Search

Your search keyword '"Maraqa, L."' showing total 20 results
Start Over Author "Maraqa, L."
20 results on '"Maraqa, L."'

1. Homozygous TAF1C variants are associated with a novel childhood‐onset neurological phenotype

Author

Knuutinen, O. (Oula), Pyle, A. (Angela), Suo-Palosaari, M. (Maria), Duff, J. (Jennifer), Froukh, T. (Tawfiq), Lehesjoki, A.-E. (Anna-Elina), Kangas, S. M. (Salla M.), Cassidy, J. (James), Maraqa, L. (Latifa), Keski-Filppula, R. (Riikka), Kokkonen, H. (Hannaleena), Uusimaa, J. (Johanna), Horvath, R. (Rita), and Vieira, P. (Päivi)

Subjects
TATAbinding protein associated factors, Pol1 transcription initiation complex proteins, brain atrophy, infantile spasms
Abstract

TATA‐box binding protein associated factor, RNA polymerase I subunit C (TAF1C) is a component of selectivity factor 1 belonging to RNA polymerase I (Pol I) transcription machinery. We report two unrelated patients with homozygous TAF1C missense variants and an early onset neurological phenotype with severe global developmental delay. Clinical features included lack of speech and ambulation and epilepsy. MRI of the brain demonstrated widespread cerebral atrophy and frontal periventricular white matter hyperintensity. The phenotype resembled that of a previously described variant of UBTF, which encodes another transcription factor of Pol I. TAF1C variants were located in two conserved amino acid positions and were predicted to be deleterious. In patient‐derived fibroblasts, TAF1C mRNA and protein expression levels were substantially reduced compared with healthy controls. We propose that the variants impairing TAF1C expression are likely pathogenic and relate to a novel neurological disease. This study expands the disease spectrum related to Pol I transcription machinery, associating the TAF1C missense variants with a severe neurological phenotype for the first time.

Published
2020

2. Multifocal and multicentric breast cancer, is it time to think again?

Author

Masannat, Y.A. Agrawal, A. Maraqa, L. Fuller, M. Down, S.K. Tang, S.S.K. Pang, D. Kontos, M. Romics, L. Heys, S.D.

Subjects
skin and connective tissue diseases
Abstract

Multifocal multicentric breast cancer has traditionally been considered a contraindication to breast conserving surgery because of concerns regarding locoregional control and risk of disease recurrence. However, the evidence supporting this practice is limited. Increasingly, many breast surgeons are advocating breast conservation in selected cases. This short narrative review summarises current evidence on the role of surgery in multifocal multicentric breast cancer and shows that when technically feasible the option of breast conservation is oncologically safe. © 2020 Royal College of Surgeons of England. All rights reserved.

Published
2020

5. Short-term safety outcomes of mastectomy and immediate implant-based breast reconstruction with and without mesh (iBRA): a multicentre, prospective cohort study

Author

Potter, Shelley, primary, Conroy, Elizabeth J, additional, Cutress, Ramsey I, additional, Williamson, Paula R, additional, Whisker, Lisa, additional, Thrush, Steven, additional, Skillman, Joanna, additional, Barnes, Nicola L P, additional, Mylvaganam, Senthurun, additional, Teasdale, Elisabeth, additional, Jain, Abhilash, additional, Gardiner, Matthew D, additional, Blazeby, Jane M, additional, Holcombe, Chris, additional, Achuthan, R, additional, Adwan, I, additional, Aggarwal, S, additional, Ahmed, M, additional, Akelund, M, additional, Akolekar, D, additional, Al-Jibury, O, additional, Amanita, M, additional, Appleton, D, additional, Archampong, D, additional, Asgiersson, K, additional, Athwal, R, additional, Augusti, A, additional, Ayaani, S, additional, Bains, S, additional, Baker, B, additional, Baker, E, additional, Baldota, S, additional, Banerjee, D, additional, Barker, S, additional, Barr, L, additional, Barry, P, additional, Basu, N, additional, Bathla, S, additional, Bishop, N, additional, Boland, G, additional, Branford, O A, additional, Bright-Thomas, R, additional, Brindle, R, additional, Brock, L, additional, Brown, V, additional, Bux, F, additional, Byrne, G, additional, Cain, H, additional, Caldon, L, additional, Callaghan, M, additional, Carbone, A, additional, Carpenter, R, additional, Cawthorn, S, additional, Chagla, L, additional, Challoner, T, additional, Chalmers, C, additional, Chalmers, R, additional, Chambers, S, additional, Chana, M, additional, Chand, N, additional, Chandran, V, additional, Chandrashekar, M, additional, Charfare, H, additional, Chatterjee, J, additional, Chatterjee, S, additional, Chattopadhyay, R, additional, Chaudry, A, additional, Chin, K, additional, Chong, K, additional, Chouhan, A, additional, Choy, C, additional, Christopoulos, P, additional, Clarke, D, additional, Clarke, S, additional, Clayton, E, additional, Clifford, R, additional, Cocker, D, additional, Collin, T, additional, Collis, N, additional, Conroy, F, additional, Constantinou, C, additional, Conway, A, additional, Cook, J, additional, Coombs, N, additional, Cox, K, additional, Critchley, A, additional, Dakka, M, additional, Dani, M, additional, Daoud, R, additional, Darragh, L, additional, Darvesh, S, additional, Dash, I, additional, Datta, S, additional, Davies, E, additional, Dawson, S, additional, De Sousa, E, additional, Debnath, D, additional, Deol, H, additional, Devalia, H, additional, Di Micco, R, additional, Dicks, JR, additional, Dickson, J, additional, Dobner, N, additional, Dobson, G, additional, Dunne, N, additional, Egbeare, D, additional, El Sharief, D, additional, Elfadl, D, additional, Eltigani, E, additional, Enver, D, additional, Erel, E, additional, Evans, A, additional, Exarchos, G, additional, Fage, E, additional, Fatayer, H, additional, Fenn, C, additional, Ferguson, D, additional, Foulkes, R, additional, Franks, J, additional, Fung, V, additional, Galea, M, additional, Gandamihardja, T, additional, Gandhi, A, additional, Garnsey, C, additional, Gateley, C, additional, Gattuso, J, additional, Gawne, S, additional, Geerthan, N, additional, Ghattura, A, additional, Giaramadze, A, additional, Gill, J, additional, Godden, AR, additional, Goh, S, additional, Govindarajulu, S, additional, Goyal, S, additional, Graja, T, additional, Granger, S, additional, Green, M, additional, Grover, K, additional, Gui, G, additional, Gurung, R, additional, Gutteridge, E, additional, Hakim, A, additional, Halka, A, additional, Hamilton-Burke, W, additional, Hamo, I, additional, Harding-Mackean, C, additional, Hargreaves, A, additional, Harries, S, additional, Harris, K, additional, Harris, P, additional, Harrison, S, additional, Harvey, J, additional, Hashem, M, additional, Hassan, U, additional, Henderson, J, additional, Henton, J, additional, Hignett, S, additional, Hodgkins, K, additional, Horgan, K, additional, Horn, S, additional, Hu, J, additional, Hussain, A, additional, Iddon, J, additional, Iqbal, A, additional, Irri, R, additional, Irvine, T, additional, Irwin, G, additional, Iskender, A, additional, Ismail, A, additional, Ives, C, additional, James, K, additional, James, R, additional, Jiwa, N, additional, Jobson, M, additional, Joglekar, S, additional, Johnson, L, additional, Johnson, R, additional, Jones, L, additional, Ju Hwang, M, additional, Kalles, V, additional, Kanesalingam, K, additional, Karat, I, additional, Kaushik, M, additional, Kennedy, K, additional, Khalifa, E, additional, Khan, H, additional, Khanbhai, M, additional, Khawaja, S, additional, Khout, H, additional, Kiernan, T, additional, Kim, B, additional, Kirkpatrick, K, additional, Kiruparan, P, additional, Kirwan, C, additional, Kishore, M, additional, Kneeshaw, P, additional, Knight, A, additional, Kohlhardt, S, additional, Krupa, J, additional, Krupa, K, additional, Kuruvilla, R, additional, Laban, C, additional, Lai, LM, additional, Laidlaw, I, additional, Lambert, K, additional, Langlands, F, additional, Lansdown, M, additional, Laurence, N, additional, Laws, S, additional, Ledwidge, S, additional, Lefemine, V, additional, Lennon, H, additional, Linforth, R, additional, Little, K, additional, Luangsomboon, A, additional, Lund, J, additional, Maalo, J, additional, MacLennan, L, additional, Macmillan, RD, additional, MacNeil, F, additional, Mahapatra, TK, additional, Mallidis, E, additional, Mallon, P, additional, Manoloudakis, N, additional, Maraqa, L, additional, Marla, S, additional, Masood, S, additional, Massey, J, additional, Masudi, T, additional, Matey, P, additional, Mazari, F, additional, McCulley, S, additional, McEvoy, K, additional, Mcintosh, J, additional, McIntosh, S, additional, McKenzie, S, additional, McManus, P, additional, McNicholas, J, additional, Michalakis, I, additional, Mills, N, additional, Mitchell, G, additional, Monib, S, additional, Mullan, M, additional, Murphy, C, additional, Murphy, G, additional, Murphy, J, additional, Murthy, B, additional, Musa, S, additional, Nagra, G, additional, Nangalia, R, additional, Narayanan, S, additional, Nasr, R, additional, Navin, C, additional, Newton, R, additional, Nicholson, S, additional, Nuru, N, additional, O'Connell, R, additional, O'Donoghue, J, additional, Ogedegbe, A, additional, Olayinka, OS, additional, Olsen, S, additional, Osborn, G, additional, Osborne, C, additional, Osman, H, additional, Otieno, C, additional, Pakzad, F, additional, Park, A, additional, Parker, S, additional, Partlett, P, additional, Parvaiz, A, additional, Parvanta, L, additional, Patel, G, additional, Peel, A, additional, Peiris, L, additional, Pennick, M, additional, Peppe, A, additional, Perry, D, additional, Pilgrim, S, additional, Piper, J, additional, Poonawalla, S, additional, Popa, E, additional, Pope, V, additional, Pugh, P, additional, Rainsbury, D, additional, Ramsey, K, additional, Rasheed, T, additional, Rathinaezhil, R, additional, Rattay, T, additional, Ravichandran, D, additional, Reed, M, additional, Refsum, S, additional, Remoundos, D, additional, Rigby, K, additional, Robertson, S, additional, Robinson, A, additional, Robinson, J, additional, Roche, N, additional, Roy, PJ, additional, Runkel, M, additional, Rusby, J, additional, Saha, S, additional, Saidan, Z, additional, Salab, M, additional, Saleh, M, additional, Salem, F, additional, Sami, A, additional, Samlalsingh, S, additional, Sarfraz, N, additional, Shah, R, additional, Shaheed, S, additional, Sharaiha, Y, additional, Shetty, G, additional, Shotton, R, additional, Sircar, T, additional, Skene, E, additional, Sloan, S, additional, Smith, B, additional, Smith, J, additional, Soldanova, L, additional, Soliman, F, additional, Soumian, S, additional, Stevens, J, additional, Steventon, C, additional, Stewart-Parker, E, additional, Stringfellow, T, additional, Sutaria, R, additional, Sutton, R, additional, Sweetland, H, additional, Swiech, B, additional, Tadiparthi, S, additional, Tafazal, H, additional, Taheri, N, additional, Tait, C, additional, Tan, M, additional, Tang, S, additional, Tansley, A, additional, Tate, S, additional, Tayeh, S, additional, Taylor, A, additional, Taylor, J, additional, Thawdar, P, additional, Thomas, C, additional, Thomas, S, additional, Thomson, S, additional, Thorne, A, additional, Tillett, R, additional, Tolkien, Z, additional, Tomlins, A, additional, Topps, A, additional, Tsang, F, additional, Turner, EJ, additional, Turton, P, additional, Udayasankar, S, additional, Ugolini, F, additional, Vaughan Williams, E, additional, Vidya, R, additional, Vijaynagar, B, additional, Vinayagam, R, additional, Volleamere, A, additional, Voynov, V, additional, Waheed, S, additional, Walker, T, additional, Walsh, U, additional, Warner, R, additional, Waters, R, additional, Wilkins, A, additional, Williams, K, additional, Wilson, G, additional, Wiltsher, M, additional, Wooler, B, additional, Wright, C, additional, Wright, M, additional, Wyld, L, additional, Youssef, M, additional, Zabkiewicz, C, additional, Zammit, C, additional, Zeidan, B, additional, and Zheng, D, additional

Published
2019
Full Text
View/download PDF

14. Epidemiology of Phenylketonuria Disease in Jordan: Medical and Nutritional Challenges.

Author

Dababneh S, Alsbou M, Taani N, Sharkas G, Ismael R, Maraqa L, Nemri O, Al-Jawaldeh H, Kopti N, Atieh E, and Almasri A

Abstract

Background: Phenylketonuria (PKU) is the most frequent inborn error in amino acid metabolism caused by a deficiency of the phenylalanine hydroxylase enzyme (PAH). If PKU is left untreated, high concentrations of phenylalanine (Phe) accumulate in the blood, leading to severe brain dysfunction, neurodevelopmental, behavioral and psychological problems. Data concerning the epidemiology of PKU in Jordan are limited. The main objectives of our study were to determine the prevalence of PKU in Jordan, analyze the PKU phenotypes, and identify major challenges in providing dietary management to PKU patients., Methods: Data were collected utilizing the medical records of PKU patients attending the PKU clinic at the Ministry of Health in Amman, Jordan, between 2008 and 2021., Results: The total number of patients diagnosed with PKU was 294. The prevalence of PKU was estimated to be 1/5263. Most patients were Jordanians (90.8%), and 9.2% were non-Jordanians. More than half of the patients (56%) were diagnosed through the national newborn screening (NBS) program. Regarding the phenotypes of PKU, 46.6% had moderate PKU, whereas 42.9% had the classic type of PKU and only 8 (2.7%) had cofactor Tetrahydrobiopterin (BH4) deficiency (atypical PKU). According to the age of diagnosis, 66% of patients were diagnosed more than 30 days post-birth. Consanguinity was found in 87.4% of patients, and the majority of patients, 218 (74.2%), had first-degree consanguinity. The most common complication was mental retardation (31%). Most patients were committed to dietary management (83%) and developed fewer complications., Conclusion: In our study, we demonstrated the importance of the NBS program in the early identification and diagnosis of new PKU cases which allows the initiation of treatment and dietary management to prevent severe complications of PKU in Jordan.

Published
2022
Full Text
View/download PDF

15. Homozygous TAF1C variants are associated with a novel childhood-onset neurological phenotype.

Author

Knuutinen O, Pyle A, Suo-Palosaari M, Duff J, Froukh T, Lehesjoki AE, Kangas SM, Cassidy J, Maraqa L, Keski-Filppula R, Kokkonen H, Uusimaa J, Horvath R, and Vieira P

Subjects
Child, Preschool, Epilepsy diagnostic imaging, Epilepsy pathology, Female, Fibroblasts metabolism, Homozygote, Humans, Infant, Infant, Newborn, Magnetic Resonance Imaging, Male, Mutation, Missense genetics, Phenotype, Spasms, Infantile diagnostic imaging, Spasms, Infantile pathology, Epilepsy genetics, RNA Polymerase I genetics, Spasms, Infantile genetics, TATA-Binding Protein Associated Factors genetics, Transcription Factor TFIID genetics
Abstract

TATA-box binding protein associated factor, RNA polymerase I subunit C (TAF1C) is a component of selectivity factor 1 belonging to RNA polymerase I (Pol I) transcription machinery. We report two unrelated patients with homozygous TAF1C missense variants and an early onset neurological phenotype with severe global developmental delay. Clinical features included lack of speech and ambulation and epilepsy. MRI of the brain demonstrated widespread cerebral atrophy and frontal periventricular white matter hyperintensity. The phenotype resembled that of a previously described variant of UBTF, which encodes another transcription factor of Pol I. TAF1C variants were located in two conserved amino acid positions and were predicted to be deleterious. In patient-derived fibroblasts, TAF1C mRNA and protein expression levels were substantially reduced compared with healthy controls. We propose that the variants impairing TAF1C expression are likely pathogenic and relate to a novel neurological disease. This study expands the disease spectrum related to Pol I transcription machinery, associating the TAF1C missense variants with a severe neurological phenotype for the first time., (© 2020 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)

Published
2020
Full Text
View/download PDF

16. A comparative biomarker study of 514 matched cases of male and female breast cancer reveals gender-specific biological differences.

Author

Shaaban AM, Ball GR, Brannan RA, Cserni G, Di Benedetto A, Dent J, Fulford L, Honarpisheh H, Jordan L, Jones JL, Kanthan R, Maraqa L, Litwiniuk M, Mottolese M, Pollock S, Provenzano E, Quinlan PR, Reall G, Shousha S, Stephens M, Verghese ET, Walker RA, Hanby AM, and Speirs V

Subjects
Adult, Aged, Aged, 80 and over, Cluster Analysis, Female, Humans, Male, Middle Aged, Receptor, ErbB-2 metabolism, Receptors, Estrogen metabolism, Receptors, Progesterone metabolism, Sex Factors, Biomarkers, Tumor metabolism, Breast Neoplasms metabolism, Breast Neoplasms mortality, Breast Neoplasms, Male metabolism, Breast Neoplasms, Male mortality
Abstract

Male breast cancer remains understudied despite evidence of rising incidence. Using a co-ordinated multi-centre approach, we present the first large scale biomarker study to define and compare hormone receptor profiles and survival between male and female invasive breast cancer. We defined and compared hormone receptor profiles and survival between 251 male and 263 female breast cancers matched for grade, age, and lymph node status. Tissue microarrays were immunostained for ERα, ERβ1, -2, -5, PR, PRA, PRB and AR, augmented by HER2, CK5/6, 14, 18 and 19 to assist typing. Hierarchical clustering determined differential nature of influences between genders. Luminal A was the most common phenotype in both sexes. Luminal B and HER2 were not seen in males. Basal phenotype was infrequent in both. No differences in overall survival at 5 or 10 years were observed between genders. Notably, AR-positive luminal A male breast cancer had improved overall survival over female breast cancer at 5 (P = 0.01, HR = 0.39, 95% CI = 0.26-0.87) but not 10 years (P = 0.29, HR = 0.75, 95% CI = 0.46-1.26) and both 5 (P = 0.04, HR = 0.37, 95% CI = 0.07-0.97) and 10 years (P = 0.04, HR = 0.43, 95% CI = 0.12-0.97) in the unselected group. Hierarchical clustering revealed common clusters between genders including total PR-PRA-PRB and ERβ1/2 clusters. A striking feature was the occurrence of ERα on distinct clusters between genders. In female breast cancer, ERα clustered with PR and its isoforms; in male breast cancer, ERα clustered with ERβ isoforms and AR. Our data supports the hypothesis that breast cancer is biologically different in males and females suggesting implications for clinical management. With the incidence of male breast cancer increasing this provides impetus for further study.

Published
2012
Full Text
View/download PDF

17. Investigating and critically appraising the expression and potential role of androgen receptor in breast carcinoma.

Author

Peter MB, Shaaban AM, Rajan SS, Maraqa L, Horgan K, and Speirs V

Abstract

The potential role of the androgen receptor (AR) as a predictive or prognostic factor in breast cancer remains unclear. We aimed to determine the prognostic significance of AR in a cohort of breast carcinomas with long-term follow-up and to critically appraise this in the context of existing literature. Four hundred and eight cases of invasive breast cancer were incorporated into tissue microarrays (TMAs). All received tamoxifen and comprised 108 cases which relapsed and 300 cases which did not. Mean follow-up time for the former was 84 months (range 1-142, SD 38.8) and for the latter was 77 months (range 11-229, SD 49.7). TMAs were immunohistochemically stained with AR and scored as a continuous variable and using the Allred score. AR expression was significantly associated with grade, recurrence on tamoxifen, non-breast cancer death estrogen receptor alpha (ERα) and progesterone receptor (PR). AR correlated significantly with better overall survival (OS) and disease-free survival (DFS) using an Allred cut-off of 4 (log rank=0.0053 and 0.0044, respectively), and 20% positive tumor cells (log rank=0.0027 and 0.0059, respectively). AR expression was additionally associated with a reduced risk of recurrence following endocrine therapy. In summary, AR positive breast tumors have better OS and DFS and are less likely to recur following endocrine treatment.

Published
2011
Full Text
View/download PDF

18. Phosphorylation of estrogen receptor beta at serine 105 is associated with good prognosis in breast cancer.

Author

Hamilton-Burke W, Coleman L, Cummings M, Green CA, Holliday DL, Horgan K, Maraqa L, Peter MB, Pollock S, Shaaban AM, Smith L, and Speirs V

Subjects
Breast Neoplasms pathology, Cell Line, Tumor, Chi-Square Distribution, Female, Flow Cytometry, Humans, Immunohistochemistry, Kaplan-Meier Estimate, Phosphorylation, Prognosis, RNA, Small Interfering, Tissue Array Analysis, Breast Neoplasms metabolism, Estrogen Receptor beta metabolism, Serine metabolism
Abstract

Estrogen receptor (ER) action is modulated by posttranslational modifications. Although ERalpha phosphorylation correlates with patient outcome, ERbeta is similarly phosphorylated but its significance in breast cancer has not been addressed. We investigated whether ERbeta that is phosphorylated at serine 105 (S105-ERbeta) is expressed in breast cancer and assessed potential clinical implications of this phosphorylation. Following antibody validation, S105-ERbeta expression was studied in tissue microarrays comprising 108 tamoxifen-resistant and 351 tamoxifen-sensitive cases and analyzed against clinical data. S105-ERbeta regulation in vitro was assessed by Western blot, flow cytometry, and immunofluorescence. Nuclear S105-ERbeta was observed in breast carcinoma and was associated with better survival (Allred score > or =3), even in tamoxifen-resistant cases, and additionally correlated with ERbeta1 and ERbeta2 expression. Distinct S105-ERbeta nuclear speckles were seen in some higher grade tumors. S105-ERbeta levels increased in MCF-7 cells in response to 17beta-estradiol, the ERbeta-specific agonist diarylpropionitrile, and the partial ERbeta-agonist genistein. S105-ERbeta nuclear speckles were also seen in MCF-7 cells and markedly increased in size and number at 24 hours following 17beta-estradiol and, in particular diarylpropionitrile, treatment. These speckles were coexpressed with ERbeta1 and ERbeta2. Presence of S105-ERbeta in breast cancer and association with improved survival, even in endocrine resistant breast tumors suggest S105-ERbeta might be a useful additional prognostic marker in this disease.

Published
2010
Full Text
View/download PDF

19. Carcinoembryonic antigen cell adhesion molecule 6 predicts breast cancer recurrence following adjuvant tamoxifen.

Author

Maraqa L, Cummings M, Peter MB, Shaaban AM, Horgan K, Hanby AM, and Speirs V

Subjects
Antigens, CD genetics, Antineoplastic Agents, Hormonal pharmacology, Breast, Breast Neoplasms genetics, Breast Neoplasms metabolism, Cell Adhesion Molecules genetics, Cell Line, Tumor, Cell Proliferation drug effects, Chemotherapy, Adjuvant, Drug Resistance, Neoplasm, Estradiol pharmacology, Estrogen Antagonists pharmacology, GPI-Linked Proteins, Humans, Neoplasm Recurrence, Local, Prognosis, RNA Interference, Selective Estrogen Receptor Modulators pharmacology, Tamoxifen analogs & derivatives, Tamoxifen pharmacology, Tissue Array Analysis, Antigens, CD metabolism, Antineoplastic Agents, Hormonal therapeutic use, Breast Neoplasms drug therapy, Cell Adhesion Molecules metabolism, Tamoxifen therapeutic use
Abstract

Purpose: Tamoxifen remains therapy of choice for premenopausal estrogen receptor alpha-positive breast cancer. However, resistance and recurrence are serious problems. Our previous work indicated that carcinoembryonic antigen cell adhesion molecule 6 (CEACAM6) was significantly up-regulated in tamoxifen-resistant (TAMr) MCF-7 derivatives. The aim of this study was to determine the functional role of CEACAM6 in endocrine-resistant breast cancer and to retrospectively test whether it was predictive of resistance in a large cohort of breast cancers with long-term follow-up., Experimental Design: siRNA silencing of CEACAM6 was done in TAMr cells and effects on clonogenicity and endocrine sensitivity were determined. CEACAM6 immunohistochemistry was done on a tissue microarray comprising 108 relapsed primary human breast cancers and 243 tamoxifen-sensitive controls., Results: siRNA-mediated silencing of CEACAM6 reduced both clonogenicity and anchorage-dependent and anchorage-independent growth of TAMr cells. Importantly, CEACAM6 silencing restored sensitivity of TAMr cells to 4-hydroxytamoxifen and proliferative response to 17beta-estradiol. Immunohistochemistry showed significantly more CEACAM expression in the relapsed group compared with nonrelapsed controls [35 of 108 (33.3%) and 32 of 243 (13.2%), respectively; odds ratio, 3.16 (95% confidence interval, 1.83-5.47); P < 0.0001]. Additionally, we derived an outcome predictor model based on CEACAM expression that restratified patients in the Nottingham prognostic index intermediate-risk group into either higher-risk or lower-risk group., Conclusions: Our data support an important role for CEACAM6 in endocrine resistance, which can serve as a powerful predictor of future recurrence.

Published
2008
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results