bluuebunny/crossref_metadata_2025_split huggingface dataset:
Regulation of cell survival in burkitt lymphoma: Implications from studies of apoptosis following cold‐shock treatment
Authors: Gregory Christopher D. , Milner Anne E. 
Published: February 2007

AbstractBurkitt lymphoma (BL) tumour‐cell populations are known to display high rates both of proliferation and of apoptosis in vivo, but the mechanisms which determine whether a BL cell continues to cycle or engages its cell‐death programme are not understood. Group‐I BL‐derived cell lines, which retain in vitro the proliferateve and apoptotic capacities of the parental cells, selectively entered apoptosis when returned to 37°C after a brief period at low temperature (1°C). The induction of apoptosis by cold treatment, as determined by morphological characteristics and DNA fragmentation, was readily detectable within the first 1 to 2 hr of re‐incubation at 37°C, reaching a maximum at 4 to 6 hours. Commitment to enter apoptosis occurred after as little as 20 to 30 min at 1°C. Significant cell death at 1°C occurred only during prolonged incubation in the cold and displayed the characteristics of necrosis. Both bc1‐2‐dependent and ‐independent survival pathways were found to provide protection from cold‐induced apoptosis, but only if engaged before cold‐shock treatment. These results indicate that continued cycling of group‐1 BL cells is dependent upon their capacity to inhibit or circumvent their normally constitutively active apoptotic programme, and are consistent with the notion that the synthesis of one or more critical “survival” proteins of short half‐life is necessary to guarantee successful passage through the cell cycle. Notably, high levels of apoptosis were also inducible in group‐1 BL cells by inhibitors of RNA and protein synthesis. © 1994 Wiley‐Liss, Inc.
Developmental stages in experimental liver metastases: Relation to invasiveness
Authors: Dingemans Koert P. , van den Bergh Weerman Marius A. , Keep Robert F. , Das Pranab K. 
Published: February 2007

AbstractWe have previously reported that an invasive morphotype can be evoked in a rat colon carcinoma by transplanting it into pre‐induced subcutaneous granulation tissue. We have now studied the interaction of the same tumor with liver tissue, which is extremely poor in connective tissue in comparison with the subcutaneous site. Tumor cells were injected into the portal system and the resulting experimental liver metastases were examined by electron microscopy and immunohistochemistry. Early metastases consisted of well‐differentiated acini, fully surrounded by connective tissue that was derived from the periportal stroma. In a later stage, this connective tissue was overgrown by tumor cells and, almost immediately, acinar differentiation was lost. Most metastases eventually reached the liver capsule, which reacted by forming a layer of granulation tissue. Only in this layer, we observed invasion by thin tumor cell strands, which were often intimately associated with fibroblasts or with blood capillaries. The tumor cells remained smooth and rounded during this process. After fully penetrating the granulation tissue, the tumor cell strands reached the liver surface, where they formed poorly structured papillary masses that were nearly devoid of stroma. Our observations indicate that, even in a relatively homogeneous organ like the liver, the tumor‐host interaction is highly complex and dynamic. They also confirm the notion that granulation tissue stimulates tumor invasiveness. Finally, they show that tumor cells can actively invade host tissues without exhibiting a “fibroblastic” morphology. © 1994 Wiley‐Liss, Inc.
Correlation between p53 gene expression and tumor‐cell proliferation in oropharyngeal cancer
Authors: Bourhsis J. , Boso J. , Wilson G. D. , Bressac M. , Talbot M. , Leridant A. M. , Dendale R. , Janin N. , Armand J. P. , Luboinski B. , Malaise E. P. , Wibault P. , Eschwege F. 
Published: February 2007

AbstractThe aim of our study was to analyze the correlation between tumor‐cell kinetics measured in vivo and p53 gene expression in a series of 49 oropharyngeal cancers. The duration of the S phase (TS), the labelling index (LI) and the potential doubling time (Tpot) were obtained by flow‐cytometry measurements of a tumor biopsy obtained after i.v. injection of 200 mg bromode‐oxyuridine into patients. An adjacent section of the same samples was studied by immunohistochemistry for the detection of p53 protein. Over‐expression of the p53 protein, as defined by strong p53 immunostaining of tumor nuclei, was found in 23/49 of the samples. Aneuploid tumors showed a higher LI, a shorter Tpot and a higher proportion of p53 gene over‐expression. A significant correlation was seen between p53 over‐expression and short Tpots. Indeed 87.5% of the tumors with a very short Tpot (⩽ 3 days) had p53 over‐expression, as compared with 27% of tumors with a longer Tpot (>3 days). Our data strongly suggest that over‐expression of the p53 gene is associated with rapid tumor‐cell proliferation in this type of cancer. © 1994 Wiley‐Liss, Inc.
Karyotypic characterization of bronchial large cell carcinomas
Authors: Johansson Maria , Dietrich Claudia , Mandahl Nils , Hambraeus Göran , Johansson Leif , Clausen Per Praetorius , Mitelman Felix , Heim Sverre 
Published: February 2007

AbstractCytogenetic analysis of short‐term cultures from 26 primary bronchial large cell carcinomas and 1 metastasis from a primary large cell carcinoma revealed clonal chromosome abnormalities in 20 tumors and a normal karyotype in 6. No outgrowth was obtained in 1 case. Simple aberrations were present in 3 tumors; in 1, the only change was a reciprocal translocation between chromosomes 1 and 6, in another the sole anomaly was a supernumerary marker ring chromosome and in a third loss of the Y chromosome was the only clonal change. The remaining 17 tumors had complex karyotypes. The chromosomes most frequently involved in structural rearrangements were chromosomes 1, 2, 3, 5, 6, 7, 6, 10, 11, 13, 14 and 17. The bands most frequently affected were 1q11‐12, 1p13. 7q11, and 17p11‐13. The rearrangements led to repeated losses of 1p, 1q, 3p, 6q, 7q and 17p and gains of 5q and 7p. The emerging karyotypic picture of large cell lung carcinomas indicates more similarities with adenocarcinomas than with other pathologic subgroups of lung cancer. © 1994 Wiley‐Liss, Inc.
Inhibition of growth of MKN45 human gastric‐carcinoma xenografts in nude mice by treatment with bombesin/gastrin‐releasing‐peptide antagonist (RC‐3095) and somatostatin analogue RC‐160
Authors: Pinski Jucek , Halmos Gabor , Yano Tetsu , Szepeshazi Karoly , Qin Yunfeng , Ertl Tibor , Schally Andrew V. 
Published: February 2007

AbstractNude mice bearing xenografts of the gastrin‐responsive human gastric carcinoma MKN45 cell line were treated for 4 to 5 weeks with bombesin/gastrin‐releasing‐peptide(GRP) antagonist (RC‐3095), somatostatin analogues RC‐160 and SMS 201‐995, or the combination of RC‐3095 and RC‐160. Tumor volumes and weights were reduced significantly to a similar extent by RC‐160 and SMS 201‐995, administered by daily s.c. injections at a dose of 100 μg/day. Bombesin/GRP antagonist RC‐3095, given s.c. at a dose of 20 μg/day, had the greatest inhibitory effect on tumor growth. The combination of RC‐3095 with RC‐160 did not further potentiate the suppression of tumor growth. Histologically, the number of mitotic cells decreased significantly in the groups treated with RC‐160 or the combination of RC‐3095 with RC‐160. Serum gastrin levels were significantly diminished in all treated groups. Therapy with RC‐160 or the combination also significantly decreased levels of serum growth hormone. Receptor assays on tumor membranes showed that bombesin was bound to 2 classes of receptor sites, one with high affinity and low capacity, the other with low affinity and high capacity. Binding sites for epidermal growth factor (EGF) were down‐regulated in tumor cells after treatment with RC‐3095, RC‐160 or the combination of RC‐3095 with RC‐160. In studies in vitro, both RC‐160 and RC‐3095 significantly inhibited the proliferation of MKN45 cells in culture as measured by cell number. These data demonstrate, for the first time, that the growth of human gastric cancer in nude mice can be inhibited not only by somatostatin analogues, but also by administration of modern bombesin/GRP antagonists, such as RC‐3095. © 1994 Wiley‐Liss, Inc.
Adoptive immunotherapy of established tumors. Acquisition of radioresistance by tumor‐specific T cells after passive transfer into tumor‐bearing recipients
Authors: Dunn Pamela L. , North Robert J. 
Published: February 2007

AbstractThe present study was undertaken to determine the sensitivity to ionizing irradiation of T cells from mice immunized against the Meth‐A fibrosarcoma and P815 mastocytoma after the transfer of these cells into tumor‐bearing recipients. It was found that T cells from memory‐immune donors were destroyed by exposing recipients to 500 rad of gamma irradiation up to 46 hr after transfer of the cells, but not thereafter. In contrast, activated immune cells were resistant to irradiation immediately after transfer. T cells were considered to be actively immune if they were harvested from donors in the process of rejecting their tumor, and were replicating, as evidenced by sensitivity to vinblastine. Memory‐immune cells, on the other hand, were T cells that were harvested long after rejection of the immunizing tumor and were vinblastine‐resistant. Additional results showed that CDB+ memory T cells were needed to cause regression of Meth‐A tumor in recipients, whereas CD4+ memory T cells were needed for P8IS tumor regression. These results support the idea that T cells that mediate tumor regression in this model of adoptive immunotherapy are radiosensitive while resting, and radioresistant after becoming activated. This knowledge needs to be taken into account when considering ionizing radiation as an immunomodulating agent for tumor immunotherapy. © 1994 Wiley‐Liss, Inc.
Flow‐cytometric and quantitative histologic parameters as prognostic indicators for occult retroperitoneal disease in clinical‐stage‐I non‐seminomatous testicular germ‐cell tumors
Authors: de Riese Werner T. W. , de Riese Cornelia , Ulbright Thomas M. , Walker Edwin B. , Messemer Jon , Jones Jeffrey A. , Reister Terry , Albers Peter , Allhoff Ernst P. , Foster Richard S. , Donohue John P. 
Published: February 2007

AbstractOur study was performed to clarify whether the combination of DNA flow‐cytometric and quantitative histopathological parameters improves the prediction of occult metastatic disease in clinical stage‐I non‐seminomatous testicular germ‐cell tumors (NSGCT). We used archival paraffin primary‐tumor tissue of 67 clinical stage‐I NSGCT patients who had undergone retroperitoneal lymph‐node dissection (RPLND). According to the RPLND specimens, 24 patients were at pathological stage I and 43 at pathological stage II. Archival blocks were redissected for histological re‐evaluation. In addition, 50 μm sections were prepared according to the Hedley technique in order to obtain nuclear suspensions which were processed for flow cytometry (FC). In univariate analysis, the percentage of embryonal carcinoma, the percentage of immature teratoma and vascular invasion were the most accurate predictive histopathological parameters. The percentage of aneuploid cells in S‐phase was the best predictive FC parameter. In multivariate analysis, the percentage of embryonal carcinoma and the S‐phase fraction of aneuploid cells were the only independent markers for occult metastatic disease. According to this statistical approach, 91.0% of pathological stage‐I and stage‐II cases were correctly classified. Sensitivity was 95.3% and specificity was 83.3%. Using histopathological criteria alone, only 56.7% NSGCT patients were correctly classified.
Prognostic factors in renal‐cell carcinoma: Immunohistochemical detection of p53 protein versus clinico‐pathological parameters
Authors: But Fredrik J. , Godschalk Josian C. J. , Krishnadath Kausilia K. , Van Kwast Theo H. M. Der , Bosman Fred T. 
Published: February 2007

AbstractImmunoreactivity forp53 protein was assessed in 100 cases of primary renal‐cell carcinoma (RCC). The results were correlated with clinical survival data (follow‐up 24 to 84 months: mean: 39 months) and with clinico‐pathological parameters, including nuclear grade, tumour stage, cell type, tumour architecture and tumour diameter. In all, 32% of the tumours were p53‐positive; there was no difference in survival between p53‐positive and ‐negative cases. Similarly, p53 expression did not correlate with any of the clinico‐pathological parameters mentioned. Nuclear grade (grade 1 + 2 vs. grade 3 + 4) had a striking impact on prognosis and so, to a lesser extent, did tumour stage and the occurrence of a spindle‐cell component. The immunohistochemical detection of p53 in RCC is not of prognostic value. The estimation of nuclear grade, however is a major predictor of prognosis.
Nutrients and gastric cancer risk. A population‐based case‐control study in Sweden
Authors: Hansson Lars‐Erik , Nykén Olof , Beagström Reinhold , Wolk Alicja , Lindgren Anders , Baron John , Adami Hans‐Olov 
Published: February 2007

AbstractA population‐based case‐control study of gastric cancer was conducted in areas with contrasting incidence rates in Sweden. Face‐to‐face interviews were carried out with 338 (74.1 %) of all eligible cases and 679 (77.3%) of the selected controls. Consumption of selected nutrients during adolescence and 20 years prior to interview was estimated, together with life‐time intake of vitamin supplements. Ascorbic acid and β‐carotene had an unequivocal protective effect, but α‐tocopherol and nitrate were also negatively associated with gastric‐cancer risk. In a multivariate analysis including all of these factors, only ascorbic acid remained a significant protective factor. The only macronutrient positively associated with the risk of gastric cancer was fat: intake 20 years prior to interview, but not during adolescence, was found to have a significant impact. Supplementation with vitamins almost halved the risk after adjustment for dietary intake of the corresponding vitamins. While the protective effect of vitamin C and β‐carotene could conceivably be ascribed to other agents in the diet, the strong negative association between supplementation with vitamin C and risk of gastric cancer supports the hypothesis of a protective role of this anti‐oxidant.
Genetic alterations of the putative envelope proteins encoding region of the hepatitis C virus in the progression to relapsed phase from acute hepatitis: Humoral immune response to hypervariable region 1
Authors: Sekiya Hitomi , Kato Nobuyuki , Ootsuyama Yuko , Nakazawa Takahide , Yamauchi Katsumi , Shimotohno Kunitada 
Published: February 2007

AbstractHypervariable region I (HVRI) of the putative second envelope glycoprotein (gp70) of hepatitis C virus (HCV) undergoes sequential alterations at intervals of several months during the chronic phase of hepatitis. To evaluate the implications of sequence variability in HVRI of HCV, we investigated the sequence variability of the whole envelope‐protein(gp35 and gp70)‐coding regions of HCV genome derived from patient M in acute and relapsed phases (8‐month interval) of hepatitis. From this analysis, we found that a Leu (position 405) in HVRI substituted to Pro, and that 4 additional substitutions could be detected in gp70 during the relapsed phase. Sequence‐specific antibody against HVRI derived from patient M was first detected in the serum at 8 months after the onset of hepatitis, but no other specific antibodies against peptides containing aminoacid position(s) substituted in regions other than HVRI could be detected. Epitope mapping using the sequence of HVRI derived from the acute phase of hepatitis was also performed, and a B‐cell epitope (positions 397 to 407) of 11 amino acids was identified. However, the Pro variant at position 405 did not display an escape pattern from the antibody produced at 8 months after the onset. In addition, we demonstrated the existence of important a mi no‐acid residue positions which are recognized by the anti‐HVRI antibody produced in patient M using introduction point mutations within HVRI.
Neuroblastoma cell detection by reverse transcriptase‐polymerase chain reaction (RT‐PCR) for tyrosine hydroxylase mRNA
Authors: Burchill S. A. , Bradbury F. M. , Smith B. , Lewis I. J. , Selby P. 
Published: February 2007

AbstractThe presence of tumour cells in peripheral blood of neuroblastoma patients is of considerable clinical importance. Nucleic acid amplification offers an opportunity to detect very small numbers of such cells, but in neuroblastoma a frequent specific abnormality in the tumour DNA suitable for this purpose has yet Co be identified. To facilitate the detection of such cells we have developed RT‐PCR using tyrosine hydroxylase (TH) as a tissue‐specific target gene. TH mRNA was detected in 3 neuroblastoma cell lines and in all neuroblastoma tumours examined, but was undetectable in peripheral blood from children without neuroblastoma. The method was highly sensitive, detecting 1‐10 neuroblastoma cells per 107 blood cells. Thirty blood samples from 24 patients were analysed and results were compared with known disease status. At diagnosis 4/7 patient blood specimens were positive; the four positive samples were from stage‐4 patients. In blood samples from these patients 6‐8 weeks after the initiation of treatment, TH mRNA was undetectable. Of 7 samples taken at the time of clinical relapse, 5 were positive; 4 of these were from patients with evidence of disseminating disease. Of 16 blood samples from disease‐free patients, 14 were negative and 2 were positive. One positive patient in this group subsequently had a clinical relapse. These results show that this technique is of value for detecting neuroblastoma cells in peripheral blood. The significance of these cells at diagnosis, during treatment or on follow‐up requires further evaluation.
Deletion mapping of chromosome 19 in human gliomas
Authors: von Deimling Andreas , Nagel Judith , Bender Bernhard , Lenartz Doris , Schramm Johannes , Louis David N. , Wiestler Otmar D. 
Published: February 2007

AbstractThere is evidence that a putative glioma tumor suppressor locus resides on the long arm of chromosome 19. We present data on 161 gliomas from IS6 patients, which were studied by microsatellite analysis for loss of heterozygosity (LOH) on chromosome 19. Eight loci on the long arm and 2 loci on the short arm of chromosome IV were examined. LOH on I9qwas observed in 3/19 astrocytomas (WHO grade II), 12/27 anaplastic astrocytomas (WHO grade III), 16/76 cases of glioblastoma multiforme WHO (grade IV), 4/9 oligodendrogliomas (WHO grade II), 3/5 anaplastic oligodendrogliomas (WHO grade III), 5/9 mixed oligo‐astrocytomas (WHO grade II) and 8/10 anaplastic oligo‐astrocytomas (WHO grade III). While 31 of the tumors with LOH on chromosomal arm I9q exhibited allelic loss at every informative locus, 20 tumors showed terminal or interstitial deletions. In contrast to astrocytomas and glioblastomas, tumors with an oligodendroglial component had predominantly lost the entire long arm of chromosome 19. The common region of overlap in gliomas was located on 19q 13.2‐q 13.4 between the markers D 19S 178 and D 19S 180. Our data confirm the involvement of a putative tumor suppressor gene on chromosomal arm 19q in gliomas and assign this gene to 19q 13.2‐q 13.4.
Incidence of breast cancer in women with fibroadenoma
Authors: Levi Fabio , Randimrison Lalao , Te Van‐Cong , la Vecchia Carlo 
Published: February 2007

AbstractThere is a general agreement that fibroadenoma is associated with a certain increase in breast cancer risk, but the risk estimates appear heterogeneous according to various studies. To provide further quantitative and population‐based estimates of breast cancer risk in women with histologically confirmed fibroadenomas, we linked data of 1,461 incident cases of fibroadenoma (median age, 37 years) to the Cancer Registry of the Swiss Canton of Vaud (about 600,000 inhabitants) over the period 1977–1991. After exclusion of 57 synchronous breast neoplasms, a total of 17 cases of breast cancer were observed vs. 10.9 expected (standardised incidence ratio, SIR, 1.6; 90% confidence interval: 1.1‐2.1). The SIR was similar in the short term (3–5 years) and in the medium‐long term (>5 years) following diagnosis of fibroadenoma. The cumulative risk of invasive breast cancer was 0.7% after 5 years and 2.2% after 12 years following diagnosis of fibroadenoma. This is not negligible on account of the young age of our cohort.
Characterization of a bombesin/gastrin‐releasing peptide receptor on a human gastric‐cancer cell line
Authors: Preston Shaun R. , Woodhouse Linda F. , Gokhale Jay , Miller Glenn V. , Primrose John N. 
Published: February 2007

AbstractThis study examined the expression of receptors of the bombesin (BBS) family in human gastric‐cancer cell lines. Of 5 cell lines screened, only one, St42, demonstrated specific binding sites for 125I‐Tyr4‐BBS, which have been further characterized. This binding was saturable, and temperature‐ and time‐dependent. Scatchard analysis of displacement data performed at 37°C revealed 2 binding sites: a high‐affinity, low‐capacity site (KD = 0.13 nM, Bmax = 1500 sites/cell) and a lower‐affinity, higher‐capacity site (KD = 11 nM, Bmax = 35,000 sites/cell); the latter was lost when internalization of peptide was prevented, suggesting that it may be an artefact. Displacement assays with gastrin‐releasing peptide (GRP) and neuromedin B (NMB) revealed that the receptor was of the GRP‐preferring sub‐type (GRP IC50 = 0.35 nM; NMB IC50 = 112 nM). Co‐valent cross‐linking of 125I‐Tyr4‐BBS to the receptor demonstrated the presence of a single band corresponding to a molecular weight of 37 to 44 kDa on SDS‐PAGE, similar to that of the cloned GRP receptor protein core. G‐protein linkage of this receptor was demonstrated by selective inhibition of 125I‐Tyr4‐BBS binding by guanosine nucleotides. The binding of BBS to the receptor resulted in a rise in intracellular calcium. Three of four structurally distinct BBS antagonists bound to the receptor with high affinity, but [DPhe12, Leu14]‐bombesin did not cause any displacement of 125I‐Tyr4‐BBS even at 10 mM. The functional significance of GRP receptors on human gastric‐cancer cells is as yet unknown, but further studies may determine whether such receptors have importance in the therapy of gastric cancer.