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1.
Flavia RM Latini Jefferson P Hemerly Beatriz CG Freitas Gisele Oler Gregory J Riggins Janete M Cerutti 《BMC cancer》2011,11(1):11
Background
Mounting evidence has indicated that ABI3 (ABI family member 3) function as a tumor suppressor gene, although the molecular mechanism by which ABI3 acts remains largely unknown. 相似文献2.
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Background
Pituitary tumor transforming gene (PTTG) is a novel oncogene that is expressed abundantly in most tumors. Overexpression of PTTG induces cellular transformation and promotes tumor formation in nude mice. PTTG has been implicated in various cellular processes including sister chromatid separation during cell division as well as induction of apoptosis through p53-dependent and p53-independent mechanisms. The relationship between PTTG and p53 remains unclear, however. 相似文献4.
Takakuwa O Oguri T Ozasa H Uemura T Kasai D Miyazaki M Maeno K Sato S 《Cancer chemotherapy and pharmacology》2011,68(3):669-676
Purpose
Amrubicin, a totally synthetic 9-aminoanthracycline anticancer drug, has shown promising activity for lung cancer, but little is known about the mechanism of resistance for this agent. This study was aimed to clarify the role of P-glycoprotein (P-gp) in amrubicinol, an active metabolite of amrubicin, resistance in lung cancer cells. 相似文献5.
Joanne Kotsopoulos Jacek Gronwald Henry T. Lynch Andrea Eisen Susan L. Neuhausen Nadine Tung Peter Ainsworth Jeffrey N. Weitzel Tuya Pal William D. Foulkes Charis Eng Christian F. Singer Leigha Senter Ping Sun Jan Lubinski Steven A. Narod the Hereditary Breast Cancer Clinical Study Group 《Breast cancer research and treatment》2018,168(2):421-431
Purpose
Exercise has been shown to reduce fatigue during cancer treatment. Hypothesized mechanisms include inflammatory pathways. Therefore, we investigated effects of exercise on markers of inflammation in breast cancer patients during adjuvant chemotherapy.Methods
We pooled data from two randomized controlled exercise intervention trials with breast cancer patients during adjuvant chemotherapy (n = 130), which had previously shown beneficial effects of exercise on fatigue. Exercise comprised a 12-week resistance training (BEATE study) or an 18-week combined resistance and aerobic training (PACT study). Serum IL-6, IL-1ra, and the IL-6/IL-1ra ratio were quantified at baseline, mid-intervention, post-intervention, and 6–9 months post-baseline.Results
Mixed effect models showed significant increases in IL-6 and IL-6/IL-1ra ratio during chemotherapy and decreases afterwards. Differences between exercise and control group were not significant at any time point. Changes in total cancer-related fatigue were significantly correlated with changes in IL-6/IL-1ra ratio (partial correlation r = 0.23) and IL-6 (r = 0.21), and changes in physical cancer-related fatigue with changes in IL-6/IL-1ra ratio (r = 0.21).Conclusions
Changes in fatigue were slightly correlated with changes in inflammatory markers, and there was a strong inflammatory response to adjuvant chemotherapy. The supervised exercise training did not counteract this increase in inflammation, suggesting that beneficial effects of exercise on fatigue during adjuvant chemotherapy for breast cancer are not essentially mediated by IL-6, IL-1ra, or the IL-6/IL-1ra ratio.6.
Taila Hartley Luca Cavallone Nelly Sabbaghian Rachel Silva-Smith Nancy Hamel Olga Aleynikova Erika Smith Valerie Hastings Pedro Pinto Marc Tischkowitz Eva Tomiak William D Foulkes 《Hereditary cancer in clinical practice》2014,12(1):19
Background
PALB2 has emerged as a breast cancer susceptibility gene. Mutations in PALB2 have been identified in almost all breast cancer populations studied to date, but the rarity of these mutations and lack of information regarding their penetrance makes genetic counseling for these families challenging. We studied BRCA1/2 -negative breast and/or ovarian cancer families to a) assess the contribution of PALB2 mutations in this series and b) identify clinical, pathological and family history characteristics that might make PALB2 screening more efficient.Methods
The coding region of the PALB2 gene was analyzed in 175 probands with family histories of breast and/or ovarian cancer ascertained from a single Canadian institution in Eastern Ontario.Results
We identified 2 probands with PALB2 mutations that are known or strongly considered to be pathogenic and 3 probands with missense mutations that are possibly pathogenic. One of the identified truncating mutations [c.3113G > A (p.Gly1000_Trp1038del – major product)], has been previously described while the other four mutations [c.3507_3508delTC (p.H1170Ffs*19), c.1846G > C (p.D616H), c.3418 T > G (p.W1140G), c.3287A > G (p.N1096S)] have not been previously reported. Loss of heterozygosity was detected in two breast tumors from one c.3507_3508delTC mutation carrier but not in other available tumors from that family or in tumors from carriers of other mutations.Conclusions
PALB2 mutation screening identifies a small, but significant number of mutations in BRCA1/2 -negative breast and/or ovarian cancer families. We show that mutations are more likely to be found in families with three or more breast cancers as well as other BRCA2-related cancers. In our cohort, both clearly pathogenic mutations were identified in premenopausal breast cancer cases (2/77, 2.6%). Testing should be preferentially offered to affected women from such families. 相似文献7.
Andelko Hrzenjak Farid Moinfar Marie-Luise Kremser Bettina Strohmeier Edgar Petru Kurt Zatloukal Helmut Denk 《Molecular cancer》2010,9(1):49
Background
Uterine sarcomas are very rare malignancies with no approved chemotherapy protocols. Histone deacetylase (HDAC) inhibitors belong to the most promising groups of compounds for molecular targeting therapy. Here, we described the antitumor effects of suberoylanilide hydroxamic acid (SAHA; vorinostat) on MES-SA uterine sarcoma cells in vitro and in vivo. We investigated effects of vorinostat on growth and colony forming ability by using uterine sarcoma MES-SA cells. We analyzed the influence of vorinostat on expression of different HDACs, p21WAF1 and activation of apoptosis. Finally, we examined the antitumor effects of vorinostat on uterine sarcoma in vivo. 相似文献8.
Francisco Acevedo Zhengyi Deng Victor D. Armengol Kevin Hughes 《Current breast cancer reports》2018,10(2):74-82
Purpose of Review
The use of panel testing of multiple cancer-causing genes has allowed to find a subset of patients with harmful mutations in moderate penetrance genes. While extensive information is available regarding patients with BRCA1 and BRCA2 pathogenic variants, information regarding these less common genes and their management remains scarce. The aim of this review is to discuss penetrance, incidence, and management recommendations for PALB2, ATM, and CHEK2.Recent Findings
NCCN guidelines now provide management recommendation for patients with pathogenic variants in these genes. In addition, more widespread testing has provided more information on penetrance and incidence. Although this is a huge step toward improving quality of care, prospective studies are still needed. We summarize the NCCN and other guidelines/suggestions for these genes and deliver our insight on the matter based on the best information we could find.Summary
PALB2, ATM, and CHEK2 are less penetrant than BRCA1–2 and have a different spectrum, suggesting differing management. Data about incidence and penetrance along with management recommendations for these genes are provided.9.
Edneia AS Ramos Anamaria A Camargo Karin Braun Renata Slowik Iglenir J Cavalli Enilze MSF Ribeiro Fábio de O Pedrosa Emanuel M de Souza Fabrício F Costa Giseli Klassen 《BMC cancer》2010,10(1):23
Background
CXCL12 is a chemokine that is constitutively expressed in many organs and tissues. CXCL12 promoter hypermethylation has been detected in primary breast tumours and contributes to their metastatic potential. It has been shown that the oestrogen receptor α (ESR1) gene can also be silenced by DNA methylation. In this study, we used methylation-specific PCR (MSP) to analyse the methylation status in two regions of the CXCL12 promoter and ESR1 in tumour cell lines and in primary breast tumour samples, and correlated our results with clinicopathological data. 相似文献10.
<Emphasis Type="Italic">FGFR1</Emphasis> amplification in breast carcinomas: a chromogenic <Emphasis Type="Italic">in situ</Emphasis>hybridisation analysis 总被引:3,自引:1,他引:2
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Elbauomy Elsheikh S Green AR Lambros MB Turner NC Grainge MJ Powe D Ellis IO Reis-Filho JS 《Breast cancer research : BCR》2007,9(2):R23
Background
The amplicon on 8p11.2 is reported to be found in up to 10% of breast carcinomas. It has been demonstrated recently that this amplicon has four separate cores. The second core encompasses important oncogene candidates, including the fibroblast growth factor receptor 1 (FGFR1) gene. Recent studies have demonstrated that specific FGFR1 amplification correlates with gene expression and that FGFR1 activity is required for the survival of a FGFR1 amplified breast cancer cell line. 相似文献11.
Zhao Y Li Y Wang S Lu H Chen J Zhang Z Jin Y Zhu ZZ 《International journal of clinical oncology / Japan Society of Clinical Oncology》2011,16(6):679-685
Background
The prognosis of lung cancer remains poor and clinically applicable prognostic markers have not yet been satisfactory identified. Several chromosomal copy number alterations (CNAs) have been associated with metastasis, relapse, and survival of patients with lung cancer; however, no study has focused exclusively on identifying CNAs at a gene level. The aim of this study was to identify genes whose CNAs are associated with survival of patients with lung adenocarcinoma. 相似文献12.
Background
Hepatocellular carcinoma (HCC), one of the most common cancers world-wide occurs twice as often in men compared to women. Predisposing conditions such as alcoholism, chronic viral hepatitis, aflatoxin B1 ingestion, and cirrhosis all contribute to the development of HCC. 相似文献13.
Olga A Patutina Nadezda L Mironova Nelly A Popova Vasily I Kaledin Valery P Nikolin Valentin V Vlassov Marina A Zenkova 《BMC cancer》2010,10(1):204
Background
One of the main obstacles for successful cancer polychemotherapy is multiple drug resistance phenotype (MDR) acquired by tumor cells. Currently, RNA interference represents a perspective strategy to overcome MDR via silencing the genes involved in development of this deleterious phenotype (genes of ABC transporters, antiapoptotic genes, etc.). 相似文献14.
Objective|
The Wnt signaling pathway is crucial for pulmonary development and differentiation; dysregulation of the Wnt signaling pathway may impair lung function. Indeed, single nucleotide polymorphisms (SNPs) of Wnt pathway-related genes have been suggested as risk factors for certain types of cancers. In this study, we aimed to evaluate the influence of SNPs in Wnt-related genes (TCF2, MMP9) on susceptibility to lung cancer. 相似文献15.
Zhong-Zhe Lin Yung-Ming Jeng Fu-Chang Hu Hung-Wei Pan Hsin-Wei Tsao Po-Lin Lai Po-Huang Lee Ann-Lii Cheng 《BMC cancer》2010,10(1):461
Background
To investigate the significance of Aurora B expression in hepatocellular carcinoma (HCC). 相似文献16.
Background
The early to intermediate stages of the majority of colorectal tumours are thought to be driven by aberrations in the Wnt (APC, CTNNB1) and Ras (K-ras) pathways. A smaller proportion of cancers shows mismatch repair deficiency. The aim of this study was to analyse the co-occurrence of these genetic alterations in relation to tumour and patient characteristics. 相似文献17.
Yanbin Jia Christina Persson Lifang Hou Zongli Zheng Meredith Yeager Jolanta Lissowska Stephen J. Chanock Wong-Ho Chow Weimin Ye 《Cancer causes & control : CCC》2010,21(2):313-321
Objective
MUC1, MUC5AC, and MUC6 are main constituents of the mucus barrier in the stomach, which protects the underlying epithelium from acid, proteases, mechanical trauma, and pathogenic microorganisms. Accumulating evidence implicates potential roles of MUC1, MUC5AC, and MUC6 genetic variation in the development of stomach cancer. 相似文献18.
Relationship of patients' age to histopathological features of breast tumours in <Emphasis Type="Italic">BRCA1</Emphasis> and <Emphasis Type="Italic">BRCA2</Emphasis>and mutation-negative breast cancer families 总被引:1,自引:0,他引:1
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Eerola H Heikkilä P Tamminen A Aittomäki K Blomqvist C Nevanlinna H 《Breast cancer research : BCR》2005,7(4):R465-R469
Introduction
Our aim was to evaluate the relationship of patients' age to histopathological features of hereditary breast tumours in a series of breast cancer families not selected for age at diagnosis. In sporadic breast cancer, tumours from premenopausal patients have been shown to differ from those of postmenopausal patients, but this phenomenon has been little studied among familial patients. 相似文献19.
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