for identifying genetic events and the temporal relationships between these events in the primary and metastatic tumors within an individual.

35. Breast cancer brain metastases: evidence for neuronal-like adaptation in a ‘breast-to-brain’ transition?

Author

Van Swearingen, Amanda E, Siegel, Marni B, and Anders, Carey

Subjects
3. Good health
Abstract

Brain metastases remain a significant challenge in the treatment of breast cancer patients due to the unique environment posed by the central nervous system. A better understanding of the biology of breast cancer cells that have metastasized to the brain is required to develop improved therapies. A recent Proceedings of the National Academy of Sciences article demonstrates that breast cancer cells in the brain microenvironment express γ-aminobutyric acid (GABA)-related genes, enabling them to utilize GABA as an oncometabolite, thus gaining a proliferative advantage. In this viewpoint, we highlight these findings and their potential impact on the treatment of breast cancer brain metastases.

Catalog

Books, media, physical & digital resources
See catalog results