bluuebunny/crossref_metadata_2025_split huggingface dataset:
A prospective study of the independent effects of parity and age at first birth on breast cancer incidence in England and Wales
Authors: Leon D. A. 
Published: February 2007

AbstractThe independent effects of parity and age at first birth on breast cancer incidence are investigated in a 1% sample of women aged 16 to 59 from the 1971 Census of England and Wales. Over the period 1971–81, 1,003 breast cancer cases occurred in the cohort of 113,263 women who were either married, widowed or divorced at the time of Census. Age at first birth was positively related to breast cancer risk, women giving birth to their first child after 35 years being at greater risk than nulliparous women. This effect remained, after adjustment for number of live‐born children. Breast cancer risk showed a statistically significant decline with increasing parity even after adjustment for age at first birth. These results are consistent with other published evidence which suggests that other births subsequent to the first have an independent effect on breast cancer risk.
Binding of epidermal growth factor and insulin‐like growth‐factor I in renal carcinoma and adjacent normal kidney tissue
Authors: Pekonen Fredrika , Partanen Seppo , Rutanen Eeva‐Marja 
Published: February 2007

AbstractThe binding of epidermal growth factor (EGF) and insulinlike growth factor I (IGF‐1) to cell membranes was determined in 14 renal cancers and in 13 normal kidney tissues adjacent to the tumors. The soluble 34K 1GF binding protein (34K IGF‐BP) content and the phosphotyrosyl‐protein phosphatase activity in renal cancer tissue and adjacent normal tissue were also determined. The specific EGF receptor binding in renal cancers was 12.7 ± 2.5% (mean ± SEM) as compared to 2.6 ± 0.2% (mean ± SEM) in normal tissues (p < 0.01). Phosphotyrosyl‐protein phosphatase activity in renal cancer tissue was less than half of that observed in normal renal tissue (p < 0.01). The highest IGF‐1 binding was observed in 5 renal cancers although no consistent differences between IGF‐1 binding to tumor and normal tissues were observed. Both EGF and IGF binding to kidney tissue were higher than binding to gastro‐intestinal tissue irrespective of whether normal or malignant tissues were compared. All normal kidney tissues and 7 of 8 kidney tumors contained measurable amounts of 34K IGF‐BP as determined by RIA and the cross‐linking technique. In 2 tumor tissue samples the 34K IGF‐BP content was increased 8‐ and 15‐fold over that seen in adjacent normal kidney tissue, whereas in the 6 other renal cancers the 34K IGF‐BP was similar to that observed in normal kidney tissue.
High frequency of Ki‐ras codon 12 mutations in pancreatic adenocarcinomas
Authors: Grünewald Kurt , Lyons John , Fröhlich Anja , Feichtinger Hans , Weger Richard A. , Schwab Gerhard , Janssen Johannes W. G. , Bartram Claus R. 
Published: February 2007

AbstractThe frequency of Ki‐ras gene mutations was studied in 100 paraffin‐embedded sections obtained from 63 pancreatic adenocarcinomas by in vitro amplification of target sequences via polymerase chain reaction (PCR) and selective oligonucleotide hybridization. Forty‐seven (75%) of the tumors contained a Ki‐ras mutation at codon 12. No predominant amino acid substitution or nucleotide transition at this codon was observed. Two carcinomas exhibited 2 distinct Ki‐ras mutations. No particular correlation could be established between the incidence of Ki‐ras mutation and clinical parameters (sex, age, survival), tumor grade or tumor stage.
Age‐ and sex‐specific cumulative rate and risk of ATLL for HTLV‐I carriers
Authors: Kondo Toshifumi , Kono Hidehisa , Miyamoto Naoaki , Yoshida Ryouichi , Toki Hironobu , Matsumoto Isao , Hara Masamichi , Inoue Hiroo , Inatsuki Akira , Funatsu Takashi , Yamano Norio , Bando Fumihiro , Iwao Eiichi , Miyoshi Isao , Hinuma Yorio , Hanaoka Masao 
Published: February 2007

AbstractWe have surveyed the incidence of adult T‐cell leukemia/lymphoma (ATLL) in an endemic area of 290,464 inhabitants for 7 years. We now revise our previous results on the basis of additional findings and estimate the age‐ and sex‐specific cumulative rate for HTLV‐I carriers, the adoption of which is recommended by current cancer epidemiology as a new age‐standardized incidence rate. An unequivocal age‐dependent increase in seroprevalence was observed for both sexes with a characteristic predominance in females. The age‐dependent seroconversion in females may be partly explained by additional infection from infected husbands to their wives but the reason for men remains obscure. The mean annual number of incident cases of ATLL was 11.4, giving 3.9 ATLL patients annually per 105 inhabitants, 6.1 per 105 inhabitants aged over 30, and 85.0 per 105 seropositives aged over 30. Crude annual incidence rate of ATLL among 105 male seropositives aged over 30 was 145.3 and that for females was 55.2 and 95% confidence intervals of ATLL incidence rates were 34.8 to 255.7 for males and 6.4 to 104.1 for females, respectively. Although the sex ratio of 80 ATLL patients was 1.35, males are more prone to the disease (46 male patients among 4,522 male seropositives aged over 30 vs. 34 female patients among 8,801 female seropositives aged over 30; p < 0.001) for unknown reason(s). Morbidity in male seropositives aged over 30 is 2.6 times as high as that of females. Decennial incidence rates in males in their fifties and sixties were significantly higher than those in females. The remarkable male preponderance in oncogenicity of HTLV‐I may be due to the fact that men are more prone to the disease and the number of female carriers in the denominator used to calculate the incidence rate is larger than that of males. The whole life span (0–79) cumulative risk for males was 6.9% and significantly higher than that of females (2.95%).
Characterization of a novel mouse reticular cell sarcoma M5076 subline resistant to cisplatin
Authors: Ferrari A. , Damia G. , Erba E. , Rossi C. , Mandelli R. , D'incalci M. 
Published: February 2007

AbstractA novel murine tumor resistant to cis‐diamminedichloroplatinum (cisplatin, DDP) was obtained (M5/DDP) after 22 passages in which mice bearing the ovarian reticular cell sarcoma M5076 (M5) were treated with DDP. Although DDP conserved some inhibitory activity on growth of M5/DDP, it was much less effective than on M5. Treatment with DDP did not prolong the survival time of mice with M5/DDP, whereas it markedly prolonged survival of M5‐bearing mice. MS and M5/DDP tumors shared many biological and biochemical features. They were similar histologically, they metastasized reproducibly to the liver and were poorly immunogenic. Their growth rates were comparable; their DNA index, percentage of cells in S phase and intra‐cellular glutathione content were also similar. In both tumors, DDP caused an accumulation of cells in S late‐G2‐M within 24 hr after drug treatment. However, this was efficiently reversed in M5/DDP, whereas it worsened and persisted longer in M5. Cross‐resistance was observed between DDP and its analogues carboplatin and iproplatin, but tetraplatin retained marginal activity on M5/DDP tumor. Several alkylating agents tested [L‐phenylalanine mustard (L‐PAM); cyclophosphamide (CTX); chlorambucil (CLB); 1,3‐bis(2‐chloroethyl)‐I‐nitrosourea (BCNU) and dacarbazine (DTIC)] were not totally cross‐resistant to DDP, but showed greater activity on M5 than on M5/DDP. Other non‐alkylating anti‐neoplastic drugs showed a similar degree of activity on M5 and M5/DDP. 5‐Aza‐2′‐deoxycytidine (Aza‐d‐Cyd) was very effective on both tumors, etoposide (VP‐16) and cytosine arabinoside (Ara‐C) had no activity and Adriamycin (ADR) was weakly effective.
Distinct chromosomal abnormalities in murine leukemia virus‐induced T‐ and B‐cell lymphomas
Authors: Vasmel W. L. E. , Matthews E. A. , Gillis C. P. M. , Nieland J. , Borst E. A. , Leupers C. J. M. , Melief C. J. M. , Slater R. M. 
Published: February 2007

AbstractWe performed a cytogenetic study on 16 murine mature B‐cell lymphomas and 10 T‐cell lymphomas, using G‐banding techniques. All tumors, with the exception of 3 spontaneous B‐cell tumors, were induced by various slowly transforming murine leukemia virises (MuLV). Metaphases were obtained from primary (10 B‐cell tumors) and first or second transplant generation lymphomas (6 B‐cell and 10 T‐cell tumors), all of which were well characterized with respect to phenotypic, histologic and genotypic features. In the T‐cell tumors we found relatively simple karyotypic abnormalities, including various numerical aberrations, such as trisomy 15, in line with many earlier reports. However, the majority of B‐cell tumors showed a great variety of both structural and numerical chromosomal anomalies. Three B‐cell lymphomas had an apparently normal karyotype. No single cytogenetic abnormality occurred commonly in the B‐cell lymphomas, but some structural abnormalities were found in more than one stemline, in particular, ins (11) (A1; A2) in 3 tumors, and deletions involving the D‐region of chromosome 14 in 3 other lymphomas. These cytogenetic results clearly indicate that the pathogenic mechanisms involved in MuLV‐induced (long latency) B‐cell lymphomagenesis and (short latency) T‐cell lymphomagenesis differ considerably.
Retrovirally induced murine B‐cell tumors rarely show proviral integration in sites common in T‐cell tumors
Authors: Matthews E. A. , Vasmel W. L. E. , Schoenmakers H. J. , Melief C. J. M. 
Published: February 2007

AbstractThe molecular etiology of retrovirally induced T‐cell tumors has been shown in many cases to involve proviral integration near a cellular oncogene, c‐myc, N‐myc, Pim‐1 and pvt‐1 being frequent targets for insertional activation. Murine B‐cell tumors induced by infection with murine leukemia virus have been studied for rearrangements in these and other loci. In contrast to the T‐cell lymphomas, tumors of the B‐cell lineage, either early B‐cell tumors induced in nude mice or late B‐cell tumors in immunocompetent mice, did not show disruption of N‐myc or Pim‐1 in any of the tumors studied, although those lymphomas had acquired many new proviruses. The loci c‐abl, bcl‐2, fis‐1, c‐erbB, c‐myb, and neu were likewise not involved. Rearrangement of c‐myc was seen in 1 out of 71 and rearrangement of the pvt‐1 locus in 4 out of 73 (5%) of the B‐cell tumors. Thus it appears that mechanistic differences exist in the development of T‐cell tumors and B‐cell tumors caused by the same etiological agent.
Quantitative determination of water‐ and lipid‐soluble antioxidants in neoplastic and non‐neoplastic human breast tissue
Authors: Langemann H. , Torhorst J. , Kabiersch A. , Krenger W. , Honegger C. G. 
Published: February 2007

AbstractAscorbic acid, cysteine, glutathione and uric acid were determined by reverse‐phase high‐pressure liquid chromatography (HPLC) in 46 breast tissue samples [neoplastic (C) and non‐neoplastic (N) from the same patient]. Cholesterol, α‐tocopherol and γ‐tocopherol were quantified in 64 similar samples by extraction into heptane followed by direct‐phase HPLC. DNA was measured in all samples and the percentages of epithelium, fat and connective tissue were estimated in sections adjacent to the sample. Results confirm previous findings that ascorbic acid and glutathione, expressed as μmol/g DNA, were greatly increased in the epithelium of neoplastic tissue. Similar increases in cysteine could be accounted for by the presence of inflammatory cells. Although values of α‐ and γ‐tocopherol correlated with the percentage of fat in both types of tissue, these compounds were also present in the epithelium. Because of the varying amounts of fat in the samples, no significant difference could be found between N and C values. Cholesterol correlated with fat in N and epithelium in C. Consideration of 10 cases with equal amounts of fat in C and N tissue suggests that cholesterol is reduced in C in the epithelial cells.
Growth rate, kinetics of tumor cell proliferation and long‐term outcome in human breast cancer
Authors: Tubiana Maurice , Pejovic Marie Héléne , Koscielny Serge , Chavaudra Nicole , Malaise Edmond 
Published: February 2007

AbstractThymidine labelling index (LI) was prospectively assayedin vitroin a series of 128 consecutive patients with breast cancer. The follow‐up was longer than 15 years for all patients. The distribution of LI was log normal and patients were subdivided into 3 groups (patients with LI = m ± σ, lower than m — σ and greater than m + σ where m is the geometrical mean). The incidence of relapse and death remained significantly lower in the group with a low LI than in the 2 other groups, whereas the difference between the 2 other groups faded away when follow‐up exceeded 10 years. Multivariate analyses show that LI is one of the two most important independent prognostic indicators for relapse or death, the other being histological grading. Data concerning 2,648 patients treated at our Institute, prior to the introduction of chemotherapy into treatment protocols, have been used to investigate the influence of tumor growth rate on the probability of distant dissemination. A model of the natural history was used, in order to generate metastasis appearance curves, in 3 subgroups of patients, according to the value of the tumor doubling time (TDT). Our results show that after a follow‐up exceeding 8 years, there is no longer any difference between the subgroups of patients with rapid or intermediate growth rate, whereas after 25 years large and highly significant differences in relapse and survival between the slow‐growing tumors and the other two subgroups still remain. These two sets of data concur to show that tumor growth rate or proliferation rate correlates with the probability of metastatic dissemination.
Nuclear DNA, serum sialic acid and measured depth in malignant melanoma for predicting disease recurrence and survival
Authors: Silver Hulbert K. B. , Karim Karim A. , Riche Jean Le , Jong Gary De , Spinelli John , Worth Ann , McLean David I. , Gallagher Richard 
Published: February 2007

AbstractIn a previous multivariate analysis of 151 malignant melanoma patients we identified measured depth of primary lesion (Breslow) and serum N‐acetyl‐neuraminic acid (NANA) concentration as significant independent predictors of recurrence. Our present study examines the contribution of flow cytometric DNA analysis to prediction of recurrence and survival. Fixed, paraffin‐embedded specimens of primary lesions were evaluated from 63 of the previously studied patients. These were prepared for DNA analysis. Of the 28 primaries identified as aneuploid 17 later recurred, while this was true for only 9 of the 35 diploid tumors. On multivariate analysis measured depth was again the most significant predictor of recurrence (p< 0.001). Additional independent predictors were DNA ploidy (p= 0.02) and NANA (p= 0.05). For survival the independent predictors were measured depth (p= 0.003) and NANA (p= 0.05). Measured depth, DNA ploidy and NANA can be used to construct a model predicting the recurrence risk for stage‐1 melanoma.
Early diagnosis of bilateral retinoblastoma reduces death and blindness
Authors: Derkinderen D. J. , Koten J. W. , Van Romunde L. K. J. , Nagelkerke N. J. D. , Tan K. E. W. P. , Beemer F. A. , Den Otter W. 
Published: February 2007

AbstractThe influence of early diagnosis on sight and survival was studied in 130 patients with bilateral retinoblastoma. Nineteen patients died of this condition. Statistical analysis predicted that 12 of these 19 early deaths could have been prevented if doctors' delay had been less than I week. Consequently, a reduction of 65% in mortality is possible. Similarly, statistical analysis also predicted that the number of patients with resulting blindness could be reduced by 40%. Central registration and monitoring of retinoblastoma families would greatly improve early diagnosis.
Cytogenetic study on eleven cutaneous neoplasms and two pre‐tumoral lesions from xeroderma pigmentosum patients
Authors: Aledo Rosa , Dutrillaux Bernard , Lombard Martine , Aurias Alain 
Published: February 2007

AbstractEleven independent tumors (5 basal‐cell carcinomas, 5 squamous‐cell carcinomas and 1 malignant melanoma), 2 pre‐tumoral lesions and one common nevus, developing in the skin of 10 unrelated XP patients were cytogenetically analyzed. No specific chromosomal changes were observed. Two features were relevant, however: emergence of several independent clones and over‐involvement of telomeric and cen‐tromeric regions in the formation of chromosomal rearrangements, jumping translocations were observed in 2 squamous‐cell carcinomas involving telomeric and centromeric regions.
Interleukin‐1β induces tumor necrosis and early morphologic and metabolic changes in transplantable mouse tumors. Similarities with the anti‐tumor effects of tumor necrosis factor α or β
Authors: Belardelli F. , Proietti E. , Ciolli V. , Sestili P. , Carpinelli G. , Di Vito M. , Ferretti A. , Woodrow D. , Boraschi D. , Podo F. 
Published: February 2007

AbstractPeri‐tumoral injection of recombinant human interleukin‐I ß in mice transplanted s.c. with Friend erythroleukemia cells (FLC) resulted in marked inhibition of tumor growth and increased survival. However, in vitro treatment of FLC (745 or 3CI‐8) with IL‐Iß barely inhibited cell multiplication. IL‐Iß, injected into established solid tumors, induced marked morphologic changes. Vascular congestion and focal extravasation of erythrocytes were observed as early as 6 hr after injection with IL‐Iß of FLC and L1210 tumors and HeJ16 fibrosarcomas. Focal areas of disaggregation of tumor cells and tumor necrosis were observed 6 and 24 hr after IL‐I injection. These morphologic changes were similar to those observed in FLC tumors or HeJ16 fibrosarcomas treated with TNF‐α or ß. These cytokines determined morphological changes in tumor blood vessels of FLC tumors within I hr of injection. Freshly dissected FLC tumors and their tissue extracts were studied by Nuclear Magnetic Resonance (NMR) spectroscopy, shortly after peri‐tumoral injection of IL‐Iß or TNF‐ß. After 6 hr, both cytokines induced a 3‐fold reduction in the levels of two catabolites, glycerophosphorylcholine and glycerophospho‐rylethanolamine, an accumulation of sn‐glycerol 3‐phosphate and a more than 10‐fold increase in the choline/phosphoryl‐choline ratio. These results are similar to those reported for TNF‐α, and can be interpreted on the basis of an activation of glycerophosphorylcholine phosphodiesterase (EC 3.1.4.2) and partial inhibition of choline kinase (EC 2.7.1.32). IL‐Iß and TNF‐ß (like TNF‐α) also induced alkaline shifts (0.10‐0.25 units) in the average intratumoral pH value. We suggest that alterations of tumor blood vessels may be the primary events in solid tumors treated with IL‐Iß or TNF. Such alterations lead to early changes in tumor metabolism and subsequent tumor cell degeneration.
Enhanced tumor growth and metastatic spread of an mh 134 variant lacking a part of the mm antigen: A possible role of antibody‐dependent cellular cytotoxicity in control of tumor growth and metastases
Authors: Hara Hideki , Kawase Ichiro , Komuta Kiyoshi , Masuno Tomiya , Kishimoto Susumu 
Published: February 2007

AbstractThe role of antibody‐dependent cellular cytotoxicity (ADCC) in host defense against tumor growth and metastasis was investigated with MH134, an MM antigen‐positive murine hepatoma, and MH134‐M, a variant with enhanced tumori‐genesis and metastasis, in syngeneic C3H/HeN mice. When inoculated subcutaneously into C3H/HeN mice, MH134‐M tumors grew more rapidly than did MH134 tumors and consistently metastasized to the draining lymph nodes, whereas MH134 tumors did not. Also, MH134‐M exhibited a significantly greater lung colonization potential than did MH134, when inoculated intravenously into C3H/HeN mice. In BALB/c nu/nu mice, however, solid MH134 tumors grew and metastasized to the same extent as MH134‐M, indicating that there is no significant intrinsic difference between these two tumor lines in proliferative or metastatic capacity. Enzyme‐linked immunosorbent assay (ELISA) and immunoblotting, performed after SDS‐PAGE analysis of cellular extracts with a monoclonal antibody (MAb) that recognizes a part of the MM antigen, revealed that the cells of MH134‐M lack at least a part of the MM antigen. Sera of C3H/HeN mice bearing solid MH134 tumors were found to contain anti‐MM‐antigen antibodies, when tested by immunoblotting of SDS‐PAGE‐developed materials. Cytotoxicity testing in which thioglycol‐late‐induced peritoneal macrophages were used as effector cells revealed that antibodies present in sera strongly induced ADCC to MH134 but not to MH134‐M. On the other hand, sera of MH134‐M tumor‐bearing C3H/HeN mice neither contained anti‐MM‐antigen antibodies nor induced ADCC to MH134 or MH134‐M tumor cells. Intravenous injection of car‐rageenan into C3H/HeN mice bearing solid MH134 tumors significantly enhanced tumor growth, whereas the growth of subcutaneously injected MH134‐M tumors was not influenced by this treatment. These results suggest that the enhanced tumorigenesis and metastasis of the MH134‐M line in C3H/ HeN mice are based, at least in part, on significant loss of the MM antigen and the resultant inability to induce ADCC‐triggering antibody production during tumor growth.
Identification by C‐banding of two human prostate tumour cell lines, 1013L and DU 145
Authors: Hartley‐Asp Beryl , Billström Anita , Kruse Elisabeth 
Published: February 2007

AbstractTwo human prostate carcinoma cell lines are easily distinguished by C‐banding. DU 145 has one metacentric chromosome with a large centromeric band, I metacentric and 2 acrocentric chromosomes with interstitial C‐bands. The Y chromosome was present in 48% and 42% of the cells at passages 83 and 106, respectively, whereas in I0I3L only one metacentric chromosome contained distinct extra C bands—one at the centromere and one interstitially. The Y chromosome was present in 72% of the cells at passage 15 and in 20% at passage 22, but by passage 44 it had disappeared. Karyotype analysis using G‐banding revealed that DU 145 had retained several of its original markers, and demonstrated multiple marker chromosomes in 1013L.
Abnormal DNA content in liver‐cell dysplasia: A flow cytometric study
Authors: Roncalli M. , Borzio M. , Brando B. , Colloredo G. , Servida E. 
Published: February 2007

AbstractTo clarify the true nature of liver‐cell dysplasia (LCD), a flow cytometric study has been performed. The DNA content of hepatocytes from 26 cases of cirrhosis with diffuse areas of LCD was investigated and compared to that of hepatocytes from 21 control patients with non‐neoplastic and neoplastic liver conditions. Flow cytometric analysis was performed on propidium‐stained nuclei from archival paraffin‐embedded material. Analysis was directed to assessment of diploid as well as non‐diploid peaks by calculation of DNA index (Dl), using normal hepatocytes present in each sample as individual and specific references. Since only samples containing at least 10,000 nuclei were considered suitable for analysis, 4 of the 26 LCD cases were discarded. Eight of 22 LCD cases had an abnormal DNA content compared with 0/11 non‐neoplastic cases (p < 0.05) and 8/10 hepatocellular carcinomas (p < 0.05). Nonneoplastic control cases displayed uniformly diploid stemlines whereas hepatocellular carcinomas had in 8/10 cases bimodal or trimodal populations. Thus, LCD is a heterogeneous lesion in terms of ploidy, and the abnormal DNA content observed in some cases supports its pre‐neoplastic nature.