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4. Studies of molecular motions in selected polymer systems

Author

Henshall, S. A. E.

Subjects
547.7, Polymers, Molecular dynamics
Abstract

Torsional Braid Analysis, TBA, of various polysaccharide derivatives and of members of the poly (di-n-alkylitaconate) series, complemented by a limited number of Differential Scanning Calorimeter thermograms, has enabled the mclecular motions associated with several secondary glass transitions to be tentatively identified. A damping peak observed at less than -190° to -166°C in TBA thermograms for polymers with side groups containing n-alkyl moitiés as large as the n-propyl group has been attributed to the onset of rotational motion of this alkyl group alone. TBA of higher poly (di-n-alkylitaconates) also revealed a large secondary transition between -70° and -45°C; from the relationship between their temperatures these two transitions were identified with the glass and melting transitions of the n-alkyl side-chains and it was suggested that the g-transition for the entire polymer also contributes to the high damping associated with the latter process. Two of the secondary transitions that are visible in TBA thermograms for various polysaccharide derivatives may be associated with absorbed water: the damping maximum occurring between 15° and 33°C has been attributed to the rupture of hydrogen bonds, the increased mobility of bonded water molecules possibly being responsible for the damping variation at about -1U°C. It was suggested that motion of the oxycarbonyl portion of ester groups and/or of the C6 oxymethylene group may be initiated at approximately -55°C. It was concluded that chair-chair conformational interchange of main-chain glucose rings becomes energetically feasible between -90 and -140°C, the temperature of this secondary transition being particularly dependent on the structure of substituent groups. The glass transition temperature was also determined for each available sample, the variety in their structures enabling the relationship between these two parameters to be discussed.

Published
1974

6. An analysis of a multiple biomarker panel to better predict prostate cancer metastasis after radical prostatectomy

Author

Zhang, AY, Chiam, K, Haupt, Y, Fox, S, Birch, S, Tilley, W, Butler, LM, Knudsen, K, Comstock, C, Rasiah, K, Grogan, J, Mahon, KL, Bianco-Miotto, T, Ricciardelli, C, Bohm, M, Henshall, S, Delprado, W, Stricker, P, Horvath, LG, Kench, JG, Zhang, AY, Chiam, K, Haupt, Y, Fox, S, Birch, S, Tilley, W, Butler, LM, Knudsen, K, Comstock, C, Rasiah, K, Grogan, J, Mahon, KL, Bianco-Miotto, T, Ricciardelli, C, Bohm, M, Henshall, S, Delprado, W, Stricker, P, Horvath, LG, and Kench, JG

Abstract

A plethora of individual candidate biomarkers for predicting biochemical relapse in localized prostate cancer (PCa) have been proposed. Combined biomarkers may improve prognostication, and ensuring validation against more clinically relevant endpoints are required. The Australian PCa Research Centre NSW has contributed to numerous studies of molecular biomarkers associated with biochemical relapse. In the current study, these biomarkers were re-analyzed for biochemical relapse, metastatic relapse and PCa death with extended follow-up. Biomarkers of significance were then used to develop a combined prognostic model for clinical outcomes and validated in a large independent cohort. The discovery cohort (n = 324) was based on 12 biomarkers with a median follow-up of 16 years. Seven biomarkers were significantly associated with biochemical relapse. Three biomarkers were associated with metastases: AZGP1, Ki67 and PML. Only AZGP1 was associated with PCa death. In their individual and combinational forms, AZGP1 and Ki67 as a dual BM signature was the most robust predictor of metastatic relapse (AUC 0.762). The AZPG1 and Ki67 signature was validated in an independent cohort of 347 PCa patients. The dual BM signature of AZGP1 and Ki67 predicted metastasis in the univariable (HR 7.2, 95% CI, 1.6-32; p = 0.01) and multivariable analysis (HR 5.4, 95% CI, 1.2-25; p = 0.03). The dual biomarker signature marginally improved risk prediction compared to AZGP1 alone (AUC 0.758 versus 0.738, p < 0.001). Our findings indicate that biochemical relapse is not an adequate surrogate for metastasis or PCa death. The dual biomarker signature of AZGP1 and Ki67 offers a small benefit in predicting metastasis over AZGP1 alone.

Published
2019

13. Cytokine profiling of docetaxel-resistant castration-resistant prostate cancer

Author

Mahon, K L, primary, Lin, H-M, additional, Castillo, L, additional, Lee, B Y, additional, Lee-Ng, M, additional, Chatfield, M D, additional, Chiam, K, additional, Breit, S N, additional, Brown, D A, additional, Molloy, M P, additional, Marx, G M, additional, Pavlakis, N, additional, Boyer, M J, additional, Stockler, M R, additional, Daly, R J, additional, Henshall, S M, additional, and Horvath, L G, additional

Published
2015
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15. Cytokines' profiles to predict chemotherapy outcome in castration-resistant prostate cancer (CRPC).

Author

Mahon, K. L., primary, Chatfield, M. D., additional, Lee-Ng, M., additional, Breit, S. N., additional, Brown, D. A., additional, Molloy, M. P., additional, Marx, G. M., additional, Pavlakis, N., additional, Boyer, M. J., additional, Stockler, M. R., additional, Wykes, R., additional, Henshall, S. M., additional, Sutherland, R. L., additional, and Horvath, L., additional

Published
2011
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22. Aberrent hedgehog signaling is an early event in breast cancer development.

Author

O'Toole, S, primary, Swarbrick, A, additional, Millar, E, additional, McLeod, D, additional, McNeil, C, additional, Qiu, M, additional, Lopez-Knowles, E, additional, Caldon, E, additional, Oakes, S, additional, Ormandy, C, additional, Morey, A, additional, Musgrove, E, additional, Henshall, S, additional, and Sutherland, R, additional

Published
2009
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25. EXPRESSION OF S100A2 CALCIUM-BINDING PROTEIN PREDICTS RESPONSE TO PANCREATECTOMY FOR PANCREATIC CANCER

Author

Biankin, A. V., primary, Kench, J. G., additional, Colvin, E. K., additional, Segara, D., additional, Scarlett, C. J., additional, Nguyen, N. Q., additional, Chang, D. K., additional, Morey, A. L., additional, Lee, C.-S., additional, Pinese, M., additional, Kuo, S. C. L., additional, Susanto, J. M., additional, Cosman, P. H., additional, Lindeman, G. J., additional, Visvader, J. E., additional, Merrett, N. D., additional, Musgrove, E. A., additional, Henshall, S. M., additional, and Sutherland, R. L., additional

Published
2008
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27. Erratum: The E3 ubiquitin ligase EDD is an adverse prognostic factor for serous epithelial ovarian cancer and modulates cisplatin resistance in vitro

Author

O'Brien, P M, primary, Davies, M J, additional, Scurry, J P, additional, Smith, A N, additional, Barton, C A, additional, Henderson, M J, additional, Saunders, D N, additional, Gloss, B S, additional, Patterson, K I, additional, Clancy, J L, additional, Heinzelmann-Schwarz, V A, additional, Murali, R, additional, Scolyer, R A, additional, Zeng, Y, additional, Williams, E D, additional, Scurr, L, additional, DeFazio, A, additional, Quinn, Di, additional, Watts, C K W, additional, Hacker, N F, additional, Henshall, S M, additional, and Sutherland, R L, additional

Published
2008
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28. Stage migration and the Kattan nomogram

Author

Horvath, L., primary, Thanigasalam, R., additional, Rasiah, K., additional, Stricker, P., additional, Earnest, A., additional, Haynes, A., additional, Sutherland, S., additional, Sutherland, R., additional, and Henshall, S., additional

Published
2008
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29. The E3 ubiquitin ligase EDD is an adverse prognostic factor for serous epithelial ovarian cancer and modulates cisplatin resistance in vitro

Author

O'Brien, P M, primary, Davies, M J, additional, Scurry, J P, additional, Smith, A N, additional, Barton, C A, additional, Henderson, M J, additional, Saunders, D N, additional, Gloss, B S, additional, Patterson, K I, additional, Clancy, J L, additional, Heinzelmann-Schwarz, V A, additional, Scolyer, R A, additional, Zeng, Y, additional, Williams, E D, additional, Scurr, L, additional, DeFazio, A, additional, Quinn, D I, additional, Watts, C K W, additional, Hacker, N F, additional, Henshall, S M, additional, and Sutherland, R L, additional

Published
2008
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30. Expression of LMO4 and outcome in pancreatic ductal adenocarcinoma

Author

Murphy, N C, primary, Scarlett, C J, additional, Kench, J G, additional, Sum, E Y M, additional, Segara, D, additional, Colvin, E K, additional, Susanto, J, additional, Cosman, P H, additional, Lee, C-S, additional, Musgrove, E A, additional, Sutherland, R L, additional, Lindeman, G J, additional, Henshall, S M, additional, Visvader, J E, additional, and Biankin, A V, additional

Published
2008
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34. A distinct molecular profile associated with mucinous epithelial ovarian cancer

Author

Heinzelmann-Schwarz, V A, primary, Gardiner-Garden, M, additional, Henshall, S M, additional, Scurry, J P, additional, Scolyer, R A, additional, Smith, A N, additional, Bali, A, additional, Bergh, P Vanden, additional, Baron-Hay, S, additional, Scott, C, additional, Fink, D, additional, Hacker, N F, additional, Sutherland, R L, additional, and O'Brien, P M, additional

Published
2006
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43. BAG-1 predicts patient outcome and tamoxifen responsiveness in ER-positive invasive ductal carcinoma of the breast.

Author

Millar, E. K. A., Anderson, L. R., McNeil, C. M., O'Toole, S. A., Pinese, M., Crea, P., Morey, A. L., Biankin, A. V., Henshall, S. M., Musgrove, E. A., Sutherland, R. L., and Butt, A. J.

Subjects
TAMOXIFEN, BREAST cancer, CANCER patients, CANCER invasiveness, CANCER cell proliferation, HORMONE antagonists, GENETIC regulation, IMMUNOHISTOCHEMISTRY, RNA analysis, BREAST cancer chemotherapy, PROTEIN analysis, RESEARCH, RESEARCH methodology, ESTROGEN antagonists, MEDICAL cooperation, EVALUATION research, DUCTAL carcinoma, COMPARATIVE studies, DNA-binding proteins, TRANSCRIPTION factors, CELL lines, BREAST tumors
Abstract

BAG-1 (bcl-2-associated athanogene) enhances oestrogen receptor (ER) function and may influence outcome and response to endocrine therapy in breast cancer. We determined relationships between BAG-1 expression, molecular phenotype, response to tamoxifen therapy and outcome in a cohort of breast cancer patients and its influence on tamoxifen sensitivity in MCF-7 breast cancer cells in vitro. Publically available gene expression data sets were analysed to identify relationships between BAG-1 mRNA expression and patient outcome. BAG-1 protein expression was assessed using immunohistochemistry in 292 patients with invasive ductal carcinoma and correlated with clinicopathological variables, therapeutic response and disease outcome. BAG-1-overexpressing MCF-7 cells were treated with antioestrogens to assess its effects on cell proliferation. Gene expression data demonstrated a consistent association between high BAG-1 mRNA and improved survival. In ER+ cancer (n=189), a high nuclear BAG-1 expression independently predicted improved outcome for local recurrence (P=0.0464), distant metastases (P=0.0435), death from breast cancer (P=0.009, hazards ratio 0.29, 95% CI: 0.114-0.735) and improved outcome in tamoxifen-treated patients (n=107; P=0.0191). BAG-1 overexpression in MCF-7 cells augmented antioestrogen-induced growth arrest. A high BAG-1 expression predicts improved patient outcome in ER+ breast carcinoma. This may reflect both a better definition of the hormone-responsive phenotype and a concurrent increased sensitivity to tamoxifen. [ABSTRACT FROM AUTHOR]

Published
2009
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45. Aberrant p16(INK4A) and DPC4/Smad4 expression in intraductal papillary mucinous tumours of the pancreas is associated with invasive ductal adenocarcinoma.

Author

V, Biankin A, A, Biankin S, G, Kench J, L, Morey A, C-S, Lee, R, Head D, P, Eckstein R, B, Hugh T, M, Henshall S, and L, Sutherland R

Abstract

BACKGROUND AND AIMS: Intraductal papillary mucinous tumours (IPMT) of the pancreas constitute a unique pathological entity with an overall incidence of associated invasive malignancy of 20%. The malignant potential of an individual IPMT cannot be accurately predicted. Preoperative estimation of the risk of associated invasive malignancy with IPMT would be of significant clinical benefit. As aberrations in cell cycle regulatory genes are associated with the progression of precursor pancreatic ductal lesions to invasive adenocarcinoma, we examined expression of key cell cycle regulatory genes in the cyclin D1/retinoblastoma pathway and the transforming growth factor beta/Smad4 signalling pathway in a cohort of patients with surgically resected IPMT. METHODS: Sections of formalin fixed paraffin embedded pancreatic tissue from a cohort of 18 patients with IPMT were examined using immunohistochemistry for protein expression of cell cycle regulatory genes p16(INK4A), p21(CIP1), p27(KIP1), cyclin D1, pRb, and p53, as well as the cell signalling molecule Smad4. A comparison of expression levels was made between adenoma/borderline IPMT (10 patients) and intraductal papillary mucinous carcinoma (IPMC) (eight patients, four of whom harboured invasive carcinoma). Statistical analysis was performed using the chi(2) and Fisher's exact tests. RESULTS: Aberrant expression of the proteins examined increased in frequency from adenoma/borderline IPMT to IPMC. Specifically, there was a significantly greater incidence of loss of p16(INK4A) expression in IPMC: 8/8 lesions (100%) compared with 1/10 (10%) adenoma/borderline IPMT (p&lt;0.001). Similarly, loss of Smad4 expression was associated with IPMC: 3/8 (38%) versus adenoma/borderline IPMT 0/10 (p&lt;0.03). Loss of Smad4 expression within the IPMT was the best marker for the presence of invasive carcinoma (p&lt;0.001). CONCLUSIONS: These data indicate that loss of p16(INK4A) and Smad4 expression occur more frequently in IPMC alone, or with associated invasive carcinoma, compared with adenoma/borderline IPMT. Aberrant protein expression of these cell cycle regulatory genes in IPMT and pancreatic intraepithelial neoplasia in the current model of pancreatic cancer progression suggest similarities in their development and may also represent the subsequent risk of invasive carcinoma.

Published
2002

47. Preclinical validation of anti-TMEFF2-auristatin E-conjugated antibodies in the treatment of prostate cancer

Author

Afar, D. E. H., Bhaskar, V., Ibsen, E., Breinberg, D., Henshall, S. M., Kench, J. G., Drobnjak, M., Powers, R., Wong, M., Evangelista, F., O Hara, C., Powers, D., Dubridge, R. B., Ingrid Caras, Winter, R., Anderson, T., Solvason, N., Stricker, P. D., Cordon-Cardo, C., Scher, H. I., Grygiel, J. J., Sutherland, R. L., Murray, R., Ramaskrishnan, V., and Law, D. A.

Subjects
Male, Follistatin, Cancer Research, DNA, Complementary, Time Factors, Recombinant Fusion Proteins, Molecular Sequence Data, Antineoplastic Agents, Transfection, Mice, Animals, Humans, Amino Acid Sequence, RNA, Messenger, Cloning, Molecular, Neoplasm Metastasis, Cell Proliferation, Oligonucleotide Array Sequence Analysis, Hybridomas, Sequence Homology, Amino Acid, Cell Membrane, Prostate, Antibodies, Monoclonal, Brain, Membrane Proteins, Prostatic Neoplasms, Surface Plasmon Resonance, Flow Cytometry, Immunohistochemistry, Neoplasm Proteins, Protein Structure, Tertiary, Kinetics, Microscopy, Fluorescence, Oncology, Lymphatic Metastasis, Oligopeptides
Abstract

Current treatments for advanced stage, hormone-resistant prostate cancer are largely ineffective, leading to high patient mortality and morbidity. To fulfill this unmet medical need, we used global gene expression profiling to identify new potential antibody-drug conjugate (ADC) targets that showed maximal prostate cancer-specific expression. TMEFF2, a gene encoding a plasma membrane protein with two follistatin-like domains and one epidermal growth factor–like domain, had limited normal tissue distribution and was highly overexpressed in prostate cancer. Immunohistochemistry analysis using a specific monoclonal antibody (mAb) to human TMEFF2 showed significant protein expression in 74% of primary prostate cancers and 42% of metastatic lesions from lymph nodes and bone that represented both hormone-naïve and hormone-resistant disease. To evaluate anti-TMEFF2 mAbs as potential ADCs, one mAb was conjugated to the cytotoxic agent auristatin E via a cathepsin B–sensitive valine-citrulline linker. This ADC, Pr1-vcMMAE, was used to treat male severe combined immunodeficient mice bearing xenografted LNCaP and CWR22 prostate cancers expressing TMEFF2. Doses of 3 to 10 mg/kg of this specific ADC resulted in significant and sustained tumor growth inhibition, whereas an isotype control ADC had no significant effect. Similar efficacy and specificity was shown with huPr1-vcMMAE, a humanized anti-TMEFF2 ADC. No overt in vivo toxicity was observed with either murine or human ADC, despite significant cross-reactivity of anti-TMEFF2 mAb with the murine TMEFF2 protein, implying minimal toxicity to other body tissues. These data support the further evaluation and clinical testing of huPr1-vcMMAE as a novel therapeutic for the treatment of metastatic and hormone-resistant prostate cancer.

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