Recurrent or residual pelvic bowel cancer: accuracy of MRI local extent before salvage surgery.
AffiliationDepartments of Diagnostic Radiology, Christie Hospital NHS Trust, Manchester, UK.
MetadataShow full item record
AbstractPURPOSE: To determine pre-operative MRI accuracy in assessing local disease extent in recurrent/residual pelvic bowel cancer by comparing MRI assessment and staging examination under anaesthesia (EUA), with laparotomy/histopathological findings. MATERIALS AND METHODS: Twenty-seven consecutive patients with recurrent (n = 21) or residual (n = 6) pelvic bowel cancer (13 of the rectum, eleven of the anus and three of the colon) underwent EUA and pelvic MRI (1T) using a phased array pelvic coil. Retrospective analysis of eight specific anatomical regions for tumour involvement on MRI was performed. Findings at EUA and biopsy were recorded. The MRI and EUA findings were correlated with findings at surgery and histopathology. Statistical comparison between MRI and EUA results was performed using the chi-squared test. RESULTS: Overall MRI accuracy in determining tumour invasion for all sites assessed was 452/499 (91%), sensitivity was 95/109 (87%), specificity was 357/390 (92%), positive predictive value (PPV) was 95/128 (74%) and negative predictive value (NPV) was 357/371 (96%). PPV and NPV for specific areas were 21/38 (55%) and 134/136 (99%) for genitourinary tract, 4/6 (67%) and 61/65 (94%) for pelvic side wall, 21/26 (81%) and 40/41 (98%) for pelvic floor, 1/6 (17%) and 40/43 (93%) for the posterior pelvis pre-sacrum/sacrum. For those anatomical sites evaluated by both EUA and MRI, MRI was superior to EUA, with an accuracy of 89% vs 73% (P < 0.05). CONCLUSION: MRI is an accurate technique for assessing disease extent in recurrent/residual pelvic bowel cancer.
CitationRecurrent or residual pelvic bowel cancer: accuracy of MRI local extent before salvage surgery. 2002, 57 (6):514-22 Clin Radiol
- Local staging of rectal cancer using combined pelvic phased-array and endorectal coil MRI.
- Authors: Tatli S, Mortele KJ, Breen EL, Bleday R, Silverman SG
- Issue date: 2006 Apr
- Pre-operative assessment of extramural invasion and sphincteral involvement in rectal cancer by magnetic resonance imaging with phased-array coil.
- Authors: Ferri M, Laghi A, Mingazzini P, Iafrate F, Meli L, Ricci F, Passariello R, Ziparo V
- Issue date: 2005 Jul
- Routine follow-up by magnetic resonance imaging does not improve detection of resectable local recurrences from colorectal cancer.
- Authors: Titu LV, Nicholson AA, Hartley JE, Breen DJ, Monson JR
- Issue date: 2006 Mar
- Comparison between 3-T magnetic resonance imaging and multi-detector row computed tomography for the preoperative evaluation of rectal cancer.
- Authors: Kim CK, Kim SH, Choi D, Kim MJ, Chun HK, Lee SJ, Lee JM
- Issue date: 2007 Nov-Dec
- Transrectal ultrasound versus magnetic resonance imaging for detection of rectal wall invasion by prostate cancer.
- Authors: Leibovici D, Kamat AM, Do KA, Pettaway CA, Ng CS, Evans RB, Rodriguez-Bigas M, Skibber J, Wang X, Pisters LL
- Issue date: 2005 Jan 1
Showing items related by title, author, creator and subject.
AZD8186 study 1: phase I study to assess the safety, tolerability, pharmacokinetics (PK), pharmacodynamics (PD) and preliminary anti-tumour activity of AZD8186 in patients with advanced castration-resistant prostate cancer (CRPC), squamous non-small cell lung cancer, triple negative breast cancer and with PTEN-deficient/mutated or PIK3CB mutated/amplified malignancies, as monotherapy and in combination with vistusertib (AZD2014) or abiraterone acetate.Lillian, S; De Bono, J; Higano, C; Shapiro, G; Brugger, W; Mitchell, P; Colebrook, S; Klinowska, T; Barry, S; Dean, Emma J; et al. (2016-12)
Mitochondrial oxidative stress in cancer-associated fibroblasts drives lactate production, promoting breast cancer tumor growth: understanding the aging and cancer connection.Balliet, R M; Capparelli, C; Guido, C; Pestell, T G; Martinez-Outschoorn, U E; Lin, Z; Whitaker-Menezes, D; Chiavarina, B; Pestell, R G; Howell, Anthony; et al. (2011-12-01)Increasing chronological age is the most significant risk factor for cancer. Recently, we proposed a new paradigm for understanding the role of the aging and the tumor microenvironment in cancer onset. In this model, cancer cells induce oxidative stress in adjacent stromal fibroblasts. This, in turn, causes several changes in the phenotype of the fibroblast including mitochondrial dysfunction, hydrogen peroxide production, and aerobic glycolysis, resulting in high levels of L-lactate production. L-lactate is then transferred from these glycolytic fibroblasts to adjacent epithelial cancer cells and used as "fuel" for oxidative mitochondrial metabolism. Here, we created a new pre-clinical model system to directly test this hypothesis experimentally. To synthetically generate glycolytic fibroblasts, we genetically-induced mitochondrial dysfunction by knocking down TFAM using an sh-RNA approach. TFAM is mitochondrial transcription factor A, which is important in functionally maintaining the mitochondrial respiratory chain. Interestingly, TFAM-deficient fibroblasts showed evidence of mitochondrial dysfunction and oxidative stress, with the loss of certain mitochondrial respiratory chain components, and the over-production of hydrogen peroxide and L-lactate. Thus, TFAM-deficient fibroblasts underwent metabolic reprogramming towards aerobic glycolysis. Most importantly, TFAM-deficient fibroblasts significantly promoted tumor growth, as assayed using a human breast cancer (MDA-MB-231) xenograft model. These increases in glycolytic fibroblast driven tumor growth were independent of tumor angiogenesis. Mechanistically, TFAM-deficient fibroblasts increased the mitochondrial activity of adjacent epithelial cancer cells in a co-culture system, as seen using MitoTracker. Finally, TFAM-deficient fibroblasts also showed a loss of caveolin-1 (Cav-1), a known breast cancer stromal biomarker. Loss of stromal fibroblast Cav-1 is associated with early tumor recurrence, metastasis, and treatment failure, resulting in poor clinical outcome in breast cancer patients. Thus, this new experimental model system, employing glycolytic fibroblasts, may be highly clinically relevant. These studies also have implications for understanding the role of hydrogen peroxide production in oxidative damage and "host cell aging," in providing a permissive metabolic microenvironment for promoting and sustaining tumor growth.
Penetrance estimates for BRCA1 and BRCA2 based on genetic testing in a Clinical Cancer Genetics service setting: risks of breast/ovarian cancer quoted should reflect the cancer burden in the family.Evans, D Gareth R; Shenton, Andrew; Woodward, Emma; Lalloo, Fiona; Howell, Anthony; Maher, Eamonn R; Academic Unit of Medical Genetics and Regional Genetics Service, St Mary's Hospital Manchester M13 0JH, UK. firstname.lastname@example.org (2008)BACKGROUND: The identification of a BRCA1 or BRCA2 mutation in familial breast cancer kindreds allows genetic testing of at risk relatives. However, considerable controversy exists regarding the cancer risks in women who test positive for the family mutation. METHODS: We reviewed 385 unrelated families (223 with BRCA1 and 162 with BRCA2 mutations) ascertained through two regional cancer genetics services. We estimated the penetrance for both breast and ovarian cancer in female mutation carriers (904 proven mutation carriers - 1442 females in total assumed to carry the mutation) and also assessed the effect on penetrance of mutation position and birth cohort. RESULTS: Breast cancer penetrance to 70 and to 80 years was 68% (95%CI 64.7-71.3%) and 79.5% (95%CI 75.5-83.5%) respectively for BRCA1 and 75% (95%CI 71.7-78.3%) and 88% (95%CI 85.3-91.7%) for BRCA2. Ovarian cancer risk to 70 and to 80 years was 60% (95%CI 65-71%) and 65% (95%CI 75-84%) for BRCA1 and 30% (95%CI 25.5-34.5%) and 37% (95%CI 31.5-42.5%) for BRCA2. These risks were borne out by a prospective study of cancer in the families and genetic testing of unaffected relatives. We also found evidence of a strong cohort effect with women born after 1940 having a cumulative risk of 22% for breast cancer by 40 years of age compared to 8% in women born before 1930 (p = 0.0005). CONCLUSION: In high-risk families, selected in a genetics service setting, women who test positive for the familial BRCA1/BRCA2 mutation are likely to have cumulative breast cancer risks in keeping with the estimates obtained originally from large families. This is particularly true for women born after 1940.