tbuckley/cabot-search huggingface dataset:
Abstract P6-01-11: Distinct recruitment of tumor-associated immune cells correlates with increased pro-malignant chemokines in tumors expressing epithelial atypical chemokine receptor 1 (ACKR1/DARC), indicating a unique tumor microenvironment
Authors: BD Jenkins, RN Martini, R Hire, MA Monteil, MB Davis
Journal: Cancer Research (2017)

Abstract The breast tumor microenvironment is a complex assortment of cancer and host immune cells that interact to produce a myriad of clinical outcomes for breast cancer (BrCa) patients.Chemokine receptors, such asthe Atypical Chemokine Receptor 1 (ACKR1), play an important role in maintaining the homeostasis of pro-inflammatory chemokines, as well as influencing the migration of host immune cells. ACKR1 has the ability to modify the breast tumor microenvironment in multiple ways, including sequestering chemokine activity and affecting leukocyte migration. The purpose of this study is to characterize the variation in immune cell signaling between ACKR1 positive and negative tumors, and determine any correlation between ACKR1 and CCL2 (MCP-1) and CXCL8 (IL-8) in various BrCa cell types. Primary breast tumor samples were stained using immunohistochemistry for ACKR1, in addition to various immune cells including, T-cells, B-cells, dendritic cells, and macrophages. We determined levels of circulating chemokines using a Luminex assay kit on whole blood lysate. We also tested the localization of ACKR1-associated chemokines and the abundance of ACKR1 using immunofluorescence techniques. Pilot data collected from primary breast tumor tissue suggested that differential expression of ACKR1 from various tumor subtypes leads to the recruitment of a specific subset of host immune cells to the tumor microenvironment. In our cohort, ACKR1 positive tumors tended to recruit B cells and dendritic cells to the site of the tumor, whereas ACKR1 negative cells did not. We also detected a positive correlation between ACKR1 levels in tumor tissue with CCL2 and CXCL8 levels in the circulating blood of our study group. Finally, co-localization of ACKR1 with CCL2 and CXCL8 was observed in cultured mammalian breast cancer cells. Overall, our pilot data suggests that there is differential recruitment of immune cells within the ACKR1 positive and negative BrCa tumor microenvironments, and that circulating CCL2 and CXCL8 concentrations are positively correlated with ACKR1 levels in BrCa cells. Citation Format: Jenkins BD, Martini RN, Hire R, Monteil MA, Davis MB. Distinct recruitment of tumor-associated immune cells correlates with increased pro-malignant chemokines in tumors expressing epithelial atypical chemokine receptor 1 (ACKR1/DARC), indicating a unique tumor microenvironment [abstract]. In: Proceedings of the 2016 San Antonio Breast Cancer Symposium; 2016 Dec 6-10; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2017;77(4 Suppl):Abstract nr P6-01-11.
Molecular Profiling of CD34+ Cells from Diagnosis in CML Patients Identifies Low Expression of CD7 with High Expression of Proteinase 3 or Elastase as Predictors of Longer Survival.
Authors: Agnes S.M. Yong, Richard M. Szydlo, John M. Goldman, Jane F. Apperley, Junia V. Melo
Journal: Blood (2005)
Treatment of Adolescents and Young Adults with Acute Lymphoblastic Leukemia (ALL): An Update of the GIMEMA Experience.
Authors: Luciana Annino, Marco Vignetti, Francesca Paola Paoloni, Anna Maria Testi, Giovanna Meloni, Giorgina Specchia, Giuseppe Fioritoni, Felicetto Ferrara, Nicola Cantore, Francesco Di Raimondo, Francesco Fabbiano, Andrea Camera, Enrica Morra, Pietro Leoni, Paola Fazi, Robert Foa, Franco Mandelli, Sergio Amadori
Journal: Blood (2009)
PP36. IMPROVED GLIOBLASTOMA SURVIVAL FOLLOWING THE INTRODUCTION OF A SUBSPECIALISED SURGICAL HIGH GRADE BRAIN TUMOUR SERVICE
Authors: Dr Rebecca Chave-Cox, Mr Rob Corns, Mr Gnanamurthy Sivakumar, Mr Simon Thomson
Journal: Neuro-Oncology (2017)

AIM: Glioblastoma (GBM) is a highly aggressive primary brain tumour. Whilst the prognosis remains poor, it has been noted in our centre that the three year survival of patients with GBM has improved over time. The aim of this study is to quantify the improved survival and identify causative factors. METHODS: We performed a retrospective analysis of all patients in our centre who were histologically proven to have GBM following surgery between 2008–2012 (n=353, 5 lost to follow up and excluded). Temozolomide was available throughout this time-period. We analysed survival trends and the effect of different factors including the type of surgery (biopsy vs debulking) and the introduction of a subspecialised surgical high grade brain tumour service. RESULTS: Better outcomes were seen with patients who underwent surgical debulking (median survival 11.4 months, 3 year survival 13.9%) compared to biopsy alone (median survival 3.9 months, 3 year survival 3.1%, p=0.00). There was also a survival difference between patients who were treated before and after the introduction of a high grade brain tumour service. Median survival improved from 7.0 to 8.8 months and 3 year survival improved from 7.8% to 13.1% (p=0.03). The survival of patients undergoing biopsy changed little before and after the service was introduced but the median survival of patients undergoing debulking increased from 9.7 months (3 year survival 11.5%) to 13.9 months (3 year survival 17.7%, p=0.01). CONCLUSION: Debulking confers significant benefit compared to biopsy alone. The introduction of a subspecialised high grade brain tumour service has led to improvement in survival. This is especially true for patients fit enough to undergo surgical debulking. A subspecialised high grade brain tumour service should be established in all neurosurgical units.
Adherence to Healthy Lifestyle and Cardiovascular Diseases in the Chinese Population
Authors: Jun Lv, Canqing Yu, Yu Guo, Zheng Bian, Ling Yang, Yiping Chen, Xuefeng Tang, Weiyuan Zhang, Yijian Qian, Yuelong Huang, Xiaoping Wang, Junshi Chen, Zhengming Chen, Lu Qi, Liming Li, Junshi Chen, Zhengming Chen, Rory Collins, Liming Li, Richard Peto, Daniel Avery, Ruth Boxall, Derrick Bennett, Yumei Chang, Yiping Chen, Zhengming Chen, Robert Clarke, Huaidong Du, Simon Gilbert, Alex Hacker, Michael Holmes, Andri Iona, Christiana Kartsonaki, Rene Kerosi, Ling Kong, Om Kurmi, Garry Lancaster, Sarah Lewington, Kuang Lin, John McDonnell, Winnie Mei, Iona Millwood, Qunhua Nie, Jayakrishnan Radhakrishnan, Sajjad Rafiq, Paul Ryder, Sam Sansome, Dan Schmidt, Paul Sherliker, Rajani Sohoni, Iain Turnbull, Robin Walters, Jenny Wang, Lin Wang, Ling Yang, Xiaoming Yang, Zheng Bian, Ge Chen, Yu Guo, Bingyang Han, Can Hou, Jun Lv, Pei Pei, Shuzhen Qu, Yunlong Tan, Caning Yu, Haiyan Zhou, Zeng hang Pang, Ruin Gao, Shoji Wang, Yong-Mei Liu, Ran ran Du, Yajing Zang, Liang Cheng, Xiaocao Tian, Hua Zhang, Silu Lv, Junzheng Wang, Wei Hou, Jiyuan Yin, Ge Jiang, Xue Zhou, Liqiu Yang, Hui He, Bo Yu, Yanjie Li, Huaiyi Mu, Qinai Xu, Meiling Dou, Jiaojiao Ren, Shanqing Wang, Ximin Hu, Hongmei Wang, Jinyan Chen, Yan Fu, Zhenwang Fu, Xiaohuan Wang, Min Weng, Xiangyang Zheng, Yilei Li, Huimei Li, Yanjun Wang, Ming Wu, Jinyi Zhou, Ran Tao, Jie Yang, Chuanming Ni, Jun Zhang, Yihe Hu, Yan Lu, Liangcai Ma, Aiyu Tang, Shuo Zhang, Jianrong Jin, Jingchao Liu, Zhenzhu Tang, Naying Chen, Ying Huang, Mingqiang Li, Jinhuai Meng, Rong Pan, Qilian Jiang, Weiyuan Zhang, Yun Liu, Liuping Wei, Liyuan Zhou, Ningyu Chen, Hairong Guan, Xianping Wu, Ningmei Zhang, Xiaofang Chen, Xuefeng Tang, Guojin Luo, Jianguo Li, Xiaofang Chen, Xunfu Zhong, Jiaqiu Liu, Qiang Sun, Pengfei Ge, Xiaolan Ren, Caixia Dong, Hui Zhang, Enke Mao, Xiaoping Wang, Tao Wang, Xi zhang, Ding Zhang, Gang Zhou, Shixian Feng, Liang Chang, Lei Fan, Yulian Gao, Tianyou He, Huarong Sun, Pan He, Chen Hu, Qiannan Lv, Xukui Zhang, Min Yu, Ruying Hu, Hao Wang, Yijian Qian, Chunmei Wang, Kaixue Xie, Lingli Chen, Yidan Zhang, Dongxia Pan, Yuelong Huang, Biyun Chen, Li Yin, Donghui Jin, Huilin Liu, Zhongxi Fu, Qiaohua Xu, Xin Xu, Hao Zhang, Youping Xiong, Huajun Long, Xianzhi Li, Libo Zhang, Zhe Qiu
Journal: Journal of the American College of Cardiology (2017)

Adherence to a combination of healthy lifestyle factors has been related to a considerable reduction of cardiovascular risk in white populations; however, little is known whether such associations persist in nonwhite populations like the Asian population.
RUNX1 Mutations Are the Most Frequent Leukemia Associated Mutations in Congenital Neutropenia Patients
Authors: Julia Skokowa, Doris Steinemann, Vahagn Makaryan, Maksim Klimiankou, Susanne Schnittger, Alexander Kohlmann, Brigitte Schlegelberger, Cornelia Zeidler, David C. Dale, Karl Welte
Journal: Blood (2012)
The Mutated Region of Cytoplasmatic Nucleophosmine 1 (NPM1) Elicits Both CD4+ and CD8+ T Cell Responses
Authors: Jochen Greiner, Yoko Ono, Susanne Hofmann, Vanessa Schneider, Anita Schmitt, Lu Zhang, Elmar Mehring, Marlies Götz, Konstanze Döhner, Joannis Mytilineos, Markus Wiesneth, Hartmut Döhner, Michael Schmitt
Journal: Blood (2011)
Favorable results of allogeneic bone marrow transplantation (BMT) for adults with Philadelphia (Ph)-chromosome-negative acute lymphoblastic leukemia (ALL) in first complete remission (CR): Results from the International ALL trial (MRC UKALL XII/ECOG E2993).
Authors: J M Rowe, S M Richards, A K Burnett, P H Wiernik, G Harrison, H M Lazarus, I M Franklin, G H Prentice, J I Durrant, M S Tallman, A H Goldstone
Journal: Blood (2001)
The TAL1 Complex Represses the FBXW7 Tumor Suppressor Through Mir-223 in Human T-Cell Acute Lymphoblastic Leukemia
Authors: Marc R Mansour, Takaomi Sanda, Lee N Lawton, Xiaoyu Li, Taras Kreslavsky, Carl Novina, Harald von Boehmer, Richard Young, A. Thomas Look
Journal: Blood (2012)
Abstract B05: Patient-derived GBM tumors versus patient-derived primary cells and GBM cell lines: lessons from microRNA profiling
Authors: Paula Ofek, Nir Dromi, Noga Yerushalmi, Sharon Kredo-Russo, Rachel Grossman, Zvi Ram, Ronit Satchi-Fainaro
Journal: Clinical Cancer Research (2016)

Abstract Glioblastoma multiforme is a very heterogeneous tumor, highly infiltrative, angiogenic and resistant to standard therapeutic intervention. Experimental models currently used in research are mostly based on cancer cell lines, which are grown in culture for many generations and have lost many essential biological characteristics. In consequence, the xenograft tumor models derived from those cells do not maintain genomic and phenotypic characteristics present in the original tumor. It is questionable whether these artificial preclinical models can serve as reliable platforms to select the lead candidate for a novel therapeutic approach. We utilized miRNA expression patterns to evaluate the clinical relevance of some of the currently available experimental models of GBM, searching for similarities and differences in miRNA expression levels between freshly isolated tumors, patient-derived primary cells and GBM cell lines grown in culture. The study included 22 formalin-fixed paraffin-embedded (FFPE) tumors from glioblastoma resections. Those were divided into two groups of Short Term Survivors (STS, survived up to 3 months from initial diagnosis; n=12) and Long Term Survivors (LTS, survived more than 3 years from initial diagnosis; n=10).We further tested 6 patient-derived primary cells, and 5 ATCC human GBM cell lines widely used in preclinical research. Two of the cell lines included dormant and fast-growing variants previously developed in our laboratory to resemble LTS and STS phenotypes, respectively. Samples were loaded on custom microRNA (miR) arrays, including 2172 known miRNAs (miRBase 19). We found several miRNAs that were upregulated in the STS samples while others exhibited higher expression levels in the LTS samples. Both GBM cell lines and patient-derived primary cells exhibited a miRNA profile which was very different from patient samples. Brain miRNAs used as brain markers, such as hsa-miR-124-3p), show relatively low expression levels in both patient-derived primary cells and commercial cell lines but are highly expressed in tumors. We concluded that GBM experimental models must be reevaluated and pre-clinical findings derived from long-established and commonly used in vitro and in vivo models should be further validated in patient-derived models that are more suitable to evaluate the potential clinical relevance of new therapeutics. Citation Format: Paula Ofek, Nir Dromi, Noga Yerushalmi, Sharon Kredo-Russo, Rachel Grossman, Zvi Ram, Ronit Satchi-Fainaro. Patient-derived GBM tumors versus patient-derived primary cells and GBM cell lines: lessons from microRNA profiling. [abstract]. In: Proceedings of the AACR Special Conference: Patient-Derived Cancer Models: Present and Future Applications from Basic Science to the Clinic; Feb 11-14, 2016; New Orleans, LA. Philadelphia (PA): AACR; Clin Cancer Res 2016;22(16_Suppl):Abstract nr B05.
High Hyperdiploidy and t(12; 21) (p13; q22) Translocation Is Not a so Rare Association: A Report of 4 Cases in the Experience of Armand Trousseau Hospital (Paris).
Authors: Paola Ballerini, Christine Perot, Francoise Bellmann, Anne Auvrignon, Marie-Dominique Tabone, Stephanie Haouy, Dalila Adjaoud, Jacqueline Van Den Akker, M.F. Portnoi, Luc Douay, Guy Leverger, Judith Landman-Parker
Journal: Blood (2006)
Elotuzumab in Combination with Lenalidomide and Low-Dose Dexamethasone in High-Risk and/or Stage 23 Relapsed and/or Refractory Multiple Myeloma: A Retrospective Subset Analysis of the Phase 2 Study,
Authors: Sundar Jagannath, Sagar Lonial, Andrzej J Jakubowiak, Thierry Facon, Ravi Vij, Marc S Raab, Darrell J. White, Min-Hui Wang, Teresa Parli, Blake J Bartlett, Anil K Singhal, Paul G. Richardson
Journal: Blood (2011)
Abstract P1-05-17: Interrogating the impact of pregnancy on breast cancer biology using DNA copy number profiling
Authors: B Nguyen, DN Brown, F Rothé, C Desmedt, S Majjaj, G Pruneri, F Peccatori, HA Azim, C Sotiriou
Journal: Cancer Research (2017)

Abstract Background Epidemiological evidence indicates a clear relationship between pregnancy and breast cancer (BC) risk. However, little is known regarding the impact of pregnancy on BC biology. DNA copy number aberrations (CNAs) play an important role in breast carcinogenesis. BC during pregnancy is a rare disease but yet could serve as a good model to study the impact of pregnancy on BC biology. Methods We retrospectively included 54 pregnant and 113 non-pregnant BC patients matched for age and stage with complete clinico-pathological, gene expression and 5-year follow-up data. CNAs were assessed using Affymetrix OncoScan FFPE arrays. We identified the CNAs associated with pregnancy using a multivariate logistic regression adjusted for classical clinico-pathological features. We further evaluated their impact on gene expression. Results After quality control, CNA profiles were obtained for 38 pregnant and 87 non-pregnant BC patients. We identified 13 regions with copy number gains, 11 of which were more frequently gained in pregnant compared to non-pregnant controls and 5 regions with copy number loss, 3 of which were more frequently lost in pregnant patients (p≤0.05). Of interest, we identified 4 genes previously identified as driver event associated with CNAs in breast cancer (S. Nik-Zainal et al, Nature 2016). AKT1 and CDKN2A/B were more frequently gained in the pregnant compared to the non-pregnant (23.7% vs. 8.0%, p=0.068 and 18.4% vs. 4.6% p=0.036) and ARID1B was less frequently gained in the pregnant cohort (2.6% vs. 13.8%, p=0.02). Interestingly, PAPPA which had been previously identified as a pregnancy-dependent oncogene (Takabatake Y. et al, EMBO Mol Med. 2016) was also more frequently gained in the pregnant compared to the non-pregnant patients (21.1% vs 5.8%, p=0.03). We next evaluated the effect of these CNAs on their own gene expression levels and found that AKT1 and CDKN2A/B CNAs were affected by gene-dosage effect. Conclusions In this study, we were able to identify several genomic alterations associated with pregnancy that could further elucidate the impact of pregnancy on BC risk. Moreover, by combining CNAs with gene expression, we were able to identify genes whose expression were associated with CNAs and therefore could be considered potential drivers of this rare disease. Citation Format: Nguyen B, Brown DN, Rothé F, Desmedt C, Majjaj S, Pruneri G, Peccatori F, Azim Jr HA, Sotiriou C. Interrogating the impact of pregnancy on breast cancer biology using DNA copy number profiling [abstract]. In: Proceedings of the 2016 San Antonio Breast Cancer Symposium; 2016 Dec 6-10; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2017;77(4 Suppl):Abstract nr P1-05-17.
Long-Term Follow-Up of Allogeneic Stem Cell Transplantation (SCT) with Reduced Intensity Conditioning (RIC) for Patients (pts) with Chronic Myeloid Leukemia (CML).
Authors: Partow Kebriaei, Michelle Detry, Antonio Carrasco-Yalan, Athanasios Anagnostopoulos, Daniel Couriel, Issa Khouri, Paolo Anderlini, Chitra Hosing, Amin Alousi, Sergio Giralt, Richard Champlin, Marcos de Lima
Journal: Blood (2006)
Impact of Platelet Glycoprotein Polymorphisms upon Clinical Events in Essential Thrombocythaemia Patients Enrolled in the PT1 Trial.
Authors: Susan E. Robinson, Peter J. Campbell, Georgina Buck, Keith Wheatley, Jacqueline A. Cutler, Ruth B. Wheeler, Savita Rangarajan, Beverley J. Hunt, Anthony R. Green, Claire N. Harrison
Journal: Blood (2007)
Combination of dabrafenib plus trametinib for BRAF and MEK inhibitor pretreated patients with advanced BRAFV600-mutant melanoma: an open-label, single arm, dual-centre, phase 2 clinical trial
Authors: Max Schreuer, Yanina Jansen, Simon Planken, Ines Chevolet, Teofila Seremet, Vibeke Kruse, Bart Neyns
Journal: The Lancet Oncology (2017)
Abstract B52: 2-in-1 “sniper” nanomedicines rescue dendritic cells by two pronged inhibition of JAK2/STAT-3 and p38 MAPK pathways
Authors: Siva Kumar Natarajan, Vineethkrishna Chandhrasekar, Noha Ismail, Sharada Swaminathan, Shiladitya Sengupta, Ashish Kulkarni
Journal: Cancer Research (2017)

Abstract Immunotherapy has stolen the spotlight as one of the most promising therapeutic strategies for many late stage cancers. Despite exhibiting immense potential, dendritic cell (DC) based immunotherapy has shown limited clinical benefits owing to the antagonistic effects of regulatory T cells. While regulatory T-cells dampen the immune response elicited by T effector cells through known control mechanisms, they also constitute an immune suppressive milieu with several other tumor-derived factors that impair the development and maturation of dendritic cells. This serves as a mechanism for the tumor cells to escape immune surveillance and control. It is well known that inhibition of the JAK2/STAT-3 and p38 MAPK pathways in DCs negates the tumor-induced suppression of their maturation. But it has been shown that inhibition of the STAT-3 pathway alone could counteract the suppressive effects of Interleukin-6 only and inhibition of the p38 MAPK pathway in cancer cells can be counterproductive as it is important for apoptosis. Thus it becomes essential that, to achieve a superior therapeutic response it is imperative to couple the inhibition of STAT-3 along with p38 MAPK pathway and to also ensure that it is targeted towards dendritic cells of the tumor microenvironment. We have catered to these necessities in this study by proposing a novel, supramolecular 2-in-1 nanomedicine designed by the self-assembly of patient compatible lipids that houses a STAT-3 inhibitor and a p38-α inhibitor , thus ensuring the deterministic delivery of both the drugs in a spatially constrained manner. We have shown that the 2-in-1 nanomedicine achieves superior efficacy by releasing both the drugs in a sustained manner during the differentiation of DCs and hence upregulates dendritic cell maturation markers like CD80, CD86 and MHC II. More importantly we aim to program the drug-loaded nanoparticles for selective uptake by dendritic cells of the tumor milieu. In a separate experiment we have shown that dendritic cells favor the uptake of nanoparticles with specific surface charges both in vitro and in vivo in B16F10 mouse melanoma model. Thus we conclude that the proposed 2-in-1 “sniper” nanoparticle can contribute immensely towards a targeted immunotherapy approach for rescuing dendritic cells from immune suppression in aggressive cancers like melanoma. Note: This abstract was not presented at the conference. Citation Format: Siva Kumar Natarajan, Vineethkrishna Chandhrasekar, Noha Ismail, Sharada Swaminathan, Shiladitya Sengupta, Ashish Kulkarni. 2-in-1 “sniper” nanomedicines rescue dendritic cells by two pronged inhibition of JAK2/STAT-3 and p38 MAPK pathways. [abstract]. In: Proceedings of the AACR Special Conference on Engineering and Physical Sciences in Oncology; 2016 Jun 25-28; Boston, MA. Philadelphia (PA): AACR; Cancer Res 2017;77(2 Suppl):Abstract nr B52.
CXCR7 Regulates SDF-1 Induced Adhesion and Homing in Multiple Myeloma.
Authors: Nicholas Burwick, Anne-Sophie Moreau, Xiaoying Jia, Xavier Leleu, Judith Runnels, Hai T. Ngo, Molly R. Melhem, Aldo M. Roccaro, Abdel kareem Azab, Irene M. Ghobrial
Journal: Blood (2008)
Outcomes of gemcitabine (Gem)-based palliative first-line therapy in the treatment of recurrent disease or of initially unresectable pancreatic cancer (PC).
Authors: Sina Rosenblender, Jens Stieler, Sven Bischoff, Marianne Sinn, Uwe Pelzer, Jana Kaethe Striefler, Bernd Dörken, Hanno Riess
Journal: Journal of Clinical Oncology (2015)

e15218 Background: It remains unclear, whether survival from the initiation of Gem-based first-line therapy differs between previously operated patients with or without adjuvant chemotherapy with Gem and patients receiving palliative therapy after a diagnosis of PC in an initially unresectable disease stage. Methods: We retrospectively analysed prospectively collected data of 702 PC-patients treated at “Charité Campus Virchow-Klinikum” between 1991 and 2014. Kaplan-Meier estimates of the primary endpoints PFS and OS from the initiation of palliative first-line therapy were compared with the aid of log-rank test with two-sided p-values of < 0.05 for 462 patients with Gem-based palliative first-line therapy. Among them, 140 had been operated with curative intent, 45 having, 95 not having received adjuvant therapy; 322 had been treated palliatively after first diagnosis of PC. Prognostic factors of statistical significance were established by Cox regression analysis. Results: PFS and OS were significantly longer after previous operations with (p = 0.028 and 0.01) or without adjuvant Gem-therapy (p = 0.024 and < 0.001) compared with primarily palliative chemotherapy. The biggest survival differences showed between re-uses of Gem compared with its first applications in inoperable disease stages. Here, PFS was longer by 3 months; OS was almost doubled (median 14.46, 95%-CI: 12.95-15.96 months vs. 7.29, 95%-CI: 6.49-8.10 months, p = 0.001). By contrast, PFS (p = 0.800) and OS (p = 0.972) between previously operated patients with or without adjuvant Gem did not differ significantly. The therapy context of recurrent disease proved to be a significant and independent prognostic factor for a longer PFS (p = 0.050) and OS (p = 0.006). Conclusions: In studies, numbers of patients receiving therapy in a primarily inoperable or recurrent situation should be stated, as may subgroup analyses for status of recurrence be sensible to avoid misjudgements in therapy effects when therapy status is not distributed evenly between groups. The effect of a second Gem use did not seem to be limited compared to its first utilisation in a palliative treatment context.
Spontaneous Pregnancy and Fertility Preservation Program in Women Undergoing High Dose Chemotherapy for Hematological Malignancies.
Authors: Izhar Hardan, Dror Meirow, Avichai Shimoni, Jacob Levron, Noga Shemtov, Eduard Fridman, Yaron Zalel, Abraham Kneller, Pia Raanani, Miriam Berkowicz, Izaac Ben-Bassat, Eyal Schiff, Arnon Nagler, Jehoshua Dor
Journal: Blood (2005)