bluuebunny/crossref_metadata_2025_split huggingface dataset:
Body measurements, estrogen availability and the risk of human breast cancer: A case‐control study
Authors: Bruning P. F. , Bonfrèr J. M. G. , Hart A. A. M. , van Noord P. A. H. , van der Hoeven H. , Collette H. J. A. , Battermann J. J. , de Jong‐Bakker M. , Nooijen W. J. , de Waard F. 
Published: February 2007

AbstractRecent studies on lifestyle‐related mechanisms involved in cardiovascular risk offer important clues for a better understanding of breast‐cancer epidemiology. Central body‐fat distribution promoted by an affluent dietary intake and a sedentary lifestyle over many years is related to elevated serum triglycerides and free fatty acids, with lower levels of sex‐hormone‐binding globulin (SHBG). The resulting greater availability of estradiol not bound to SHBG could help to explain the high breast‐cancer incidence in Western industrialized countries.We conducted a case‐control study comparing 225 women aged 38 to 75 years with operable (stage I or II) breast cancer and 441 women of the same age having no breast cancer who participated in a population‐based breast‐cancer screening program. Body fatness, as measured by body mass index (BMI), fat distribution as measured by waist‐to‐hip girth ratio (WHR), body height, serum lipids, SHBG and the available fraction of estradiol were analyzed in a conditional logistic regression, together with family history for breast cancer, reproductive history and smoking.Post‐menopausal cases showed no difference in body fatness (BMI), but a significant preponderance of central adiposity (WHR). In contrast, pre‐menopausal cases were significantly leaner, but had a similar body‐fat distribution as compared with controls. In all women, WHR, and less strongly BMI, was positively correlated with serum levels of triglycerides and available estradiol fractions. An independent, positive linear correlation between body height and relative risk (RR) was observed. Moreover, a significant correlation between SHBG and menarcheal age was seen in cases, but not in controls.These data support our hypothesis that lifestyle relates to breast‐cancer risk by metabolic‐endocrine mechanisms which modulate the availability of individual sex‐steroid concentrations in plasma. The findings of height as a risk factor and adult SHBG levels being correlated with menarcheal age suggest that lifestyle factors promoting breast‐cancer development already act around puberty. The leanness of pre‐menopausal cases awaits further explanation.
Pre‐cancerous lesions of the oesophagus in Argentina: Prevalence and association with tobacco and alcohol
Authors: Castelletto R. , Muñoz N. , Landoni N. , Jmelnitzky A. , Crespi M. , Belloni P. , Chopita N. , Teuchmann S. 
Published: February 2007

AbstractThe prevalence of pre‐cancerous lesions of the oesophagus and their association with alcohol and tobacco were examined in an endoscopic survey carried out in La Plata, Argentina. The study included 406 subjects over 15 years of age attending several gastroenterology clinics because of various gastrointestinal symptoms. Among males, the prevalence rates of chronic oesophagitis, epithelial atrophy and dysplasia were 42%, 3.8% and 2.4% respectively, and in females these prevalences were 36%, 2.5% and 0.0%. The presence of these pre‐cancerous lesions was significantly associated with alcohol drinking and tobacco smoking.
Maternal and perinatal risk factors for Wilms' tumor: A nationwide nested case‐control study in Sweden
Authors: Lindblad Per , Zack Matthew , Adami Hans‐Olov , Ericson Anders 
Published: February 2007

AbstractThis report describes maternal and perinatal risk factors for Wilms' tumor analyzed in a case‐control study nested in a nationwide cohort in Sweden. The Swedish National Cancer Registry ascertained 110 cases from among successive birth cohorts from 1973 through 1984, identified by the Swedish Medical Birth Registry, the latter based on medical records. From the Birth Registry, we matched 5 controls without cancer to each case by sex and date of birth. Wilms'‐tumor children were more likely to have mothers who had been exposed to penthrane (methoxyflurane) anesthesia during delivery than mothers of controls (odds ratio (OR) = 2.4; 95% confidence interval (CI) 1.1 to 5.1); this excess risk was higher in females than males and increased with age at diagnosis. Wilms'‐tumor cases were also more likely to have had physiologic jaundice (OR = 2.3; 95% CI 1.1 to 5.0). Higher parity of the mother decreased the risk of Wilms' tumor among females (OR = 0.7; 95% C1 0.5 to 1.0). We were unable to confirm the reported increased risks of Wilms' tumor for those with high birth weights or with a maternal history of hypertension or fluid retention during pregnancy, nor did we find any association with mother's age at delivery, previous stillbirth, previous live birth, gestational length or height of the child.
Chromosomal deletions and K‐ras gene mutations in human endometrial carcinomas
Authors: Imamura Toshiro , Arima Takahiro , Kato Hidenori , Miyamoto Shingo , Sasazuki Takehiko , Wake Norio 
Published: February 2007

AbstractForty‐two endometrial carcinomas of various stages of progression were analyzed to search for loss of chromosomal regions and for point mutations of ras genes and amplification of Int‐2 gene. This approach is particularly favorable for observation of genetic events and their significance in the process of neoplastic conversion by considering the clinico‐pathological characteristics of each tumor. At least 3 genetic events, including 18q, 17p deletions, and point mutations at codon 12 of the K‐ras gene, are implicated in the development of endometrial carcinomas. Likely targets for allelic losses on chromosomes 18q and 17p are the DCC gene and the p53 gene sequences, respectively. Overall numbers of allelic losses in individual tumors appeared to increase in case of advanced stage tumors, thereby indicating the association of allelic loss accumulation with tumor progression. The genetic features seen in 2 juveniletype adenocarcinomas and 2 clear‐cell carcinomas suggested the possibility that etiological factors providing selective pressure for particular mutation sub‐sets during carcinogenesis are probably heterogeneous.
CA125‐response assessment in epithelial ovarian cancer
Authors: Cruickshank D. J. , Terry P. B. , Fullerton W. T. 
Published: February 2007

AbstractTo assess the clinical potential of serial serum CA125 measurements in the follow‐up of patients with epithelial ovarian cancer, 74 consecutive unselected patients with histologically confirmed ovarian carcinoma were studied prospectively. There was an 83% concordance between clinical assessment and CA 125 assessment of response. The positive predictive values of a rising CA125 for disease progression and a falling CA125 for disease regression were 0.93 and 0.94, respectively. The absolute CA125 values during observations of complete response (mean 96 U/ml; 95% confidence interval; 33 to 128 U/ml), partial response (mean 134 U/ml; 95% confidence interval; 98 to 159 U/ml) and stable or progressive disease (mean 391 U/ml; 95% confidence interval; 282 to 545 U/ml) were significantly different. A randomized study is required to determine whether CA125 monitoring has any benefit in terms of outcome, and particularly survival, in epithelial ovarian cancer.
Defective autologous mixed lymphocyte reaction (AMLR) and killer activity generated in the AMLR in cancer patients
Authors: Iwahashi Makoto , Tanimura Hiroshi , Yamaue Hiroki , Tsunoda Takuya , Tani Masaji , Tamai Mikiko , Noguchi Kohei , Hotta Tsukasa 
Published: February 2007

AbstractThe autologous mixed lymphocyte reaction (AMLR) and the killer activity generated in the AMLR (AMLR‐killer) in the spleen and the peripheral blood of patients with gastric cancer were investigated. The AMLR in cancer patients was suppressed, especially in the spleen, compared to that seen in controls. There was no correlation between AMLR activity and the stage status of the cancer. The cytotoxic activity of AMLR‐killer cells against various tumor‐cell lines was also suppressed in the spleen, and had a tendency to be suppressed in the peripheral blood of cancer patients. The autologous tumorkilling activity of AMLR‐killer cells was developed in cancer patients with high AMLR activity, but was not induced in patients with low AMLR activity. Autotumor killing activity was decreased by the elimination of CD4+ cells, whereas the elimination of CD 16+ cells resulted in a marked reduction in cytotoxicity against K562, indicating that the non‐specific killer cells which lysed K562 were different from the specific killer cells that lysed autotumor cells. This suggests that AMLR activity is related to the differentiation and proliferation of lymphocytes with specific or non‐specific cytotoxic activity and that this activity plays an important role in immune surveillance against tumors.
Expression of myc‐family genes in established human multiple myeloma cell lines: L‐myc but not c‐myc gene expression in the U‐266 myeloma cell line
Authors: Jernberg‐Wiklund H. , Pettersson M. , Larsson L‐G. , Anton R. , Nilsson K. 
Published: February 2007

AbstractDeregulated c‐myc expression, as a consequence of translocation of the c‐myc gene to one of the immunoglobulin loci, appears to play an important role in the pathogenesis of several B‐cell tumors, including Burkitt's lymphoma, mouse plasmacytoma and rat immunocytoma. This study investigated the expression of c‐myc and 2 other members of the myc gene family, L‐ and N‐myc, at the mRNA and protein level, and analyzed for possible rearrangements of these genes in the human counterpart to the mouse plasmacytoma—multiple myeloma (MM). Nine well‐characterized MM cell lines were examined by using Northern‐ and Southern‐blot analysis and immunoprecipitation. The c‐myc gene was found to be highly expressed in most MM cell lines. The level of expression was comparable to that observed in the COLO 320 and HL‐60 cell lines, carrying amplified c‐myc genes, and to that of B‐cell lines with a higher proliferative activity than the MM cell lines. In the U‐266 MM cell line, L‐myc, but no c‐myc mRNA or protein, was found. The L‐myc gene was expressed in both early‐ and late‐passage U‐266 cells, suggesting that the L‐myc expression was not the result of the in vitro cultivation. N‐myc was not expressed in any of the MM cell lines. No rearrangements of c‐myc or L‐myc genes were found. We thus conclude that (a) in contrast to the corresponding mouse and rat B‐cell tumors, c‐myc is not frequently rearranged in MM; (b) c‐myc is highly expressed in most MM lines; and (c) L‐myc but not c‐myc is expressed in the U‐266 MM cell line.
Reactivity to TGF‐β is one step towards transformation in a murine fibroblast cell line
Authors: Götschl Michaela , Höfler Petra , Bauer Georg 
Published: February 2007

AbstractHigh doses of TGF‐β induce reactivity to TGF‐β in a distinct number of C3H10T1/2 fibroblasts suspended in soft agar. Reactive cells can be isolated and stably maintain this property. In the absence of exogenously added TGF‐β, these cells do not form colonies, but show distinct changes in their morphology and cytoskeleton. In contrast to normal C3H10T1/2 cells, they are able to form colonies when low doses of TGF‐β are added. TGF‐β‐reactive cells are more easily transformed by UV light than normal C3H10T1/2 cells, and so maintain their transformed phenotype in the absence of added TGF‐β. Reactivity for TGF‐β, therefore, represents one step towards transformation.
An in vitro fibroblast model system to study myc‐driven tumour progression
Authors: Chisholm Orin , Symonds Geoff 
Published: February 2007

AbstractWe have utilized fibroblast cell lines to investigate myc‐mediated cell transformation and tumour progression. Deregulated myc alleles were introduced into the rat fibroblast cell line, Rat‐1, and a partially‐transformed derivative of this cell line termed Rat‐1(PT). A human c‐myc gene coupled to the Moloney murine leukemia virus long terminal repeat was introduced into both cell lines by transfection. The avian MC29 v‐myc gene was introduced into the Rat‐1 cell line by retroviral infection using a Moloney murine leukemia recombinant retrovirus. For both cell lines, the introduction of exogenous myc genes resulted in an increased degree of transformation. For the non‐tumorigenic Rat‐1 cell line, this also resulted in the acquisition of tumorigenicity, while for the Rat‐1(PT) cell line the degree of tumorigenicity was increased. Various clones were isolated and, for both human c‐myc and avian v‐myc, the level of myc expression correlated with the degree of transformation and the tumorigenic potential of the cell lines. In addition, both these parameters could be increased by passaging through syngeneic recipients. Our data show that tumour progression may be driven by the deregulated expression of myc genes; that transformation and tumorigenicity correlate with the level of exogenous myc expression; that additional events involving both in vitro and in vivo selection are involved in this process; and that myc expression may increase the cells' metastatic capacity.
The geography of non‐ocular malignant melanoma in India: its association with latitude, ozone levels and UV light exposure
Authors: Krishnamurthy Sarala 
Published: February 2007

AbstractUltraviolet light from sunlight is implicated in the aetiology of non‐ocular malignant melanoma, mostly from Western studies. This study reports the relation of such melanomas from 7 cancer registries in different parts of India with latitude, altitude, ozone levels and ultraviolet (UV) light exposure. A log linear model was fitted using GLIM, assuming Poisson errors in incidence; linear and non‐linear regression techniques were also used. Results show slight negative associations of melanoma with latitude, X2 = ‐3.37, p = 0.07, and statistically nonsignificant ones with atmospheric ozone levels (r = ‐0.36, n.s.), and a positive association with UV (r = 0.30, n.s.). Melanoma incidence from 4 places relates in a parabolic curve with latitude (y = I‐0.09 X2 + 0.003 X2 in males and y = 1.73–0.17 X2 + 0.005 X2 in females). Patients originally from west coastal ethnic/linguistic communities predominate in Bombay. Geographic patterns of melanoma in Indians are similar with those in white Caucasians. Ultraviolet light exposure may also be involved in its aetiology in non‐white Caucasians, such as Indians.
Hypoxanthine‐guanine phosphoribosyl‐transferase in childhood leukemia: Relation with immunophenotype, in vitro drug resistance and clinical prognosis
Authors: Pieters R. , Huismans D. R. , Loonen A. H. , Peters G. J. , Hählen K. , van der Does‐van den Berg A. , van Wering E. R. , Veerman A. J. P. 
Published: February 2007

AbstractDecreased activity of hypoxanthine‐guanine phosphoribosyltransferase (HGPRT), responsible for the conversion of 6‐mercaptopurine and 6‐thioguanine (6‐TG) to their cytotoxic nucleotides, may cause resistance to these thiopurines in experimental leukemic systems. The clinical significance of this mechanism is as yet unclear. In 83 children with untreated acute lymphoblastic leukemia (ALL), we determined the prognostic value of HGPRT activity and the relation between HGPRT activity and resistance to thiopurines. HGPRT activity was determined radiochemically; in vitro resistance to 6‐TG with the MTT assay. HGPRT level was significantly lower in T‐ALL than in B‐lineage ALL; no differences were found between sequential differentiation stages of B‐lineage ALL. HGPRT activity was inversely related to the white‐blood‐cell count (WBC). Among patients with cALL and pre‐B‐ALL with WBC < 50 × 109/I, cases with a low HGPRT had a significantly poorer prognosis than those with a high HGPRT. WBC, age, sex, organomegaly and differentiation stage were comparable in both patient groups. No correlation was found between HGPRT activity and in vitro 6‐TG resistance in cALL and pre‐B‐ALL patients. T‐ALL cases were not more 6‐TG‐resistant than cALL and pre‐B‐ALL cases. Cells from 6 relapsed ALL cases did not show decreased HGPRT activity. We conclude that: (a) HGPRT is lower in T‐ than in B‐lineage ALL and is constant in sequential differentiation stages of B‐lineage ALL; (b) HGPRT activity is inversely related to tumor load; (c) low HGPRT activities are correlated with a poorer prognosis in precursor B‐ALL but this cannot be explained by thiopurine resistance because (d) there is no relation between HGPRT activity and in vitro 6‐TG resistance.
Doxorubicin: monoclonal antibody conjugate for therapy of human cervical carcinoma
Authors: Yeh Ming‐Yang , Roffler Steve R. , Yu Mu‐Hsien 
Published: February 2007

AbstractDoxorubicin (Dox) was conjugated via a dextran linker to the F(ab′)2 fragment of monoclonal antibody (MAb) IH10 which recognizes an antigen expressed on the surface of human cervical carcinoma cells and tissues. Drug‐antibody conjugates (IH10‐Dox) with a molar ratio of Dox to MAb ranging from 40:1 to 60:1 retained antigen‐binding and pharmacological activities. Anti‐tumor activity of the conjugate in vitro was evaluated by measuring inhibition of [5‐3H]‐uridine incorporation into cellular RNA. IH10‐Dox was found to be 30 times more toxic to cervical tumor cells than a control MAb‐Dox conjugate and 150 times more potent than Dox coupled to dextran. In addition, IH10‐Dox was less toxic to antigen‐negative cells in vitro, suggesting that IH10‐Dox killing of cervical carcinoma cells was antibody‐mediated. 125I‐labeled IH10‐Dox preferentially localized in solid human cervical carcinoma xenografts in athymic mice with tumor‐to‐blood ratios of IH10‐Dox reaching 17.9 after 24 hr and 32.8 after 48 hr. Treatment of athymic mice bearing human cervical tumors with IH10‐Dox resulted in a dose‐dependent inhibition of tumor growth. Multiple administrations of IH10‐Dox at a dose corresponding to 20 μg doxorubicin significantly suppressed the growth of human cervical tumors in nude mice without significant side effects (weight loss), and this suppression was antibody specific. Both i.p. and i.v. administration of IH10‐Dox were found to be equally effective. Our results suggest that IH10‐Dox may be useful for the treatment of human cervical carcinoma.
Human renal‐cell carcinoma cells are able to activate natural killer cells
Authors: Hayakawa Kazuhiro , Morita Tatsuo , Augustus Lazel B. , von Eschenbach Andrew C. , Itoh Kyogo 
Published: February 2007

AbstractWe previously reported that natural killer (NK) cells that had infiltrated renal‐cell carcinoma (RCC) proliferated vigorously in culture with interleukin‐2 (IL‐2) and lysed autologous tumor cells. In this study, we investigate the susceptibility of RCC cells to NK‐cell lysis and their ability to stimulate proliferation and increase phenotypic expression and function of NK cells. Cells from primary culture of RCC (p‐RCC cells) were significantly more susceptible to the lysis mediated by human NK3.3 clones than were cells from primary culture of metastatic melanomas. Both RCC‐cell clones and cells from primary culture of non‐tumorous kidneys were also susceptible to lysis by NK3.3 clones and IL‐2‐activated peripheral blood lymphocytes (PBLs). Incubation of NK3.3 clones with p‐RCC cells in the absence of IL‐2 induced proliferation of NK3.3 clones, whereas incubation with cells from primary culture of metastatic melanomas, K562 cells, or any others tested did not. The p‐RCC cells from earlier passages were more potent inducers of NK‐cell proliferation than were those from older passages. Cell‐free culture superna‐tants of p‐RCC cells with or without NK3.3 clones failed to induce NK‐cell proliferation. Incubation of CD16+ NK cells purified from PBLs with p‐RCC cells induced higher proliferation of the NK cells only in the presence of IL‐2, whereas incubation with cells from primary culture of metastatic melanomas did not. Incubation of NK3.3 clones with p‐RCC cells resulted in an increase in CD16, CD25 (IL‐2 receptor‐α), and HLA‐DR antigen expression and cytotoxicity in NK3.3 clones. In summary, these results suggest that RCC cells are able to activate NK cells, potentially through cell‐to‐cell interaction.
Pharmacodynamics and pharmacokinetics of intravesical mitomycin C upon different dwelling times
Authors: de Bruijn Ernst A. , Sleeboom Harm P. , van Helsdingen Peter J. R. O. , van Oosterom Allan T. , Tjaden Ubbo R. , Maes Robert A. A. 
Published: February 2007

AbstractThe schedule in dosing of intravesical chemotherapy has thus far received little attention. Correlation of optimal contact time with bladder toxicity, as well as maximal chemotherapeutic effect for one of the drugs of first choice for intravesical instillation, i.e. mitomycin C (MMC), is a particularly important question. In a randomized study, we treated bladder cancer patients with intravesical MMC using 30‐min and 60‐min dwelling times. There were 28 evaluable patients in each of the 2 groups. The groups were comparable with respect to mean age, sex ratio and distribution of primary or recurrent and single or multiple tumors. Stages and grades of tumors were also comparable over both treatment groups. Pharmacokinetics of MMC and degradation/metabolism were monitored during the first 4 cycles and the last (8th) cycle using HPLC and mass spectrometry. Recurrence was significantly lower in the 60‐min treatment group (35.7% vs. 14.3%, x2 test; 0.01 < p < 0.05). No recurrences were found in patients with Ta and Tl tumors when the 60‐min dwelling time was used. Toxicity was mild and transient; the incidence was, surprisingly, lower in the 60‐min group but the difference failed to reach the level of significance. Pharmacokinetics of systemic MMC and recovery in the urine was comparable over both groups and systemic absorption was calculated to be in the range of 1–5%.
High protein, saturated fat and cholesterol diet, and low levels of serum lipids in colorectal cancer
Authors: Trichopoulou A. , Tzonou A. , Hsieh C. C. , Toupadaki N. , Manousos O. , Trichopoulos D. 
Published: February 2007

AbstractIn a case‐control study probing the role of diet on the occurrence of colorectal cancer and undertaken in Athens, Greece, sera were collected from 100 cases and 100 controls, and serum total cholesterol, high‐density‐lipoprotein (HDL) cholesterol and triglycerides were determined. The biochemical results were analyzed in conjunction with nutrient intakes and a dietary score that summarizes in a linear way the dietary contrast between high‐risk (high protein, saturated fat and dietary cholesterol; low vegetable) and low‐risk (low protein, saturated fat and cholesterol; high vegetable) patterns. Cases with colorectal cancer had significantly (p < 0.001) and substantially lower values of serum total cholesterol and particularly HDL cholesterol, but these associations did not reflect dietary practices, since protein intake and, to a lesser (and nonsignificant) extent, saturated fat and dietary cholesterol intake were higher among cases than among controls. In absolute terms, the dietary effect (as summarized in the linear dietary score) is more evident among persons with low serum total cholesterol and HDL cholesterol than among those with high levels of these serum lipids. These results indicate that a diet beneficial with respect to the risk of coronary heart disease is also likely to reduce the risk of colorectal cancer, even though low levels of serum total cholesterol and particularly HDL cholesterol represent important independent correlates of clinically overt colorectal cancer.