Publications by authors named "Sergio Rodriguez-Cuevas"

40 Publications

miR‑145‑5p is associated with pathological complete response to neoadjuvant chemotherapy and impairs cell proliferation by targeting TGFβR2 in breast cancer.

Oncol Rep 2019 Jun 5;41(6):3527-3534. Epub 2019 Apr 5.

Genomics Sciences Program, Autonomous University of Mexico City, Mexico City 03100, Mexico.

Cancer patients who better benefit from neoadjuvant chemotherapy (NeoCh) are those who achieve a successful pathological complete response (pCR) represented by the absence of residual disease. Unfortunately, no highly sensitive and specific tumor biomarkers for predicting the clinical response to NeoCh have yet been defined. The aim of the present study was to ascertain whether miR‑145‑5p could discriminate between pCR and no‑pCR in triple‑negative breast cancer patients that received a cisplatin/doxorubicin‑based neoadjuvant treatment. miR‑145‑5p expression was determined in breast tumors by quantitative RT‑PCR. Our data showed that miR‑145‑5p had a significant low expression (P<0.005) in patients that achieved pCR in comparison to the non‑responder group. Kaplan Meier analysis indicated that low levels of miR‑145‑5p were associated with increased disease‑free survival. In addition, receiver operating characteristic (ROC) curve analysis suggested that miR‑145‑5p is a good predictor of pCR (P<0.003, AUC=0.7899, 95% CI, 0.6382‑0.9416). Quantitative RT‑PCR expression analysis also revealed that miR‑145‑5p was downregulated in four breast cancer cell lines relative to normal cells. To study the functions of miR‑145‑5p, its expression was restored in triple‑negative MDA‑MB‑231 cells and its effects in cell proliferation were evaluated by MTT assays and in apoptosis using Annexin V experiments. Data revealed that ectopic expression of miR‑145‑5p resulted in a significant inhibition of cell proliferation and also induced apoptosis. Moreover, miR‑145‑5p led to sensitization of breast cancer cells to cisplatin therapy. In addition, western blot assays indicated that miR‑145‑5p downregulated the TGFβR2 protein. In conclusion, miR‑145‑5p could be a potential biomarker of clinical response to NeoCh in triple‑negative breast cancer. Functionally miR‑145‑5p may regulate cell proliferation, at least in part, by targeting TGFβR2.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.3892/or.2019.7102DOI Listing
June 2019

Loss of function of miR-342-3p results in MCT1 over-expression and contributes to oncogenic metabolic reprogramming in triple negative breast cancer.

Sci Rep 2018 08 16;8(1):12252. Epub 2018 Aug 16.

Cancer Genomics Laboratory, National Institute of Genomic Medicine, Mexico City, Mexico.

Triple-negative breast cancer (TNBC) is a heterogeneous and aggressive neoplasia lacking the expression of hormonal receptors and human epidermal growth factor receptor-2. Accumulating evidence has highlighted the importance of miRNAs dysregulation in the establishment of cancer programs, but the functional role of many miRNAs remains unclear. The description of miRNAs roles might provide novel strategies for treatment. In the present work, an integrated analysis of miRNA transcriptional landscape was performed (N = 132), identifying the significant down-modulation of miR-342-3p in TNBC, probably because of the aberrant activity of estrogen receptor, which serves as a transcription factor of the miRNA, as demonstrated by a siRNA-knockdown approach. The enhanced expression of miR-342-3p significantly decreased cell proliferation, viability and migration rates of diverse TN cells in vitro. Bioinformatic and functional analyses revealed that miR-342-3p directly targets the monocarboxylate transporter 1 (MCT1), which promotes lactate and glucose fluxes alteration, thus disrupting the metabolic homeostasis of tumor cells. Optical metabolic imaging assay defined a higher optical redox ratio in glycolytic cells overexpressing miR-342-3p. Furthermore, we found that hypoxic conditions and glucose starvation attenuate miR-342-3p expression, suggesting a crosstalk program between these metabolic factors. Consistently, miR-342-3p down-modulation is associated with an increased MCT1 expression level and glycolytic score in human triple negative tumors. Overall, we described for the first time the regulatory activity of miR-342-3p on relevant metabolic carcinogenic pathways in TN breast cancers.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1038/s41598-018-29708-9DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6095912PMC
August 2018

Complete sequence of the ATP6 and ND3 mitochondrial genes in breast cancer tissue of postmenopausal women with different body mass indexes.

Ann Diagn Pathol 2018 Feb 10;32:23-27. Epub 2017 Sep 10.

Unidad de Investigación en Obesidad, Facultad de Medicina, Universidad Nacional Autónoma de México, México, D.F., México; Clínica de Obesidad, Instituto Nacional de Ciencias Médicas y Nutrición "Salvador Zubirán", México, D.F., México. Electronic address:

Due to the fact that mitochondrial defects and oxidative stress have been related with obesity and breast cancer is more aggressive in women with obesity, we investigated if postmenopausal Mexican-Mestizo women with breast cancer presented somatic mutations in the sequence of the ATP6 and/or ND3 genes. Twenty one postmenopausal Mexican-Mestizo women with breast cancer who underwent mastectomy or breast conserving surgery were studied. Height and weight were used to calculate body mass index. DNA from tumor tissue samples and blood leukocytes was amplified by polymerase chain reaction and sequenced the ATP6 and ND3 mitochondrial genes. Ages ranged from 46 to 82. According to World Health Organization criteria among the 21 women, 7 had a normal BMI, 7 were overweight and 7 had obesity. In regard to the molecular study, after sequencing the coding region of ATP6 and ND3 genes of the DNA obtained from both leukocytes and tumor tissue, we did not find somatic mutations. All of the changes that we found in both genes were polymorphisms: in ATP6, we identified in ten patients 3 non-synonymous nucleotide changes and in ND3 we observed that six patients presented polymorphisms, three of them were synonymous and two non-synonymous. To our knowledge, this constitutes the first report where the complete sequence of the ATP6 and ND3 genes has been analyzed in postmenopausal Mexican-Mestizo women with breast cancer and diverse BMI. Our results differ with those reported in Caucasian and Asian populations, possibly due to ethnic differences.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.anndiagpath.2017.09.001DOI Listing
February 2018

Phyllodes Tumor of the Breast: 307 Treated Cases, the Largest Mexican Experience at a Single Breast Disease Institution.

Iran J Pathol 2016 ;11(4):399-408

Dept. of Breast Surgical Oncology, Instituto de Enfermedades de la Mama y Fundación del Cáncer de Mama (IEM-FUCAM), Mexico City, Mexico.

Background: Phyllodes tumor (PT) of the breast in Hispanic patients is more frequently reported with large tumors and with more borderline/malignant subtypes compared with other populations. The objective of this study was to describe characteristics of patients with PT and to identify differences among subtypes in a Mexican population.

Methods: A retrospective study was conducted on patients with PT. Sociodemographic, histopathologic, and treatment characteristics were compared among subtypes, including only surgically treated cases due the complete surgical-specimen study requirement for appropriate WHO classification.

Results: During 10 years, 346 PT were diagnosed; only 307 were included (305 patients), with a mean age of 41.7 yr. Self-detected lump took place in 91.8%, usually discovered 6 months previously, with median tumor size of 4.5 cm. Local wide excisions were done in 213 (69.8%) and mastectomies in 92 (30.1%). Immediate breast reconstruction took place in 38% and oncoplastic procedures in 23%. PT were classified as benign in 222 (72.3%) cases, borderline in 50 (16.2%), and malignant in 35 (11.4%), with pathological tumor size of 4.2, 5.4, and 8.7 cm, respectively (<0.001). Patients with malignant PT were older (48 yr), with more diabetics (14.3%), less breastfeeding (37.1%), more smokers (17.1%), with more postmenopausal cases (42.9%), and older age at menopause (51.5 years) compared with the remaining subtypes (<0.05). Relapse occurred in 8.2% of patients with follow-up.

Conclusion: In comparison with other Hispanic publications, these Mexican patients had similar age, with smaller tumors, modestly higher benign PT, fewer malignant PT, and lower documented relapse cases.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5563938PMC
January 2016

Recurrent and functional regulatory mutations in breast cancer.

Nature 2017 07 28;547(7661):55-60. Epub 2017 Jun 28.

Massachusetts General Hospital Center for Cancer Research, Charlestown, Massachusetts 02129, USA.

Genomic analysis of tumours has led to the identification of hundreds of cancer genes on the basis of the presence of mutations in protein-coding regions. By contrast, much less is known about cancer-causing mutations in non-coding regions. Here we perform deep sequencing in 360 primary breast cancers and develop computational methods to identify significantly mutated promoters. Clear signals are found in the promoters of three genes. FOXA1, a known driver of hormone-receptor positive breast cancer, harbours a mutational hotspot in its promoter leading to overexpression through increased E2F binding. RMRP and NEAT1, two non-coding RNA genes, carry mutations that affect protein binding to their promoters and alter expression levels. Our study shows that promoter regions harbour recurrent mutations in cancer with functional consequences and that the mutations occur at similar frequencies as in coding regions. Power analyses indicate that more such regions remain to be discovered through deep sequencing of adequately sized cohorts of patients.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1038/nature22992DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5563978PMC
July 2017

A microRNA signature associated with pathological complete response to novel neoadjuvant therapy regimen in triple-negative breast cancer.

Tumour Biol 2017 Jun;39(6):1010428317702899

9 Posgrado en Ciencias Genómicas, Universidad Autónoma de la Ciudad de México, Ciudad de México, México.

Neoadjuvant chemotherapy aims to improve the outcome of breast cancer patients, but only few would benefit from this treatment. Pathological complete response has been proposed as a surrogate marker for the prediction of long-term clinical benefits; however, 50%-85% patients have an unfavorable pathological complete response to chemotherapy. MicroRNAs are known biomarkers of breast cancer progression; nevertheless, their potential to identify patients with pathological complete response remains poorly understood. Here, we investigated whether a microRNA profile could be associated with pathological complete response in triple-negative breast cancer patients receiving 5-fluorouracil, adriamycin, cyclophosphamide-cisplatin/paclitaxel as a novel neoadjuvant chemotherapy. In the discovery cohort, the expression of 754 microRNAs was examined in tumors from 10 triple-negative breast cancer patients who achieved pathological complete response and 8 without pathological complete response using TaqMan Low-Density Arrays. Unsupervised hierarchical cluster analysis identified 11 microRNAs with significant differences between responder and no-responder patients (fold change ≥ 1.5; p < 0.05). The differential expression of miR-30a, miR-9-3p, miR-770, and miR-143-5p was validated in an independent group of 17 patients with or without pathological complete response. Moreover, Kaplan-Meier analysis showed that expression of these four microRNAs was associated with an increased disease-free survival. Gene ontology classification of predicted microRNA targets indicated that numerous genes are involved in pathways related to chemoresistance, such as vascular endothelial growth factor, focal adhesion kinase, WNT, ERbB, phosphoinositide 3-kinase, and AKT signaling. In summary, we identified a novel microRNA expression signature associated with pathological complete response in breast cancer. We propose that the four validated microRNAs could be used as molecular biomarkers of clinical response in triple-negative breast cancer patients with pathological complete response to neoadjuvant therapy.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1177/1010428317702899DOI Listing
June 2017

Primary mucoepidermoid carcinoma of the breast.

Breast J 2017 11 10;23(6):753-755. Epub 2017 Apr 10.

Instituto de Enfermedades de la Mama, Society Surgical Oncology (American Head and Neck Society), Societé Francaise pour l'etude du cancer (Association Francaise de carcinologie cervicofaciale), Mexico City, Mexico.

View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1111/tbj.12819DOI Listing
November 2017

A Nonpalpable Nodule in Ectopic Axillary Breast Tissue: Consider Phyllodes Tumor.

Case Rep Pathol 2016 26;2016:3603262. Epub 2016 Dec 26.

Department of Breast Surgical Oncology, Instituto de Enfermedades de la Mama y Fundación del Cáncer de Mama (IEM-FUCAM), Mexico City, Mexico.

Benign and malignant pathology can develop in ectopic axillary breast tissue, such as fibroadenomas, phyllodes tumors, and breast cancer. We present a rare case of an asymptomatic 43-year-old woman with an axillary nodule which was identified during screening mammography within ectopic axillary breast tissue, initially considered as a suspicious lymph node. Radiologic studies were considered as Breast Imaging-Reporting Data System (BI-RADS) 4. A hyperdense, lobular, and well-circumscribed nodule was identified in mammogram while the nodule by ultrasound (US) was hypoechoic with indistinct microlobular margins, without vascularity by Doppler, and measuring 1.26 × 1 cm. Core-needle biopsy reported a fibroepithelial neoplasm. The patient was submitted to local wide-needle excision located in intraoperative radiography of the surgical specimen and margin evaluation. Final histopathological study reported a 1.8 × 1.2 cm benign phyllodes tumor, with irregular, pushing, and clear wide margins within normal ectopic breast tissue. The patient without surgical complications continued annual screening without recurrence during a follow-up that took place 24 months later.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1155/2016/3603262DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5220411PMC
December 2016

Dual targeting of ANGPT1 and TGFBR2 genes by miR-204 controls angiogenesis in breast cancer.

Sci Rep 2016 10 5;6:34504. Epub 2016 Oct 5.

Posgrado en Ciencias Genómicas, Universidad Autónoma de la Ciudad de México, Ciudad de México, México.

Deregulated expression of microRNAs has been associated with angiogenesis. Studying the miRNome of locally advanced breast tumors we unsuspectedly found a dramatically repression of miR-204, a small non-coding RNA with no previous involvement in tumor angiogenesis. Downregulation of miR-204 was confirmed in an independent cohort of patients and breast cancer cell lines. Gain-of-function analysis indicates that ectopic expression of miR-204 impairs cell proliferation, anchorage-independent growth, migration, invasion, and the formation of 3D capillary networks in vitro. Likewise, in vivo vascularization and angiogenesis were suppressed by miR-204 in a nu/nu mice model. Genome-wide profiling of MDA-MB-231 cells expressing miR-204 revealed changes in the expression of hundred cancer-related genes. Of these, we focused on the study of pro-angiogenic ANGPT1 and TGFβR2. Functional analysis using luciferase reporter and rescue assays confirmed that ANGPT1 and TGFβR2 are novel effectors downstream of miR-204. Accordingly, an inverse correlation between miR-204 and ANGPT1/TGFβR2 expression was found in breast tumors. Knockdown of TGFβR2, but not ANGPT1, impairs cell proliferation and migration whereas inhibition of both genes inhibits angiogenesis. Taken altogether, our findings reveal a novel role for miR-204/ANGPT1/TGFβR2 axis in tumor angiogenesis. We propose that therapeutic manipulation of miR-204 levels may represent a promising approach in breast cancer.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5050489PMC
http://dx.doi.org/10.1038/srep34504DOI Listing
October 2016

Salivary gland-like breast carcinomas: An infrequent disease.

Pathol Res Pract 2016 Nov 13;212(11):1034-1038. Epub 2016 Sep 13.

Department of Breast Surgery, Instituto de Enfermedades de la Mama (IEM-FUCAM), Mexico City, Mexico.

Objective: To show the incidence, as well as the clinical and histopathological characteristics, of patients diagnosed with mammary salivary gland-like carcinomas at our institution.

Materials And Methods: A retrospective study was conducted in all women diagnosed with breast cancer at our institution from January 2005 to February 2016. Patients with diagnosis of salivary gland-like breast carcinomas were included.

Results: In this period, 6384 patients were diagnosed with breast cancer at our institution; salivary gland-like carcinomas were found in 7 patients (0.1%), adenoid cystic carcinoma was diagnosed in 5 patients (0.07%), acinic cell carcinoma in 1 patient (0.015%) and mucoepidermoid carcinoma in 1 patient (0.015%). The triple-negative subtype was found in all of the tumors. Median follow-up was 66.3 months (range, 1-108 months). No patient developed local or distant recurrence.

Conclusions: Salivary gland-like breast tumors are extremely rare. We found a global incidence of 0.1%. Adenoid cystic, acinic cell and mucoepidermoid carcinomas were the three histologic types diagnosed. Although the triple-negative subtype is mainly found, good prognosis is expected.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.prp.2016.09.001DOI Listing
November 2016

[Clinical and pathological features of breast cancer in a population of Mexico].

Cir Cir 2017 May - Jun;85(3):201-207. Epub 2016 Sep 19.

Cirugía oncológica, Instituto de Enfermedades de la Mama, Fundación de Cáncer de Mama, A.C. (FUCAM), Ciudad de México, México.

Background: Breast cancer is the most common among women in our country, and its treatment is based on prognostic factors to categorize patients into different risk groups. In this study, the clinical and pathological features that play a role as a prognostic factor in a representative population with breast cancer in México are described.

Material And Methods: A descriptive analysis of the clinical and pathological features of women diagnosed with breast cancer, in a period from June 2005 to May 2014; registered in a database and calculated by simple frequencies.

Results: A total of 4,411 patients were included, the average age at diagnosis was 53 years, 19.7% were diagnosed by mammography screening program and 80.3% derived from any signs or symptoms. Regarding the stages at diagnosis, 6.8% were carcinoma in situ, 36% at early stages (I and IIA), 45% locally advanced (IIB to IIIC), 7.7% metastatic and 3.9% unclassifiable. A 79% were ductal histology, lobular 7.8% and the rest, other types. Of ductal carcinomas, 9.1% were grade I, 54.1% grade II, and 34.6% grade III. Regarding the biological subtypes, 65.7% were luminal, 10.9% luminal Her positive, 8.7% pure Her 2 positive and 14.6% triple negative.

Conclusion: In the present study, we described the clinical and pathologic features of a group of Mexican women with breast cancer that might reflect a national landscape, and represent the prognostic factors to determine groups of risk and treatment decisions.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.circir.2016.08.004DOI Listing
May 2018

Suppression of cell migration is promoted by miR-944 through targeting of SIAH1 and PTP4A1 in breast cancer cells.

BMC Cancer 2016 07 4;16:379. Epub 2016 Jul 4.

Universidad Autónoma de la Ciudad de México, Posgrado en Ciencias Genómicas, Ciudad de México, México.

Background: Aberrant expression of microRNAs has been associated with migration of tumor cells. In this study, we aimed to investigate the biological significance of miR-944 whose function is unknown in breast cancer.

Methods: MiR-944 expression in breast cancer cells and tumors was evaluated by Taqman qRT-PCR assays. Transcriptional profiling of MDA-MB-231 cells expressing miR-944 was performed using DNA microarrays. Cell viability, migration and invasion were assessed by MTT, scratch/wound-healing and transwell chamber assays, respectively. The luciferase reporter assay was used to evaluate targeting of SIAH1, PTP4A1 and PRKCA genes by miR-944. SIAH1 protein levels were measured by Western blot. Silencing of SIAH1 gene was performed by RNA interference using shRNAs.

Results: Our data showed that miR-944 expression was severely repressed in clinical specimens and breast cancer cell lines. Suppression of miR-944 levels was independent of hormonal status and metastatic potential of breast cancer cells. Gain-of-function analysis indicated that miR-944 altered the actin cytoskeleton dynamics and impaired cell migration and invasion. Genome-wide transcriptional profiling of MDA-MB-231 cells that ectopically express miR-944 showed that 15 genes involved in migration were significantly repressed. Notably, luciferase reporter assays confirmed the ability of miR-944 to bind the 3´UTR of SIAH1 and PTP4A1 genes, but not PRKCA gene. Congruently, an inverse correlation between miR-944 and SIAH1 protein expression was found in breast cancer cells. Moreover, SIAH1 was upregulated in 75 % of miR-944-deficient breast tumors. Finally, SIAH1 gene silencing by RNA interference significantly impaired cell migration of breast cancer cells.

Conclusions: Our results pointed out that miR-944 is a novel upstream negative regulator of SIAH1 and PTP4A1 genes and provided for the first time evidence for its functional role in migration and invasion of breast cancer cells. They also suggest that miR-944 restoration may represent a potential strategy for breast cancer therapy.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1186/s12885-016-2470-3DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4932667PMC
July 2016

Methylation Landscape of Human Breast Cancer Cells in Response to Dietary Compound Resveratrol.

PLoS One 2016 29;11(6):e0157866. Epub 2016 Jun 29.

Posgrado en Ciencias Genómicas, Universidad Autónoma de la Ciudad de México, Ciudad de México, México.

Aberrant DNA methylation is a frequent epigenetic alteration in cancer cells that has emerged as a pivotal mechanism for tumorigenesis. Accordingly, novel therapies targeting the epigenome are being explored with the aim to restore normal DNA methylation patterns on oncogenes and tumor suppressor genes. A limited number of studies indicate that dietary compound resveratrol modulates DNA methylation of several cancer-related genes; however a complete view of changes in methylome by resveratrol has not been reported yet. In this study we performed a genome-wide survey of DNA methylation signatures in triple negative breast cancer cells exposed to resveratrol. Our data showed that resveratrol treatment for 24 h and 48 h decreased gene promoter hypermethylation and increased DNA hypomethylation. Of 2476 hypermethylated genes in control cells, 1,459 and 1,547 were differentially hypomethylated after 24 h and 48 h, respectively. Remarkably, resveratrol did not induce widespread non-specific DNA hyper- or hypomethylation as changes in methylation were found in only 12.5% of 27,728 CpG loci. Moreover, resveratrol restores the hypomethylated and hypermethylated status of key tumor suppressor genes and oncogenes, respectively. Importantly, the integrative analysis of methylome and transcriptome profiles in response to resveratrol showed that methylation alterations were concordant with changes in mRNA expression. Our findings reveal for the first time the impact of resveratrol on the methylome of breast cancer cells and identify novel potential targets for epigenetic therapy. We propose that resveratrol may be considered as a dietary epidrug as it may exert its anti-tumor activities by modifying the methylation status of cancer -related genes which deserves further in vivo characterization.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0157866PLOS
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4927060PMC
July 2017

Data set of the protein expression profiles of Luminal A, Claudin-low and overexpressing HER2(+) breast cancer cell lines by iTRAQ labelling and tandem mass spectrometry.

Data Brief 2015 Sep 17;4:292-301. Epub 2015 Jun 17.

Departamento de Biología Celular, Centro de Investigación y de Estudios Avanzados del Instituto Politécnico Nacional (Cinvestav-IPN), Av. Instituto Politécnico Nacional 2508, Col. San Pedro Zacatenco, Gustavo A. Madero, C.P. 07360 México DF, Mexico.

Breast cancer is the most common and the leading cause of mortality in women worldwide. There is a dire necessity of the identification of novel molecules useful in diagnosis and prognosis. In this work we determined the differentially expression profiles of four breast cancer cell lines compared to a control cell line. We identified 1020 polypeptides labelled with iTRAQ with more than 95% in confidence. We analysed the common proteins in all breast cancer cell lines through IPA software (IPA core and Biomarkers). In addition, we selected the specific overexpressed and subexpressed proteins of the different molecular classes of breast cancer cell lines, and classified them according to protein class and biological process. Data in this article is related to the research article "Determination of the protein expression profiles of breast cancer cell lines by Quantitative Proteomics using iTRAQ Labelling and Tandem Mass Spectrometry" (Calderón-González et al. [1] in press).
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.dib.2015.04.025DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4510402PMC
September 2015

[Feasibility and cosmetic outcome of oncoplastic surgery in breast cancer treatment].

Cir Cir 2015 May-Jun;83(3):199-205. Epub 2015 Jun 6.

Departamento de Cirugía Oncológica de Mama, Instituto de Enfermedades de la Mama, FUCAM A.C., Coyoacán D.F., México.

Background: Breast cancer is the leading oncological cause of death in Mexican women over 25 years old. Given the need to improve postoperative cosmetic results in patients with breast cancer, oncoplastic surgery has been developed, which allows larger tumour resections and minor cosmetic alterations.

Objective: To determine the oncological feasibility and cosmetic outcome of oncoplastic surgery at the Instituto de Enfermedades de la Mama, FUCAM, AC.

Material And Methods: A review was conducted from January 2010 to July 2013, which included patients with breast cancer diagnosis treated with conventional breast-conserving surgery or with oncoplastic surgery in the Institute of Diseases of the Breast, FUCAM AC. Clinical and histopathological parameters were compared between the two groups, and a questionnaire of cosmetic satisfaction and quality of life was applied.

Results: Of the 171 patients included, 95 of them were treated with conventional breast-conserving surgery and 76 with oncoplastic surgery. Pathological tumour size was significantly larger in patients treated with oncoplastic surgery (p = 0.002). There were no differences found between the groups as regards the number of patients with positive surgical margin, the rate of complications, and cosmetic satisfaction.

Conclusion: This study demonstrates the oncological feasibility and high cosmetic satisfaction of oncoplastic surgery with minimal psycho-social impact on patients.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.circir.2015.05.015DOI Listing
May 2016

Determination of the protein expression profiles of breast cancer cell lines by quantitative proteomics using iTRAQ labelling and tandem mass spectrometry.

J Proteomics 2015 Jun 24;124:50-78. Epub 2015 Apr 24.

Departmento de Biología Celular, Centro de Investigación y de Estudios Avanzados del Instituto Politécnico Nacional (Cinvestav-IPN), Av. Instituto Politécnico Nacional 2508, Col. San Pedro Zacatenco, Gustavo A. Madero, C.P. 07360, México, D. F., México. Electronic address:

Unlabelled: Breast cancer is the principal cancer in women worldwide. Although there are serum tumor markers such as CEA and HER2, they are detected in advanced stages of the disease and used as progression and recurrence markers. Therefore, there is a necessity for the identification of new markers that might lead to an early detection and also provide evidence of an effective treatment. The aim of this work was to determine the differential protein expression profiles of four breast cancer cell lines in comparison to a normal control cell line by iTRAQ labelling and tandem mass spectrometry, in order to identify putative biomarkers of the disease. We identified 1,020 iTRAQ-labelled polypeptides with at least one peptide identified with more than 95% in confidence. Overexpressed polypeptides in all cancer cell lines were 78, whilst the subexpressed were 128. We categorised them with PANTHER program into biological processes, being the metabolic pathways the most affected. We detected six groups of proteins with the STRING program involved in DNA topology, glycolysis, translation initiation, splicing, pentose pathway, and proteasome degradation. The main subexpressed protein network included mitochondrial proteins involved in oxidative phosphorylation. We propose BAG6, DDX39, ANXA8 and COX4 as putative biomarkers in breast cancer.

Biological Significance: We report a set of differentially expressed proteins in the MCF7 and T47D (Luminal A), MDA-MB-231 (Claudin low) and SK-BR-3 (HER2(+)) breast cancer cell lines that have not been previously reported in breast cancer disease. From these proteins, we propose BAG6, DDX39, ANXA8 and COX4 as putative biomarkers in breast cancer. On the other hand, we propose sets of unique polypeptides in each breast cancer cell line that can be useful in the classification of different subtypes of breast cancer.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.jprot.2015.04.018DOI Listing
June 2015

Primary neuroendocrine tumor of the breast.

Breast J 2015 May-Jun;21(3):312-3. Epub 2015 Mar 23.

Instituto de Enfermedades de la Mama, FUCAM AC, Mexico City, Mexico.

View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1111/tbj.12413DOI Listing
May 2016

[Neoadjuvant Chemotherapy (NC) Response in Patients with Breast Cancer According to Immunohistochemical Intrinsic Subtypes (IHC)].

Gac Med Mex 2014 Dec;150 Suppl 2:161-70

Departamento de Oncología Mamaria Quirúrgica, Instituto de Enfermedades de la Mama (IEM), Fundación del Cáncer de Mama, A.C. (FUCAM), México, D.F.

Introduction: Breast cancer is heterogeneous, with different responses to NC even within similar histology and stages.

Objective: To evaluate clinical/pathological response to NC according to different tumor subtypes in Mexican breast cancer patients.

Patients And Methods: Retrospective study of patients with breast cancer stages II-III, and complete immunohistochemistry (IHC), such as hormonal receptors HER2 and Ki67, treated with NC and surgery. Descriptive and comparative analyses between different intrinsic subtypes were performed.

Results: A total of 117 patients were included with 48.6 ± 10.6 years of age, stage II (24%), and III (76%). We identified 20 (17.1%) cases of luminal A, 37 (31.6%) luminal B HER2-, 13 (11.1%) luminal B HER2+, 12 (10.3%) HER2+, and 35 (29.9%) triple negative. Clinical complete response (tumor and lymph nodes) in luminal A was 10%, in luminal B HER2- 10.8%, luminal B HER2+ 15.4%, HER2+ 25%, and in triple negative 14.3%. Conservative surgeries were done in 9 (7.7%) patients. There is a weak positive association between Ki67 expression and tumor clinical response. Pathological complete response occurred in 8 (6.83%) cases, being more frequent in luminal B HER2+ patients (23%).

Conclusions: Pathological complete responses were more often in luminal B HER2+ cases.
View Article and Find Full Text PDF

Download full-text PDF

Source
December 2014

[Sentinel lymph node metastasis in patients with ductal breast carcinoma in situ].

Cir Cir 2014 Mar-Apr;82(2):129-41

Departamento de Oncología Mamaria Quirúrgica, Instituto de Enfermedades de la Mama (IEM) de la Fundación del Cáncer de Mama, A. C. (FUCAM), México DF, Mexico.

Background: Sentinel lymph node biopsy in patients with ductal carcinoma in situ still controversial, with positive lymph node in range of 1.4-12.5% due occult invasive breast carcinoma in surgical specimen.

Objective: To know the frequency of sentimel node metastases in patients with ductal carcinoma in situ, identify differences between positive and negative cases.

Methods: Retrospective study of patients with ductal carcinoma in situ treated with sentinel lymph node biopsy because mastectomy indication, palpable tumor, radiological lesion = 5 cm, non-favorable breast-tumor relation and/or patients whom surgery could affect lymphatic flow drainage.

Results: Of 168 in situ carcinomas, 50 cases with ductal carcinoma in situ and sentinel lymph node biopsy were included, with a mean age of 51.6 years, 30 (60%) asymptomatic. The most common symptoms were palpable nodule (18%), nipple discharge (12%), or both (8%). Microcalcifications were common (72%), comedonecrosis pattern (62%), grade-2 histology (44%), and 28% negative hormonal receptors. Four (8%) cases had intra-operatory positive sentinel lymph node and one patient at final histo-pathological study (60% micrometastases, 40% macrometastases), all with invasive carcinoma in surgical specimen. Patients with intra-operatory positive sentinel lymph node where younger (44.5 vs 51 years), with more palpable tumors (50% vs 23.1%), and bigger (3.5 vs 2 cm), more comedonecrosis pattern (75% vs 60.8%), more indifferent tumors (75% vs 39.1%), and less cases with hormonal receptors (50% vs 73.9%), compared with negative sentinel lymph node cases, all these differences without statistic significance.

Conclusions: One of each 12 patients with ductal carcinoma in situ had affection in sentinel lymph node, so we recommend continue doing this procedure to avoid second surgeries due the presence of occult invasive carcinoma.
View Article and Find Full Text PDF

Download full-text PDF

Source
June 2015

Comparative proteomic profiling of triple-negative breast cancer reveals that up-regulation of RhoGDI-2 is associated to the inhibition of caspase 3 and caspase 9.

J Proteomics 2014 Dec 22;111:198-211. Epub 2014 Apr 22.

Oncogenomics and Cancer Proteomics Laboratory, Autonomous University of Mexico City, Mexico. Electronic address:

Unlabelled: There are no targeted therapeutic modalities for triple-negative breast cancer (TNBC), thus it is associated with poor prognosis and worst clinical outcome. Here, our aim was to identify deregulated proteins in TNBC with potential therapeutic applications. Proteomics profiling of TNBC and normal breast tissues through two-dimensional electrophoresis and ESI-MS/MS mass spectrometry revealed the existence of 16 proteins (RhoGDI-2, HSP27, SOD1, DJ1, UBE2N, PSME1, FTL, SH3BGRL, and eIF5A-1) with increased abundance in carcinomas. We also evidenced for the first time the deregulation of COX5, MTPN and DB1 proteins in TNBC that may represent novel tumor markers. Particularly, we confirmed the overexpression of the Rho-GDP dissociation inhibitor 2 (RhoGDI-2) in distinct breast cancer subtypes, as well as in metastatic cell lines derived from lung, prostate, and breast cancer. Remarkably, targeted disruption of RhoGDI-2 by RNA interference induced mitochondrial dysfunction, and facilitated caspase-3 and -9 activation in two breast cancer cell lines. Moreover, suppression of RhoGDI-2 resulted in a robust sensitization of breast cancer cells to cisplatin therapy. In conclusion, we identified novel proteins deregulated in TNBC, and confirmed the overexpression of RhoGDI-2. We propose that RhoGDI-2 inhibition may be exploited as a potential therapeutic strategy along cisplatin-based chemotherapy in breast cancer.

Biological Significance: There are no useful biomarkers neither targeted therapeutic modalities for triple-negative breast cancer, which highly contributes to the poor prognosis of this breast cancer subtype. In this work, we used two-dimensional electrophoresis and ESI-MS/MS spectrometry to identify novel deregulated proteins in breast cancer tissues. Particularly, our results showed that RhoGDI-2, a protein that has been associated to metastasis and poor survival in human cancers, is overexpressed in different subtypes of breast tumors, as well as in metastatic cell lines derived from lung, prostate, and breast cancer. Our data also provided novel insights about the role of RhoGDI-2 in apoptosis through intrinsic pathway inhibition. Importantly, they suggested that targeted modulation of RhoGDI-2 levels might be a useful strategy for breast cancer therapy.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.jprot.2014.04.019DOI Listing
December 2014

RAD50 targeting impairs DNA damage response and sensitizes human breast cancer cells to cisplatin therapy.

Cancer Biol Ther 2014 Jun 18;15(6):777-88. Epub 2014 Mar 18.

Oncogenomics and Cancer Proteomics Laboratory; Genomics Sciences Program; Autonomous University of Mexico City; Mexico DF, Mexico.

In tumor cells the effectiveness of anti-neoplastic agents that cause cell death by induction of DNA damage is influenced by DNA repair activity. RAD50 protein plays key roles in DNA double strand breaks repair (DSBs), which is crucial to safeguard genome integrity and sustain tumor suppression. However, its role as a potential therapeutic target has not been addressed in breast cancer. Our aim in the present study was to analyze the expression of RAD50 protein in breast tumors, and evaluate the effects of RAD50-targeted inhibition on the cytotoxicity exerted by cisplatin and anthracycline and taxane-based therapies in breast cancer cells. Immunohistochemistry assays on tissue microarrays indicate that the strong staining intensity of RAD50 was reduced in 14% of breast carcinomas in comparison with normal tissues. Remarkably, RAD50 silencing by RNA interference significantly enhanced the cytotoxicity of cisplatin. Combinations of cisplatin with doxorubicin and paclitaxel drugs induced synergistic effects in early cell death of RAD50-deficient MCF-7, SKBR3, and T47D breast cancer cells. Furthermore, we found an increase in the number of DSBs, and delayed phosphorylation of histone H2AX after cisplatin treatment in RAD50-silenced cells. These cellular events were associated to a dramatical increase in the frequency of chromosomal aberrations and a decrease of cell number in metaphase. In conclusion, our data showed that RAD50 abrogation impairs DNA damage response and sensitizes breast cancer cells to cisplatin-combined therapies. We propose that the development and use of inhibitors to manipulate RAD50 levels might represent a promising strategy to sensitize breast cancer cells to DNA damaging agents.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.4161/cbt.28551DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4049793PMC
June 2014

[Impact on quality of life with breast reconstructive surgery after mastectomy for breast cancer].

Ginecol Obstet Mex 2013 Sep;81(9):510-8

Fundación del Cáncer de Mama (FUCAM).

Background: Breast cancer treatment leads mutilation and destruction of breast shape, with negative effects on body image and self-esteem.

Objectives: Assessment on quality of life after breast reconstruction surgery, impact on sexuality, the cosmetic outcome experienced by the patient, and compare result with patients who refused breast reconstruction.

Material And Methods: Retrospective, observational, descriptive, analytic study. We included breast cancer patients treated between April 15 2010 to April 15, 2011. Application of "The Survey Questionnaire short form Health 36" (SF-36) with valid use on Mexican population was conducted to measure quality of life, which uses 8 concepts: physical functioning, physical role, body pain, general health, vitality, social function, emotional role and mental health, the results are transferred to a scale 0 (worst health) to 100 (best health).

Results: 37 patients whit breast reconstruction had the inclusion criteria, mean age was 48.4 years. The score of SF-36 questionnaire in reconstructed patients was 76.8, in control group was 85.19 and mastectomy patients without reconstruction was 72.6. Among the items studied those with the greatest difference was the mental health, emotional role and social function, this means that patients with breast reconstruction are less affected in their social and sexual interaction.

Conclusions: The reconstructed patients have a positive impact on quality of life slightly higher, sexuality is significantly worse in patients without breast reconstruction, it is important to inform and offer breast reconstruction because many do not require these procedures for fear or lack of information.
View Article and Find Full Text PDF

Download full-text PDF

Source
September 2013

microRNA-18b is upregulated in breast cancer and modulates genes involved in cell migration.

Oncol Rep 2013 Nov 22;30(5):2399-410. Epub 2013 Aug 22.

Oncogenomics and Cancer Proteomics Laboratory, Genomics Sciences Program, Autonomous University of Mexico City, Mexico City, Mexico.

microRNAs are small non-coding RNAs of ~22 nucleotides that function at post-transcriptional level as negative regulators of gene expression. Aberrant expression of microRNAs could promote uncontrolled proliferation, migration and invasion of human cancer cells. In this study, we analyzed the expression of microRNA-18b (miR-18b) in breast cancer cell lines and in a set of clinical specimens. Our results showed that miR-18b was upregulated in four out of five breast cancer cell lines and also in breast tumors. In order to identify potential gene targets, we carried out transcriptional profiling of MDA-MB-231 breast cancer cells that ectopically expressed miR-18b. Our results showed that 263 genes were significantly modulated in miR-18b-deficient cells (fold change >1.5; P≤0.05). We found that knock-down of miR-18b induced the upregulation of 55 olfactory receptor (OR) genes and nine genes (NLRP7, KLK3, OLFM3, POSTN, MAGED4B, KIR3DL3, CRX, SEMG1 and CEACAM5) with key roles in cell migration and metastasis. Consistently, we found that ectopic inhibition of miR-18b suppressed the migration of two breast cancer cell models in vitro. In conclusion, we have uncovered genes directly or indirectly modulated by miR-18b which may represent potential therapeutic targets in breast cancer. Our data also pointed out a role of miR-18b in migration of breast cancer cells.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.3892/or.2013.2691DOI Listing
November 2013

Sequence analysis of mutations and translocations across breast cancer subtypes.

Nature 2012 Jun 20;486(7403):405-9. Epub 2012 Jun 20.

The Broad Institute of MIT and Harvard, Cambridge, Massachusetts 02142, USA.

Breast carcinoma is the leading cause of cancer-related mortality in women worldwide, with an estimated 1.38 million new cases and 458,000 deaths in 2008 alone. This malignancy represents a heterogeneous group of tumours with characteristic molecular features, prognosis and responses to available therapy. Recurrent somatic alterations in breast cancer have been described, including mutations and copy number alterations, notably ERBB2 amplifications, the first successful therapy target defined by a genomic aberration. Previous DNA sequencing studies of breast cancer genomes have revealed additional candidate mutations and gene rearrangements. Here we report the whole-exome sequences of DNA from 103 human breast cancers of diverse subtypes from patients in Mexico and Vietnam compared to matched-normal DNA, together with whole-genome sequences of 22 breast cancer/normal pairs. Beyond confirming recurrent somatic mutations in PIK3CA, TP53, AKT1, GATA3 and MAP3K1, we discovered recurrent mutations in the CBFB transcription factor gene and deletions of its partner RUNX1. Furthermore, we have identified a recurrent MAGI3-AKT3 fusion enriched in triple-negative breast cancer lacking oestrogen and progesterone receptors and ERBB2 expression. The MAGI3-AKT3 fusion leads to constitutive activation of AKT kinase, which is abolished by treatment with an ATP-competitive AKT small-molecule inhibitor.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1038/nature11154DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4148686PMC
June 2012

Breast cancer proteomics reveals a positive correlation between glyoxalase 1 expression and high tumor grade.

Int J Oncol 2012 Aug 14;41(2):670-80. Epub 2012 May 14.

Genomics Sciences Program, Oncogenomics and Cancer Proteomics Laboratory, Autonomous University of Mexico city, Mexico City, Mexico.

Breast cancer is the neoplasia with the highest incidence in women worldwide. Proteomics approaches have accelerated the discovery of diagnostic and prognostic biomarkers. Here, we compared the proteomic profiles of breast tumors versus non-tumoral tissues in order to identify modulated proteins, which could represent potential markers associated to clinical features. By two-dimensional electrophoresis, we detected 28 differentially expressed proteins. Among these, 21 proteins were up-regulated and 7 were down-regulated in tumors (p<0.05). Proteins were identified using LC/ESI-MS/MS tandem mass spectrometry. One protein was identified as glyoxalase 1 (GLO1), an enzyme involved in detoxification of methylglyoxal, a cytotoxic product of glycolysis. GLO1 overexpression was confirmed by western blot assays in paired normal and tumor breast tissues in clinical stages I-III, and by immunohistochemistry on tissue microarrays (TMA) comprising a cohort of 98 breast tumors and 20 healthy specimens. Results from TMA demonstrated that GLO1 is overexpressed in 79% of tumors. Interestingly, GLO1 up-regulation correlates with advanced tumor grade (p<0.05). These findings demonstrate the association of GLO1 overexpression with tumor grade and pointed out for additional studies to establish the importance of GLO1 in breast cancer.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.3892/ijo.2012.1478DOI Listing
August 2012

Identification and pathway analysis of microRNAs with no previous involvement in breast cancer.

PLoS One 2012 16;7(3):e31904. Epub 2012 Mar 16.

Laboratorio de Genómica del Cáncer, Instituto Nacional de Medicina Genómica. Mexico City, Mexico.

microRNA expression signatures can differentiate normal and breast cancer tissues and can define specific clinico-pathological phenotypes in breast tumors. In order to further evaluate the microRNA expression profile in breast cancer, we analyzed the expression of 667 microRNAs in 29 tumors and 21 adjacent normal tissues using TaqMan Low-density arrays. 130 miRNAs showed significant differential expression (adjusted P value = 0.05, Fold Change = 2) in breast tumors compared to the normal adjacent tissue. Importantly, the role of 43 of these microRNAs has not been previously reported in breast cancer, including several evolutionary conserved microRNA*, showing similar expression rates to that of their corresponding leading strand. The expression of 14 microRNAs was replicated in an independent set of 55 tumors. Bioinformatic analysis of mRNA targets of the altered miRNAs, identified oncogenes like ERBB2, YY1, several MAP kinases, and known tumor-suppressors like FOXA1 and SMAD4. Pathway analysis identified that some biological process which are important in breast carcinogenesis are affected by the altered microRNA expression, including signaling through MAP kinases and TP53 pathways, as well as biological processes like cell death and communication, focal adhesion and ERBB2-ERBB3 signaling. Our data identified the altered expression of several microRNAs whose aberrant expression might have an important impact on cancer-related cellular pathways and whose role in breast cancer has not been previously described.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0031904PLOS
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3306365PMC
August 2012

MetastamiRs: non-coding MicroRNAs driving cancer invasion and metastasis.

Int J Mol Sci 2012 27;13(2):1347-79. Epub 2012 Jan 27.

Genomics Sciences Program, Oncogenomics and Cancer Proteomics Laboratory, Autonomous University of Mexico City, Avenue San Lorenzo 290, 03100, Mexico; E-Mail:

MicroRNAs (miRNAs) are small non-coding RNAs of ~22 nucleotides that function as negative regulators of gene expression by either inhibiting translation or inducing deadenylation-dependent degradation of target transcripts. Notably, deregulation of miRNAs expression is associated with the initiation and progression of human cancers where they act as oncogenes or tumor suppressors contributing to tumorigenesis. Abnormal miRNA expression may provide potential diagnostic and prognostic tumor biomarkers and new therapeutic targets in cancer. Recently, several miRNAs have been shown to initiate invasion and metastasis by targeting multiple proteins that are major players in these cellular events, thus they have been denominated as metastamiRs. Here, we present a review of the current knowledge of miRNAs in cancer with a special focus on metastamiRs. In addition we discuss their potential use as novel specific markers for cancer progression.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.3390/ijms13021347DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3291964PMC
July 2015

[Breast cancer in Mexican women under 40].

Ginecol Obstet Mex 2011 Aug;79(8):482-8

Instituto de Enfermedades de la Mama FUCAM (IEM-FUCAM).

Background: Breast cancer is the leading cause of death from malignancy in women. The incidence increases with age, but the relationship between age and survival of breast cancer patients is not well defined. It is observed that young women with breast cancer have patterns more aggressive biological.

Objective: To determine the frequency, sociodemographic, clinical and histopathological features of breast cancer in women under 40 years attending a specialist breast unit in Mexico City.

Patients And Method: Transversal, descriptive and retrospective study of patients under 40 years of age with breast cancer treated between 2005 and 2010.

Results: 1430 cases were diagnosed with breast cancer five years with a mean age of 53.64 +/- 11.87 years (range 23 to 93 years), 142 cases were women under 40 years of age (10%). The auto-detection of a breast lump was the most frequent clinical manifestation (50%).

Conclusion: The prevalence of clinical stage III in this age group suggests the difficulty of diagnosis, the high breast density, which is one factor limiting studies of screening with mammography, it diminishes their effectiveness in early detection of breast cancer.
View Article and Find Full Text PDF

Download full-text PDF

Source
August 2011

[Radiological control intraoperatory of a surgical piece in non palpable breast lesions].

Ginecol Obstet Mex 2009 Sep;77(9):407-18

Departamento de Cirugía Oncológica Mamaria, Instituto de Enfermedades de la Mama de la Fundación Mexicana de Fomento Educativo para la Prevención y Detección Oportuna del Cáncer de Mama, AC, DF México.

Background: nonconcrete the mammary injuries are frequent in programs of detection of breast cancer, estereotaxic or ecographic marking is required to realize its split. The intrasurgical radiation control of the surgical piece is indispensable to evaluate the margins of the mammary cancer.

Objective: to determine the effectiveness of the intrasurgical radiation control of the surgical piece in nonconcrete mammary injuries to diminish the surgical reinterventions to extend margins.

Patients And Method: women with nonconcrete mammary injuries to those who biopsy by split became, previous marking and intraoperating radiation control of the surgical piece to value margins (suitable margin the same or major of 10 mm, smaller inadequate margin of 10 mm). Intrasurgical reesicion in inadequate radiological margins became. The demographic characteristics, masto-ecographics images, histopathology of the injuries and the radiological-histopatol6gica correlation of the margins studied. Cross-sectional, prospective and descriptive study.

Results: 103 patients with 113 nonconcrete mammary injuries included themselves, with age average of 51,35 (32-73) years. In all the injuries the intrasurgical radiation control became of the surgical piece. The prevalence of mammary cancer was of 28.3% (32/113), that corresponds to stellar images (42.8%), suspicious microcalcifications with density (39.2%), microcalcifications (31.2%) and nodules (20%). Of the 32 cancers, 16 had inadequate radiological margins that required intraoperating reescision; suitable histopatologic margins in 100% were obtained (16/16). The 16 (62.5%) cancers without intraoperating reescisi6n by suitable radiological margins had suitable histopatologic margins and 37.5% (6/16) inadequate ones that required surgical reinterventionn to control the margins. The discrepancy between margins was related to microcalcifications in 83.3% of the injuries.

Conclusions: the intrasurgical radiation control of the surgical piece is effective to evaluate margins; the intrasurgical reescisión changed inadequate margins to suitable in 50% (16/32) of the cancers; only 18.7% (6/32) of the total of cases required another surgery to control the margins.
View Article and Find Full Text PDF

Download full-text PDF

Source
September 2009