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2. Targeting tumour-associated macrophages in hodgkin lymphoma using engineered extracellular matrix-mimicking cryogels

Author

Bahlmann, Laura C., Xue, Chang, Chin, Allysia A., Skirzynska, Arianna, Lu, Joy, Thériault, Brigitte, Uehling, David, Yerofeyeva, Yulia, Peters, Rachel, Liu, Kela, Chen, Jianan, Martel, Anne L., Yaffe, Martin, Al-awar, Rima, Goswami, Rashmi S., Ylanko, Jarkko, Andrews, David W., Kuruvilla, John, Laister, Rob C., and Shoichet, Molly S.

Published
2023
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4. Data from Heterogeneity of Circulating Tumor Cell–Associated Genomic Gains in Breast Cancer and Its Association with the Host Immune Response

Author

Kanwar, Nisha, primary, Balde, Zaldy, primary, Nair, Ranju, primary, Dawe, Melanie, primary, Chen, Shiyi, primary, Maganti, Manjula, primary, Atenafu, Eshetu G., primary, Manolescu, Sabrina, primary, Wei, Carrie, primary, Mao, Amanda, primary, Fu, Fred, primary, Wang, Dan, primary, Cheung, Alison, primary, Yerofeyeva, Yulia, primary, Peters, Rachel, primary, Liu, Kela, primary, Desmedt, Christine, primary, Sotiriou, Christos, primary, Szekely, Borbala, primary, Kulka, Janina, primary, McKee, Trevor D., primary, Hirano, Naoto, primary, Bartlett, John M.S., primary, Yaffe, Martin J., primary, Bedard, Philippe L., primary, McCready, David, primary, and Done, Susan J., primary

Published
2023
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5. Supplementary File from Heterogeneity of Circulating Tumor Cell–Associated Genomic Gains in Breast Cancer and Its Association with the Host Immune Response

Author

Kanwar, Nisha, primary, Balde, Zaldy, primary, Nair, Ranju, primary, Dawe, Melanie, primary, Chen, Shiyi, primary, Maganti, Manjula, primary, Atenafu, Eshetu G., primary, Manolescu, Sabrina, primary, Wei, Carrie, primary, Mao, Amanda, primary, Fu, Fred, primary, Wang, Dan, primary, Cheung, Alison, primary, Yerofeyeva, Yulia, primary, Peters, Rachel, primary, Liu, Kela, primary, Desmedt, Christine, primary, Sotiriou, Christos, primary, Szekely, Borbala, primary, Kulka, Janina, primary, McKee, Trevor D., primary, Hirano, Naoto, primary, Bartlett, John M.S., primary, Yaffe, Martin J., primary, Bedard, Philippe L., primary, McCready, David, primary, and Done, Susan J., primary

Published
2023
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6. Supplementary Information from Heterogeneity of Circulating Tumor Cell–Associated Genomic Gains in Breast Cancer and Its Association with the Host Immune Response

Author

Kanwar, Nisha, primary, Balde, Zaldy, primary, Nair, Ranju, primary, Dawe, Melanie, primary, Chen, Shiyi, primary, Maganti, Manjula, primary, Atenafu, Eshetu G., primary, Manolescu, Sabrina, primary, Wei, Carrie, primary, Mao, Amanda, primary, Fu, Fred, primary, Wang, Dan, primary, Cheung, Alison, primary, Yerofeyeva, Yulia, primary, Peters, Rachel, primary, Liu, Kela, primary, Desmedt, Christine, primary, Sotiriou, Christos, primary, Szekely, Borbala, primary, Kulka, Janina, primary, McKee, Trevor D., primary, Hirano, Naoto, primary, Bartlett, John M.S., primary, Yaffe, Martin J., primary, Bedard, Philippe L., primary, McCready, David, primary, and Done, Susan J., primary

Published
2023
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7. Single Section Biomarker Measurement and Colocalization via a Novel Multiplexing Staining Technology

Author

Hope, Tyna, Wang, Dan, Nofech-Mozes, Sharon, Liu, Kela, Kaanumalle, Sireesha, Al-Kohafi, Yousef, Shaikh, Kashan, Filkins, Robert, Yaffe, Martin, Hutchison, David, Series editor, Kanade, Takeo, Series editor, Kittler, Josef, Series editor, Kleinberg, Jon M., Series editor, Mattern, Friedemann, Series editor, Mitchell, John C., Series editor, Naor, Moni, Series editor, Pandu Rangan, C., Series editor, Steffen, Bernhard, Series editor, Terzopoulos, Demetri, Series editor, Tygar, Doug, Series editor, Weikum, Gerhard, Series editor, Tingberg, Anders, editor, Lång, Kristina, editor, and Timberg, Pontus, editor

Published
2016
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11. Pre-clinical Evaluation of Tumour Angiogenesis with Contrast-Enhanced Breast Tomosynthesis

Author

Hill, Melissa L., Liu, Kela, Mainprize, James G., Levitin, Ronald B., Shojaii, Rushin, Yaffe, Martin J., Hutchison, David, editor, Kanade, Takeo, editor, Kittler, Josef, editor, Kleinberg, Jon M., editor, Mattern, Friedemann, editor, Mitchell, John C., editor, Naor, Moni, editor, Nierstrasz, Oscar, editor, Pandu Rangan, C., editor, Steffen, Bernhard, editor, Sudan, Madhu, editor, Terzopoulos, Demetri, editor, Tygar, Doug, editor, Vardi, Moshe Y., editor, Weikum, Gerhard, editor, Maidment, Andrew D. A., editor, Bakic, Predrag R., editor, and Gavenonis, Sara, editor

Published
2012
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15. Heterogeneity of Circulating Tumor Cell–Associated Genomic Gains in Breast Cancer and Its Association with the Host Immune Response

Author

Kanwar, Nisha, primary, Balde, Zaldy, additional, Nair, Ranju, additional, Dawe, Melanie, additional, Chen, Shiyi, additional, Maganti, Manjula, additional, Atenafu, Eshetu G., additional, Manolescu, Sabrina, additional, Wei, Carrie, additional, Mao, Amanda, additional, Fu, Fred, additional, Wang, Dan, additional, Cheung, Alison, additional, Yerofeyeva, Yulia, additional, Peters, Rachel, additional, Liu, Kela, additional, Desmedt, Christine, additional, Sotiriou, Christos, additional, Szekely, Borbala, additional, Kulka, Janina, additional, McKee, Trevor D., additional, Hirano, Naoto, additional, Bartlett, John M.S., additional, Yaffe, Martin J., additional, Bedard, Philippe L., additional, McCready, David, additional, and Done, Susan J., additional

Published
2021
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18. Heterogeneity of Circulating Tumor Cell-Associated Genomic Gains in Breast Cancer and Its Association with the Host Immune Response.

Author

Kanwar, Nisha, Balde, Zaldy, Nair, Ranju, Dawe, Melanie, Chen, Shiyi, Maganti, Manjula, Atenafu, Eshetu EG, Manolescu, Sabrina, Wei, Carrie, Mao, Amanda, Fu, Fred, Wang, Dan, Cheung, Alison, Yerofeyeva, Yulia, Peters, Rachel, Liu, Kela, Desmedt, Christine, Sotiriou, Christos, Szekely, Borbala, Kulka, Janina, McKee, Trevor D, Hirano, Naoto, Bartlett, John M S, Yaffe, Martin MJ, Bedard, Philippe L, McCready, David, Done, Susan J, Kanwar, Nisha, Balde, Zaldy, Nair, Ranju, Dawe, Melanie, Chen, Shiyi, Maganti, Manjula, Atenafu, Eshetu EG, Manolescu, Sabrina, Wei, Carrie, Mao, Amanda, Fu, Fred, Wang, Dan, Cheung, Alison, Yerofeyeva, Yulia, Peters, Rachel, Liu, Kela, Desmedt, Christine, Sotiriou, Christos, Szekely, Borbala, Kulka, Janina, McKee, Trevor D, Hirano, Naoto, Bartlett, John M S, Yaffe, Martin MJ, Bedard, Philippe L, McCready, David, and Done, Susan J

Abstract

Tumor cells that preferentially enter circulation include the precursors of metastatic cancer. Previously, we characterized circulating tumor cells (CTC) from patients with breast cancer and identified a signature of genomic regions with recurrent copy-number gains. Through FISH, we now show that these CTC-associated regions are detected within the matched untreated primary tumors of these patients (21% to 69%, median 55.5%, n = 19). Furthermore, they are more prevalent in the metastases of patients who died from breast cancer after multiple rounds of treatment (70% to 100%, median 93%, samples n = 41). Diversity indices revealed that higher spatial heterogeneity for these regions within primary tumors is associated with increased dissemination and metastasis. An identified subclone with multiple regions gained (MRG clone) was enriched in a posttreatment primary breast carcinoma as well as multiple metastatic tumors and local breast recurrences obtained at autopsy, indicative of a distinct early subclone with the capability to resist multiple lines of treatment and eventually cause death. In addition, multiplex immunofluorescence revealed that tumor heterogeneity is significantly associated with the degree of infiltration of B lymphocytes in triple-negative breast cancer, a subtype with a large immune component. Collectively, these data reveal the functional potential of genetic subclones that comprise heterogeneous primary breast carcinomas and are selected for in CTCs and posttreatment breast cancer metastases. In addition, they uncover a relationship between tumor heterogeneity and host immune response in the tumor microenvironment. SIGNIFICANCE: As breast cancers progress, they become more heterogeneous for multiple regions amplified in circulating tumor cells, and intratumoral spatial heterogeneity is associated with the immune landscape., info:eu-repo/semantics/published

Published
2021

20. Heightened aberrant deposition of hard-wearing elastin in conduit arteries of prehypertensive SHR is associated with increased stiffness and inward remodeling

Author

Arribas, Silvia M., Briones, Ana M., Bellingham, Catherine, Gonzalez, M. Carmen, Salaices, Mercedes, Liu, Kela, Wang, Yanting, and Hinek, Aleksander

Subjects
Arteries -- Physiological aspects, Elastin -- Physiological aspects, Hypertension -- Risk factors, Biological sciences
Abstract

Elastin is a major component of conduit arteries and a key determinant of vascular viscoelastic properties. Aberrant organization of elastic lamellae has been reported in resistance vessels from spontaneously hypertensive rats (SHR) before the development of hypertension. Hence, we have characterized the content and organization of elastic lamellae in conduit vessels of neonatal SHR in detail, comparing the carotid arteries from 1-wk-old SHR with those from Wistar-Kyoto (WKY) and Sprague Dawley (SD) rats. The general structure and mechanics were studied by pressure myography, and the internal elastic lamina organization was determined by confocal microscopy. Cyanide bromide-insoluble elastin scaffolds were also prepared from l-mo-old SHR and WKY aortas to assess their weight, amino acid composition, three-dimensional lamellar organization, and mechanical characteristics. Carotid arteries from 1-wk-old SHR exhibited narrower lumen and greater intrinsic stiffness than those from their WKY and SD counterparts. These aberrations were associated with heightened elastin content and with a striking reduction in the size of the fenestrae present in the elastic lamellae. The elastin scaffolds isolated from SHR aortas also exhibited increased relative weight and stiffness, as well as the presence of peculiar trabeculae inside the fenestra that reduced their size. We suggest that the excessive and aberrant elastin deposited in SHR vessels during perinatal development alters their mechanical properties. Such abnormalities are likely to compromise vessel expansion during a critical period of growth and, at later stages, they could compromise hemodynamic function and participate in the development of systemic hypertension. remodeling; hypertension; elastic lamellae; fenestrae; spontaneously hypertensive rats

Published
2008

36. Examination of nasopharyngeal epithelium with contact endoscopy

Author

Huang Tengbo, Deng Man-quan, Huang Xiaoming, Shao Jian-yong, Liu Kela, Liang Xiaoman, Su Yong, and Mai Hai-Qiang

Subjects
Adult, Male, Pathology, medicine.medical_specialty, Adolescent, Population, In vivo, Nasopharynx, medicine, Carcinoma, Humans, Cyst, education, education.field_of_study, Mucous Membrane, medicine.diagnostic_test, business.industry, Endoscopy, Epithelial Cells, General Medicine, Anatomy, Middle Aged, medicine.disease, Epithelium, Squamous carcinoma, Methylene Blue, medicine.anatomical_structure, Nasopharyngeal Diseases, Otorhinolaryngology, Nasopharyngeal carcinoma, Female, business
Abstract

Primarily to evaluate the potential of contact endoscopy, the nasopharyngeal mucosa were examined using contact microscopy. With contact endoscopy it has been possible to visualize (60 x, 150 x ) the superficial cell layers of the nasopharyngeal epithelium, previously stained with methylene blue in vivo and in situ. Normal nasopharyngeal epithelium (20 cases) and cases with pathology (18 cases of chronic nasopharyngitis, 5 cases of nasopharyngeal cyst, and 57 cases of poorly differentiated squamous carcinoma) were assessed with contact endoscopy. The results showed that contact endoscopy can offer clear morphology and arrangement of the epithelial cells of the superficial layers and microvascular networks, such as the size and shapes of the cells or nuclei, nucleus/cytoplasm ratio, karyokinesis, etc. Our study indicated that contact endoscopy can permit the mapping of cellular alteration over mucosa and constitutes a new method of monitoring a high-risk population or precancerous lesions of nasopharyngeal carcinoma.

Published
2001

37. A novel, automated technology for multiplex biomarker imaging and application to breast cancer

Author

Clarke, Gina M, primary, Zubovits, Judit T, additional, Shaikh, Kashan A, additional, Wang, Dan, additional, Dinn, Sean R, additional, Corwin, Alex D, additional, Santamaria-Pang, Alberto, additional, Li, Qing, additional, Nofech-Mozes, Sharon, additional, Liu, Kela, additional, Pang, Zhengyu, additional, Filkins, Robert J, additional, and Yaffe, Martin J, additional

Published
2013
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50. Promoter hypermethylation: an important epigenetic mechanism for hMLH1 gene inactivation in head and neck squamous cell carcinoma.

Author

Liu K, Huang H, Mukunyadzi P, Suen JY, Hanna E, and Fan CY

Subjects
Adaptor Proteins, Signal Transducing, Carcinoma, Squamous Cell pathology, Carrier Proteins, Head and Neck Neoplasms pathology, Humans, MutL Protein Homolog 1, Nuclear Proteins, Polymerase Chain Reaction, Carcinoma, Squamous Cell genetics, DNA Methylation, Gene Silencing, Head and Neck Neoplasms genetics, Neoplasm Proteins genetics, Promoter Regions, Genetic genetics
Abstract

Objective: The hMLH1 gene is one of the mismatch DNA repair genes. Inactivation of the hMLH1 gene has been implicated in the tumorigenesis of many types of human cancers. In most sporadic forms of human cancers, promoter hypermethylation is responsible for hMLH1 gene inactivation. Lack of hMLH1 protein expression has been found in a subset of head and neck squamous cell carcinomas (HNSCCs). The purpose of this study was to investigate whether promoter hypermethylation causes hMLH1 gene inactivation in HNSCCs., Study Design: hMLH1 protein expression was determined by immunohistochemical staining in 62 cases, whereas hMLH1 gene promoter methylation was analyzed by methylation-sensitive restriction enzyme digestion, followed by polymerase chain reaction, in 35 cases of HNSCCs., Results: Sixteen (26%) of 62 cases of HNSCCs showed near-complete loss of hMLH1 protein expression on immunohistochemical staining. Twelve (92%) of 13 cases that were negative for the hMLH1 protein displayed promoter hypermethylation, whereas 17 (77%) of 22 cases positive for the protein were free of promoter methylation., Conclusions: Promoter hypermethylation may be an important mechanism for hMLH1 gene inactivation in a subset of HNSCCs.

Published
2002
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