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121 results on '"Pan, Tien-chi"'

1. Osteopontin is a therapeutic target that drives breast cancer recurrence

Author

Gu, Yu, Taifour, Tarek, Bui, Tung, Zuo, Dongmei, Pacis, Alain, Poirier, Alexandre, Attalla, Sherif, Fortier, Anne-Marie, Sanguin-Gendreau, Virginie, Pan, Tien-Chi, Papavasiliou, Vasilios, Lin, Nancy U., Hughes, Melissa E., Smith, Kalie, Park, Morag, Tremblay, Michel L., Chodosh, Lewis A., Jeselsohn, Rinath, and Muller, William J.

Published
2024
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5. B3GALT6 promotes dormant breast cancer cell survival and recurrence by enabling heparan sulfate-mediated FGF signaling

Author

Sreekumar, Amulya, primary, Lu, Michelle, additional, Choudhury, Biswa, additional, Pan, Tien-chi, additional, Pant, Dhruv K., additional, Lawrence-Paul, Matthew R., additional, Sterner, Christopher J., additional, Belka, George K., additional, Toriumi, Takashi, additional, Benz, Brian A., additional, Escobar-Aguirre, Matias, additional, Marino, Francesco E., additional, Esko, Jeffrey D., additional, and Chodosh, Lewis A., additional

Published
2023
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7. Genomic landscape of metastatic breast cancer identifies preferentially dysregulated pathways and targets

Author

Paul, Matt R., Pan, Tien-chi, Pant, Dhruv K., Shih, Natalie N.C., Chen, Yan, Harvey, Kyra L., Solomon, Aaron, Lieberman, David, Morrissette, Jennifer J.D., Soucier-Ernst, Danielle, Goodman, Noah G., Stavropoulos, S. William, Maxwell, Kara N., Clark, Candace, Belka, George K., Feldman, Michael, DeMichele, Angela, and Chodosh, Lewis A.

Subjects
Cancer genetics -- Comparative analysis, Genomes -- Comparative analysis, Progesterone -- Comparative analysis, Breast cancer -- Comparative analysis, Cancer metastasis -- Comparative analysis, Genomics -- Comparative analysis, Health care industry
Abstract

Nearly all breast cancer deaths result from metastatic disease. Despite this, the genomic events that drive metastatic recurrence are poorly understood. We performed whole-exome and shallow whole-genome sequencing to identify genes and pathways preferentially mutated or copy-number altered in metastases compared with the paired primary tumors from which they arose. Seven genes were preferentially mutated in metastases--MYLK, PEAK1, SLC2A4RG, EVC2, XIRP2, PALB2, and ESR1--5 of which are not significantly mutated in any type of human primary cancer. Four regions were preferentially copy-number altered: loss of STK11 and CDKN2A/B, as well as gain of PTK6 and the membrane-bound progesterone receptor, PAOR8. PAOR8 gain was mutually exclusive with mutations in the nuclear estrogen and progesterone receptors, suggesting a role in treatment resistance. Several pathways were preferentially mutated or altered in metastases, including mTOR, CDK/ RB, cAMP/PKA, WNT, HKMT, and focal adhesion. Immunohistochemical analyses revealed that metastases preferentially inactivate pRB, upregulate the mTORC1 and WNT signaling pathways, and exhibit nuclear localization of activated PKA. Our findings identify multiple therapeutic targets in metastatic recurrence that are not significantly mutated in primary cancers, implicate membrane progesterone signaling and nuclear PKA in metastatic recurrence, and provide genomic bases for the efficacy of mTORC1, CDK4/6, and PARP inhibitors in metastatic breast cancer., Introduction Breast cancer is the most prevalent cancer in the United States and the leading cause of cancer mortality worldwide among women (1). Although 5-year survival rates approach 90%, up [...]

Published
2020
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26. Notch promotes recurrence of dormant tumor cells following HER2/neu-targeted therapy

Author

Abravanel, Daniel L., Belka, George K., Pan, Tien-chi, Pant, Dhruv K., Collins, Meredith A., Sterner, Christopher J., and Chodosh, Lewis A.

Subjects
Recurrence (Disease) -- Development and progression -- Health aspects -- Analysis -- Risk factors -- Genetic aspects -- Research, Breast cancer -- Development and progression -- Genetic aspects -- Research, Health care industry
Abstract

Breast cancer mortality is principally due to recurrent tumors that arise from a reservoir of residual tumor cells that survive therapy. Remarkably, breast cancers can recur after extended periods of clinical remission, implying that at least some residual tumor cells pass through a dormant phase prior to relapse. Nevertheless, the mechanisms that contribute to breast cancer recurrence are poorly understood. Using a mouse model of recurrent mammary tumorigenesis in combination with bioinformatics analyses of breast cancer patients, we have identified a role for Notch signaling in mammary tumor dormancy and recurrence. Specifically, we found that Notch signaling is acutely upregulated in tumor cells following HER2/neu pathway inhibition, that Notch signaling remains activated in a subset of dormant residual tumor cells that persist following HER2/ neu downregulation, that activation of Notch signaling accelerates tumor recurrence, and that inhibition of Notch signaling by either genetic or pharmacological approaches impairs recurrence in mice. Consistent with these findings, meta- analysis of microarray data from over 4,000 breast cancer patients revealed that elevated Notch pathway activity is independently associated with an increased rate of recurrence. Together, these results implicate Notch signaling in tumor recurrence from dormant residual tumor cells and provide evidence that dormancy is a targetable stage of breast cancer progression., Introduction Improvements in the early detection of breast cancers--coupled with advances in surgery, radiotherapy, and adjuvant therapy--have led to substantial increases in 5-year survival rates for breast cancer patients over [...]

Published
2015
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28. Erratum to: Comparative clinical utility of tumor genomic testing and cell-free DNA in metastatic breast cancer

Author

Maxwell, Kara N., Soucier-Ernst, Danielle, Tahirovic, Emin, Troxel, Andrea B., Clark, Candace, Feldman, Michael, Colameco, Christopher, Kakrecha, Bijal, Langer, Melissa, Lieberman, David, Morrissette, Jennifer J. D., Paul, Matt R., Pan, Tien-chi, Yee, Stephanie, Shih, Natalie, Carpenter, Erica, Chodosh, Lewis A., and DeMichele, Angela

Published
2017
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29. Additional file 4 of Cellular dormancy in minimal residual disease following targeted therapy

Author

Ruth, Jason R., Pant, Dhruv K., Pan, Tien-chi, Seidel, Hans E., Baksh, Sanjeethan C., Keister, Blaine A., Singh, Rita, Sterner, Christopher J., Bakewell, Suzanne J., Moody, Susan E., Belka, George K., and Chodosh, Lewis A.

Subjects
fungi
Abstract

Additional file 4:. Table S1. Gene sets down-regulated in dormant residual tumor cells. Clusters of SP-PIR Keywords identified by DAVID functional ontology analysis of genes down-regulated in dormant residual tumor cells compared to all other cell types (false discovery rate (FDR) 1.5-fold).

Published
2021
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30. Additional file 5 of Cellular dormancy in minimal residual disease following targeted therapy

Author

Ruth, Jason R., Pant, Dhruv K., Pan, Tien-chi, Seidel, Hans E., Baksh, Sanjeethan C., Keister, Blaine A., Singh, Rita, Sterner, Christopher J., Bakewell, Suzanne J., Moody, Susan E., Belka, George K., and Chodosh, Lewis A.

Abstract

Additional file 5: Figure S4. Analysis of gene expression data for mitosis-related genes and mTOR pathway activity. (a, b) Expression of all differentially expressed cyclins and cyclin-dependent kinases in HER2/neu (a) and Wnt1 (b) models. (c) Relative expression of all ribosomal proteins, and unsupervised hierarchical clustering for HER2/neu (left) and Wnt1 (right) tumors. (d) Expression of mTOR signature in primary tumor (PT), residual lesion (RL), recurrent tumor (RT) and recurrent tumor stromal cells (RS), for individual (circles) and mean (black line) of pathway activity for HER2/neu (left) and Wnt1 (right) tumors. p-value vs. RL for mTOR signature of HER2/neu: PT

Published
2021
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31. Additional file 7 of Cellular dormancy in minimal residual disease following targeted therapy

Author

Ruth, Jason R., Pant, Dhruv K., Pan, Tien-chi, Seidel, Hans E., Baksh, Sanjeethan C., Keister, Blaine A., Singh, Rita, Sterner, Christopher J., Bakewell, Suzanne J., Moody, Susan E., Belka, George K., and Chodosh, Lewis A.

Subjects
animal structures, embryonic structures, skin and connective tissue diseases
Abstract

Additional file 7: Figure S5. HER2/neu-Prim1 residual disease is enriched for mesenchymal tumor cells. (a-c) IF staining for Hoechst 33258 (blue) and H2B-eGFP (green) along with luminal epithelial marker CK8 (red, top) or myoepithelial marker CK14 (red, bottom), on sections of H2B-eGFP-labeled orthotopic HER2/neu-Prim1 (a) or Wnt1-Prim1 (b) primary tumor (left), residual lesion 28 d after doxycycline withdrawal (right), or normal mammary gland (c). (d-g) Flow cytometry for CD49e vs. CD24 (d, e) or PDGFR-β vs. CD24 (f, g) on H2B-eGFP+DAPI- tumor cells from orthotopic H2B-eGFP-labeled orthotopic HER2/neu-Prim1 primary tumors (d, f) or MRLs (e, g). Scale bars 200 μm for all images.

Published
2021
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32. Additional file 11 of Cellular dormancy in minimal residual disease following targeted therapy

Author

Ruth, Jason R., Pant, Dhruv K., Pan, Tien-chi, Seidel, Hans E., Baksh, Sanjeethan C., Keister, Blaine A., Singh, Rita, Sterner, Christopher J., Bakewell, Suzanne J., Moody, Susan E., Belka, George K., and Chodosh, Lewis A.

Subjects
skin and connective tissue diseases, neoplasms
Abstract

Additional file 11: Table S5. TIC Frequency for Tumor Cells from H2B-eGFP-labeled Orthotopic HER2/neu-Prim1 Primary Tumors or Residual Lesions. Calculation of TIC frequencies for GFP + CD45-DAPI- singlet tumor cells from H2B-eGFP-labeled HER2/neu-Prim1 primary tumors or residual lesions, injected into nu/nu mice either on (HER2/neu transgene expressed), or not on (HER2/neu transgene not expressed), doxycycline.

Published
2021
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33. Additional file 8 of Cellular dormancy in minimal residual disease following targeted therapy

Author

Ruth, Jason R., Pant, Dhruv K., Pan, Tien-chi, Seidel, Hans E., Baksh, Sanjeethan C., Keister, Blaine A., Singh, Rita, Sterner, Christopher J., Bakewell, Suzanne J., Moody, Susan E., Belka, George K., and Chodosh, Lewis A.

Abstract

Additional file 8: Figure S6. HER2/neu-Prim1 residual tumor cells do not express luminal or myoepithelial markers. (a-p) IF staining for Hoechst 33258 (blue) and H2B-eGFP (green) along with epithelial markers (red) CK5 (a, i), CK18 (b, j), CK19 (c, k), EpCAM (e, m), E-Cadherin (f, n), P-Cadherin (g, o), and p63 (h, p), or with a Pan-CK antibody (d, l), on sections of MRLs from H2B-eGFP-labeled orthotopic HER2/neu-Prim1 tumors (a-h) or normal mammary ducts (i-p). Scale bar 50 μm for all images.

Published
2021
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34. Additional file 3 of Cellular dormancy in minimal residual disease following targeted therapy

Author

Ruth, Jason R., Pant, Dhruv K., Pan, Tien-chi, Seidel, Hans E., Baksh, Sanjeethan C., Keister, Blaine A., Singh, Rita, Sterner, Christopher J., Bakewell, Suzanne J., Moody, Susan E., Belka, George K., and Chodosh, Lewis A.

Subjects
endocrine system, animal structures, cardiovascular system
Abstract

Additional file 3 CD31 co-localizes with intravenously injected lectin-AF647. (a-f) Fluorescence microscopy for Hoechst 33258 (blue, a), IF for CD31 (red, b), H2B-eGFP (Green, d), lectin-AF647 (Yellow, eE), merge of CD31 and Lectin-AF647 (c), or merge of all channels (f) on H2B-eGFP-labeled orthotopic HER2/neu-Prim1 MRL. Scale bar 100 μm for all images.

Published
2021
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35. Additional file 2 of Cellular dormancy in minimal residual disease following targeted therapy

Author

Ruth, Jason R., Pant, Dhruv K., Pan, Tien-chi, Seidel, Hans E., Baksh, Sanjeethan C., Keister, Blaine A., Singh, Rita, Sterner, Christopher J., Bakewell, Suzanne J., Moody, Susan E., Belka, George K., and Chodosh, Lewis A.

Abstract

Additional file 2: Figure S2. ECM protein expression in minimal residual lesions. (a-d) IF staining showing Hoechst 33258 (blue), H2B-eGFP (green) and either collagen type-I (red, a, c) or fibronectin (red, b, d) on H2B-eGFP-labeled orthotopic HER2/neu-Prim1 MRLs (a, b) or normal mammary ducts (c, d), labeled to show duct epithelial cells (D), or lumen (Lu). Scale bar 50 μm for all images.

Published
2021
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36. Additional file 6 of Cellular dormancy in minimal residual disease following targeted therapy

Author

Ruth, Jason R., Pant, Dhruv K., Pan, Tien-chi, Seidel, Hans E., Baksh, Sanjeethan C., Keister, Blaine A., Singh, Rita, Sterner, Christopher J., Bakewell, Suzanne J., Moody, Susan E., Belka, George K., and Chodosh, Lewis A.

Subjects
fungi
Abstract

Additional file 6:. Table S2. Gene sets up-regulated in dormant residual tumor cells. Clusters of SP-PIR Keywords identified by DAVID functional ontology analysis of genes up-regulated in dormant residual tumor cells compared to all other cell types (FDR 1.5-fold).

Published
2021
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37. Additional file 9 of Cellular dormancy in minimal residual disease following targeted therapy

Author

Ruth, Jason R., Pant, Dhruv K., Pan, Tien-chi, Seidel, Hans E., Baksh, Sanjeethan C., Keister, Blaine A., Singh, Rita, Sterner, Christopher J., Bakewell, Suzanne J., Moody, Susan E., Belka, George K., and Chodosh, Lewis A.

Subjects
cardiovascular diseases
Abstract

Additional file 9: Table S3. TIC frequency for syngeneic orthotopic MTB;TetO-HER2/neu;TTC;rYFP primary tumors and residual lesions. Calculation of TIC frequencies for YFP+ CD45-DAPI- singlet tumor cells from syngeneic orthotopic primary tumors or residual lesions in nu/nu mice generated from the same MTB;TetO-HER2/neu;TTC;rYFP donor tumors, injected into nu/nu mice on doxycycline.

Published
2021
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41. Abstract 618: Comparison of mutational spectra in metastatic tumors and cell-free DNA in breast cancer patients

Author

Maxwell, Kara N., primary, Soucier-Ernst, Danielle J., additional, Carpenter, Erica L., additional, Troxel, Andrea B., additional, Colameco, Christopher, additional, Clark, Candace, additional, Feldman, Michael D., additional, Kakrecha, Bijal, additional, Langer, Melissa, additional, Lee, Joy, additional, Lewis, David A., additional, Lieberman, David, additional, Morrissette, Jennifer, additional, Pan, Tien-chi, additional, Yee, Stephanie S., additional, Shih, Natalie, additional, Chodosh, Lewis A., additional, and DeMichele, Angela M., additional

Published
2015
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