bluuebunny/crossref_metadata_2025_split huggingface dataset:
Exploring feminist evaluation: The ground from which we rise
Authors: Sielbeck‐Bowen Kathryn A. , Brisolara Sharon , Seigart Denise , Tischler Camille , Whitmore Elizabeth 
Published: December 2002

AbstractThis chapter is the fruit of discussions among several evaluators with feminist inclinations. The authors explore numerous ideas or guidelines pertinent to feminist inquiry and begin the conversation that continues throughout this volume.
Gender matters: Feminist research in educational evaluation
Authors: Pillow Wanda S. 
Published: December 2002

AbstractThe key insights and shifts in first‐, second‐, and third‐wave feminism are examined, along with the impact on methodological thinking of what may be broadly termed “race‐based” feminisms, lesbian theory, postcolonial feminist theory, and post‐structuralism. This overview provides a present‐day portrait of where feminist theory is now and the continued importance of paying attention to gender, particularly in education.
Feminist evaluation in the international development context
Authors: Bamberger Michael , Podems Donna R. 
Published: December 2002

AbstractThis chapter reviews U.S. and other Western researchers' treatment of issues affecting women in evaluations of the impacts of international development assistance. In most cases, the evaluations do not adopt a specifically feminist approach but rather a women‐in‐development (WID) or, more recently, a gender approach. The authors discuss the extent to which these approaches address feminist research concerns and how a more explicitly feminist approach could strengthen the evaluation design.
Inhibitory effect of p27KIP1 gene transfer on head and neck squamous cell carcinoma cell lines
Authors: Koh Tae‐Yong , Park Seok‐Woo , Park Kyung‐Ho , Lee Sang‐Goo , Seol Jae‐Goo , Lee Dong‐Wook , Lee Choon‐Taek , Heo Dae‐Seog , Kim Kwang‐Hyun , Sung Myung‐Whun 
Published: December 2002

AbstractBackground.Although p27 gene mutations are rarely found in cancer, the level of p27 protein expression decreases during tumor development. In several tumors, including laryngeal cancer, decreased expression of p27 is associated with a poor prognosis.Methods.The proliferation‐inhibitory effect of p27 gene transfer on human head and neck squamous cell carcinoma (HNSCC) cell lines (SNU‐1041, SNU‐1066, and SNU‐1076) by adenoviral vector was investigated.Results.On transduction of the human HNSCC cell line with adenovirus‐p27 (Ad‐p27), a high level of p27 expression and increase of cyclin D1 and E were observed. Cell cycle analysis showed a marked decrease in the proportion of cells in S phase and an increase in G1 phase. Soft agar clonogenic assay showed a marked decrease in clonogenicity.Conclusion.These results suggested that overexpression of p27 could show proliferation‐inhibitory effects on HNSCC cell lines. Thus, gene therapy using adenovirus‐p27 seemed to have a potential to develop into a new cancer gene therapy modality. © 2002 Wiley Periodicals, Inc. Head Neck 25: 000–000, 2003
Transcervical superior mediastinal lymphadenectomy in the management of papillary thyroid carcinoma
Authors: Khoo Mark L. C. , Freeman Jeremy L. 
Published: December 2002

AbstractAim.Surgery is the treatment of choice for lymph node metastases in papillary thyroid carcinoma. When adequately treated by surgical extirpation, the presence of lymph node involvement does not seem to have a negative impact on cure rates or survival. Surgical lymphadenectomy for metastatic papillary thyroid carcinoma has been well described for both the central and the lateral compartments of the neck. Superior mediastinal lymphadenectomy, however, has only sporadically been mentioned. We describe our experience with transcervical superior mediastinal lymphadenectomy (TSML) that avoids the morbidity of the traditional sternal split.Materials and Methods.This retrospective analysis included 30 patients (24 women and 6 men; age range, 17–72 years) who underwent TSML by the senior author (JLF) for papillary carcinoma metastatic to the superior mediastinum between 1985 and 1999. Histopathologic examination confirmed positive nodes in all the mediastinal dissections. All patients received postoperative I131.Results.All the patients are alive after a median follow‐up of 5 years (range, 1–14 years). Twenty‐nine of 30 patients remain free of disease, whereas one patient is alive with lung and bone metastases. No patient has had local or regional relapse. The only significant complication was a high incidence of temporary (70%) and later permanent (50%) hypoparathyroidism.Conclusions.TSML is a safe and effective treatment for superior mediastinal metastases in papillary thyroid carcinoma. © 2002 Wiley Periodicals, Inc. Head Neck 24: 000–000, 2002
Prognostic impact of reoxygenation in advanced cancer of the head and neck during the initial course of chemoradiation or radiotherapy alone
Authors: Dietz Andreas , Vanselow Bernhard , Rudat Volker , Conradt Christian , Weidauer Hagen , Kallinowski Friedrich , Dollner Ralph 
Published: December 2002

AbstractBackground.Previous studies have shown that radiation of hypoxic tumors can result in reoxygenation phenomenon. The relevance of this phenomenon for prognosis is unclear. This study analyzes whether the presence of hypoxia, or the extent to which reoxygenation occurs during the initial phase of primary chemoradiation or radiotherapy, can predict the clinical outcome in advanced tumors of the head and neck.Methods.The distribution of oxygen partial pressures was determined using pO2 histography (Kimoc 6650, Sigma pO2‐Histograph, Eppendorf, Hamburg, Germany). In cervical lymph node metastases of 37 patients with advanced carcinoma of the head and neck (stage IV, UICC), these values were determined before the start of primary chemoradiation or radiotherapy alone (pO2x). Thirty‐two of 37 patients were reexamined after 1 week of therapy, and measurements were taken again in the same nodes (pO2y). The results obtained from these measurements were correlated with both, the initial response to therapy and follow‐up results (43 months).Results.In all patients, pronounced hypoxia (median pO2, 3.2 mmHg) was found before therapy. In 19 of 32 patients, chemoradiation/radiotherapy induced reoxygenation (ΔO2 = pO2y − pO2x), with median ΔpO2 increasing to 6.5 mmHg after 1 week (p = .049). The group of patients with a complete or partial response showed only a slight increase of median ΔpO2 (1 mmHg) compared with a strong reoxygenation effect in the group of patients with no change (mean value of median ΔpO2 = 10.3 mmHg; p = .0062). The group of patients with ΔpO2 values lower than median showed significantly better survival rates compared with the other group (p = .036).Conclusion.These data suggest that reoxygenation under therapy may have prognostic relevance in patients with advanced carcinoma of the head and neck treated by primary chemoradiation or radiation therapy. Remarkably, however, a poor outcome was associated with a higher degree of reoxygenation. © 2002 Wiley Periodicals, Inc. Head Neck 24: 000–000, 2002
The treatment of squamous cell carcinoma of the tonsil with neck node metastases
Authors: Jones Andrew Simpson , Fenton John Eugene , Husband David John 
Published: December 2002

AbstractBackground.Patients with tonsillar carcinoma and neck nodes seen at the clinic are not an uncommon occurrence in head and neck practice. Over the years, treatment has ranged from radical jaw neck dissection to radical neck dissection for the nodes and primary radiotherapy to the primary site. Much controversy exists as to which treatment modality yields the best survival. Certainly, surgery to the oropharynx leads to gross morbidity, with problems of swallowing, speech, and cosmesis, although it has been claimed that radiotherapy with neck dissection yields a lower cure rate.Methods.We investigated a retrospective series of 96 patients all of whom had squamous cell carcinoma of the tonsil and associated lymph node metastases. Of these, 44 primary tumors were treated with surgery and 52 with irradiation. All 44 patients in the surgery group had a radical neck dissection, as did all but 12 in the radiotherapy group.Results.Of the tabulations, patients in good general condition were more likely to receive primary surgery. Overall cause‐specific survival for all patients was 69%. Multiple logistic regression revealed no associations; thus, the radiotherapy and surgery groups were well matched. Five‐year actuarial survival for those having irradiation was 74%. The five‐year survival for the group receiving surgery was 63% (p= .4372). This lack of difference between survival for surgery and radiotherapy was confirmed using Cox's proportional hazards model.Conclusion.We conclude that tonsillar carcinoma with lymph nodes can be safely treated by applying appropriate radiotherapy to the tonsillar region and treating the neck with radical surgery, if the disease is more than N1. © 2002 Wiley Periodicals, Inc. Head Neck 24: 000–000, 2002
Targeting epidermal growth factor receptor in head and neck cancer
Authors: Ford Allison Carter , Grandis Jennifer Rubin 
Published: December 2002

AbstractIt is well known that growth factors play an important role in normal cell proliferation by means of stimulation of growth factor receptors located on the surface of cells. Tumor cells express high levels of growth factor receptors that can theoretically serve as therapeutic targets in cancer treatment. Tyrosine kinase (type 1) growth factor receptors include the family of erbB receptors. The most extensively studied receptor in the erbB family is the human epidermal growth factor receptor (EGFR), also known as erbB1. Studies have shown that overexpression of EGFR is involved in the development and progression of head and neck squamous cell carcinoma (HNSCC). Blocking this receptor in HNSCC cell lines and animal models inhibits tumor growth. Strategies have been developed to target EGFR, including monoclonal antibodies, tyrosine kinase–specific inhibitors, ligand‐linked immunotoxins, and antisense approaches. Laboratory studies and clinical trials are under way to explore the safety and efficacy of these various approaches in a variety of cancers, including HNSCC. Preliminary results from early phase clinical trials are encouraging and may lead to the incorporation of these EGFR targeting strategies into the management of HNSCC. © 2002 Wiley Periodicals, Inc. Head Neck 25: 000–000, 2003
Health‐related quality of life of children with acute lymphoblastic leukaemia: Comparisons and correlations between parent and clinician reports
Authors: Waters Elizabeth B. , Wake Melissa A. , Hesketh Kylie D. , Ashley David M. , Smibert Elizabeth 
Published: December 2002

AbstractThe improving prognosis for children with cancer refocusses attention to long‐term outcomes with an emphasis on quality of life. Few studies have examined relationships and differences in reported results between the parent, child and clinician. We examined parent‐proxy and clinician‐reported functional status and health‐related quality of life for children and adolescents with acute lymphoblastic leukemia (ALL). Children and adolescents, 5–18 years, in the maintenance phase of treatment for ALL attending the Haematology/Oncology outpatient clinic at the Royal Children's Hospital, Melbourne, were eligible. Measures included: 1) parent‐reported functional health and well‐being (Child Health Questionnaire [CHQ]); 2) parent‐reported condition specific quality of life (Pediatric Cancer Quality of Life inventory [PCQL]); 3) clinician ratings of physical and psychosocial health; and 4) clinical indicators. Insufficient numbers of older patients prohibited collection of adolescent self‐reports. We had a 94% response and 31 participants. Mean time since diagnosis: 1.5 (SD 0.4) years. Parents reported significantly lower functioning and well‐being than population norms for all CHQ scales, whereas cancer‐specific quality of life was comparable to PCQL norms. Clinician reports of the child's global physical and psychosocial health were moderately associated with each other (rs = 0.56, p < 0.001), and with the parent‐reported physical (rs = 0.47, p < 0.01) and psychosocial (rs = 0.56, p < 0.001) CHQ summary scores. Clinician reports of the child's psychosocial health were not associated with any clinical indicators reported regularly. The results demonstrate that the social, physical and emotional health and well‐being of children with ALL is significantly poorer than the health of their community‐based peers. Routinely collected indicators of clinical progress conceal the psychosocial burden of ALL. Data on health, well‐being and quality of life can easily be incorporated into clinical care. © 2002 Wiley‐Liss, Inc.
TCDD‐dependent downregulation of γ‐catenin in rat liver epithelial cells (WB‐F344)
Authors: Dietrich Cornelia , Faust Dagmar , Moskwa Matthias , Kunz Anja , Bock Karl‐Walter , Oesch Franz 
Published: December 2002

AbstractTCDD (2,3,7,8‐tetrachlorodibenzo‐p‐dioxin) is the most potent tumor promoter ever tested in rodents. Although it is known that most of the effects of TCDD are mediated by binding to the aryl hydrocarbon receptor (AHR), the mechanisms leading to tumor promotion still remain to be elucidated. Loss of contact‐inhibition is a characteristic hallmark in tumorigenesis. In WB‐F344 cells, TCDD induces a release from contact‐inhibition manifested by a 2‐ to 3‐fold increase in DNA‐synthesis and the emergence of foci when TCDD (1 nM) is given to confluent cells. We focussed our interest on potential cell membrane proteins mediating contact‐inhibition in WB‐F344 cells, namely E‐cadherin, α,‐ β,‐ and γ‐catenin (plakoglobin). Using indirect immunofluorescence, E‐cadherin, α‐, β‐ and γ‐catenin were detected at cell adhesion sites in untreated, confluent cells. After TCDD‐exposure, γ‐catenin was exclusively localized in the cytoplasm whereas localization of E‐cadherin, α‐ and β‐catenin remained unaffected. Cytoplasmic γ‐catenin could be extracted by Triton X‐100 treatment, demonstrating that γ‐catenin was no longer bound to the actin cytoskeleton. Western blot analysis showed downregulation of γ‐catenin protein levels. This effect was not blocked by pre‐incubation with the selective proteasome inhibitor MG‐132, indicating that proteolytical degradation of γ‐catenin by the proteasome system was not increased by TCDD. Because mRNA‐levels of γ‐catenin were markedly diminished after TCDD‐exposure, we conclude that transcriptional downregulation or destabilization of the mRNA contributes to the decrease in γ‐catenin protein levels in response to TCDD. Because γ‐catenin is considered to be a tumor suppressor, our findings might give more insight into the tumor promoting actions of TCDD. © 2002 Wiley‐Liss, Inc.
Potent activity of soluble B7RP‐1‐Fc in therapy of murine tumors in syngeneic hosts
Authors: Ara Gulshan , Baher Angelo , Storm Neal , Horan Tom , Baikalov Claudia , Brisan Emil , Camacho Reuben , Moore Alison , Goldman Hartt , Kohno Tadahiko , Cattley Russell C. , Van Gwyneth , Gaida Kevin , Zhang Ming , Whoriskey John S. , Fong David , Yoshinaga Steven K. 
Published: December 2002

AbstractWe have characterized a receptor:ligand pair, ICOS:B7RP‐1, that is structurally and functionally related to CD28:B7.1/2. We reported previously that B7RP‐1 costimulates T cell proliferation and immune responses (Yoshinaga et al., Nature 1999;402:827–32; Guo et al., J Immunol 2001;166:5578–84; Yoshinaga et al., Int Immunol 2000;12:1439–47). We report that B7RP‐1‐Fc causes rejection or growth inhibition of Meth A, SA‐1 and EMT6 tumors in syngeneic mice. Established Meth A tumors were rejected effectively with a single dose of B7RP‐1‐Fc, however, the treatment was less effective on larger tumors. Mice that rejected Meth A tumors previously by Day 30, also rejected a subsequent Meth A challenge on Day 60, without additional B7RP‐1‐Fc treatment, indicating a long‐lived memory response. Tumor cells believed to be less immunogenic, such as P815 and EL‐4 cells, were less responsive to this treatment. The EL‐4 responsiveness to the B7RP‐1‐Fc treatment was enhanced, however, by pre‐treatment of the mice with cyclophosphamide. As expected, T cells appeared to be targeted by B7RP‐1‐Fc treatment. Thus, the administration of soluble B7RP‐1‐Fc may have therapeutic value in generating or enhancing anti‐tumor activity in a clinical setting. © 2002 Wiley‐Liss, Inc.
Multiple meningiomas: Investigating the molecular basis of sporadic and familial forms
Authors: Heinrich Bianca , Hartmann Christian , Stemmer‐Rachamimov Anat O. , Louis David N. , MacCollin Mia 
Published: December 2002

AbstractMeningiomas are common tumors of the coverings of the central nervous system (CNS), comprising 20% of intracranial neoplasms. The only genes known to be associated with sporadic meningiomas are NF2 on chromosome 22 and the related cytoskeleton element DAL‐1 on chromosome 18. Between 1 and 8% of patients with meningiomas develop multiple meningiomas, a trait transmitted occasionally in an autosomal dominant fashion. We investigated the DAL‐1 and NF2 loci in 7 unrelated multiple meningioma patients without clinical evidence of NF2 by mutational and pathological analysis. Five novel intragenic microsatellite polymorphisms were developed for specific detection of loss of heterozygosity (LOH) at the DAL‐1 locus. Three of 7 patients had affected relatives and all affected individuals were female. No tumors from familial patients were of a fibroblastic subtype. Truncating NF2 mutations were detected in 3 tumor specimens, but were not present in the corresponding blood samples. Two tumors showed LOH at the NF2 locus. All tumors showing mutations at the NF2 locus originated from patients without affected relatives and were of the fibroblastic subtype. Five non‐truncating alterations in the DAL‐1 gene were found, however, LOH of chromosome 18 markers was not seen in any tumor. In contrast to the NF2 results, all DAL‐1 alterations were found in paired blood specimens. Our findings provide further evidence that the molecular basis of sporadic and familial multiple meningiomas is fundamentally different and extend this dichotomy to pathologic subtypes. DAL‐1 does not function as a true tumor suppressor in these patients. © 2002 Wiley‐Liss, Inc.
Natural killer, but not natural killer T, cells play a necessary role in the promotion of an innate antitumor response induced by IL‐18
Authors: Hashimoto Wataru , Tanaka Fumiaki , Robbins Paul D. , Taniguchi Masaru , Okamura Haruki , Lotze Michael T. , Tahara Hideaki 
Published: December 2002

AbstractIL‐18 administration promotes innate immunity resulting in significant antitumor effects in multiple murine tumor models. Here, we examined the effector population mediating the innate immunity. Most NK cells and some NKT cells express IL‐18Rs without prior stimulation (65% positive in NK cells, 18% positive in NKT cells), though few naive T cells do. In vivo depletion of NK cells, but not NKT cells, using AsGM1 antibody significantly reduces IL‐18‐induced cytotoxicity. However, NK‐like activity of hepatic MNCs for the NK target YAC‐1 was present in Vα 14 NKT cell–deficient animals. Furthermore, administration of rIL‐18 greatly reduced B16 pulmonary metastases in vivo in NKT cell–deficient animals. When sorted NK and NKT cells were exposed to IL‐18 in vitro, NK cells showed more IFN‐γ production and cytolysis against YAC‐1 than NKT cells in response to IL‐18. These results are consistent with the notion that NK cells, but not NKT cells, are the major effectors in IL‐18‐induced innate immunity. © 2002 Wiley‐Liss, Inc.
Hodgkin's lymphoma cell lines are characterized by frequent aberrations on chromosomes 2p and 9p including REL and JAK2
Authors: Joos Stefan , Granzow Martin , Holtgreve‐Grez Heidi , Siebert Reiner , Harder Lana , Martín‐Subero José I. , Wolf Jürgen , Adamowicz Martyna , Barth Thomas F.E. , Lichter Peter , Jauch Anna 
Published: December 2002

AbstractFour Hodgkin's lymphoma cell lines (KM‐H2, HDLM‐2, L428, L1236) were analyzed for cytogenetic aberrations, applying multiplex fluorescence in situ hybridization, chromosome banding and comparative genomic hybridization. Each line was characterized by a highly heterogeneous pattern of karyotypic changes with a large spectrum of different translocated chromosomes (range 22–57). A recurrent finding in all cell lines was the presence of chromosomal rearrangements of the short arm of chromosome 2 involving the REL oncogene locus. Furthermore, multiple translocated copies of telomeric chromosomal segments were frequently detected. This resulted in a copy number increase of putative oncogenes, e.g., JAK2 (9p24) in 3 cell lines, FGFR3 (4p16) and CCND2 (12p13) in 2 cell lines as well as MYC (8q24) in 1 cell line. Our data confirm previous cytogenetic results from primary Hodgkin's tumors suggesting an important pathogenic role of REL and JAK2 in this disease. In addition, they provide evidence for a novel cytogenetic pathomechanism leading to increased copy numbers of putative oncogenes from terminal chromosomal regions, most probably in the course of chromosomal stabilization by telomeric capture. © 2002 Wiley‐Liss, Inc.
Multigene analysis of Rb pathway and apoptosis control in esophageal squamous cell carcinoma identifies patients with good prognosis
Authors: Güner Dilek , Sturm Isrid , Hemmati Philipp , Hermann Sandra , Hauptmann Steffen , Wurm Reinhard , Budach Volker , Dörken Bernd , Lorenz Matthias , Daniel Peter T. 
Published: December 2002

AbstractDeregulation of cell‐cycle G1‐restriction point control by disruption of Rb‐pathway components is a frequent event in cancer. In concert with the inactivation of cell death pathways, such events not only contribute to tumor development but also determine the intrinsic and acquired resistance to cancer therapy and, ultimately, disease prognosis. We previously observed that the cyclin‐dependent kinase inhibitor p16INK4a and the proapoptotic Bcl‐2 homolog Bax are positive prognostic factors and identify patients with good prognosis in esophageal squamous cell carcinoma (SCC). In the present study, we therefore extend our analysis to additional genes controlling the G1 restriction point and apoptosis, respectively. This retrospective analysis was performed in a cohort of 53 patients undergoing surgery for esophageal SCC with curative intent, i.e., R0 resection. Protein expression profiles of cyclin D1, p16INK4a, Rb, p21CIP/WAF‐1, p53, Bax and Bcl‐2 were analyzed by immunohistochemistry and compared to p53 mutational status, as determined by SSCP‐PCR of exons 5–8. Loss of p16INK4a, Rb, p21CIP/WAF‐1 or Bax and overexpression of cyclin D1 were associated individually with shorter overall survival, while Bcl‐2 expression and p53 mutation were not of prognostic relevance. The longest survival was observed in a subgroup of patients whose tumors bore a combination of favorite genotypes, i.e., low cyclin D1 and high Rb, p21CIP/WAF‐1, p16INK4a and Bax protein expression. These results show that multigene analyses based on limited sets of functionally linked genes reliably identify patients with good vs. poor prognosis. © 2003 Wiley‐Liss, Inc.