Cancer Genetics and Cytogenetics最新文献

{"title":"FISH-negative cryptic PML–RARA rearrangement detected by long-distance polymerase chain reaction and sequencing analyses: a case study and review of the literature","authors":"Min Jin Kim ,&nbsp;Sun Young Cho ,&nbsp;Myeong-Hee Kim ,&nbsp;Jae Jin Lee ,&nbsp;So Young Kang ,&nbsp;Eun Hae Cho ,&nbsp;Jungwon Huh ,&nbsp;Hwi-Joong Yoon ,&nbsp;Tae Sung Park ,&nbsp;Woo-In Lee ,&nbsp;Rolf Marschalek ,&nbsp;Claus Meyer","doi":"10.1016/j.cancergencyto.2010.08.026","DOIUrl":"10.1016/j.cancergencyto.2010.08.026","url":null,"abstract":"<div><p>Although a normal karyotype according to conventional cytogenetic analysis in association with cryptic t(15;17) has been infrequently reported in cases of acute promyelocytic leukemia (APL), a fluorescence in situ hybridization (FISH)-negative cryptic <em>PML–RARA</em> rearrangement is even more rare, with only 12 such APL cases of FISH-negative cryptic <em>PML–RARA</em> rearrangements in the literature. Reported here is an additional clinical APL case with a FISH-negative cryptic <em>PML–RARA</em> rearrangement, confirmed by long-distance DNA polymerase chain reaction method. Discussion includes a relevant literature review of similar cases. DNA-PCR can be a useful tool for the analysis of complex and cryptic rearrangements.</p></div>","PeriodicalId":55596,"journal":{"name":"Cancer Genetics and Cytogenetics","volume":"203 2","pages":"Pages 278-283"},"PeriodicalIF":0.0,"publicationDate":"2010-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.cancergencyto.2010.08.026","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"29534052","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A pericentric inv(9)(p22q34) of the der(9)t(9;22)(q34;q11.2) is a recurrent secondary anomaly in Ph-positive leukemia","authors":"Jinlan Pan,&nbsp;Yongquan Xue,&nbsp;Huiying Qiu,&nbsp;Suning Chen,&nbsp;Jun Zhang,&nbsp;Yafang Wu,&nbsp;Juan Shen,&nbsp;Yong Wang","doi":"10.1016/j.cancergencyto.2010.05.009","DOIUrl":"10.1016/j.cancergencyto.2010.05.009","url":null,"abstract":"<div><p>A pericentric inv(9)(p22q34) of the derivative chromosome 9 that resulted from a standard t(9;22)(q34;q11.2) was identified by R-banding karyotypic analysis and fluorescence in situ hybridization (FISH) assays in 4 (0.18%) of 2,200 Philadelphia chromosome (Ph)-positive leukemia patients, including 3 with chronic myeloid leukemia (CML) in chronic phase and 1 with acute myeloid leukemia (AML) in our hospital since 2004. All four patients had two malignant clones: one with only t(9;22)(q34;q11.2) and another with der(9)t(9;22)(q34;q11.2)inv(9)(p22q34) that resulted in the separation of the <em>ABL1/BCR</em> fusion gene. No metaphases with only inv(9)(p22q34) were seen in any of them. FISH also found a deletion of partial sequence of BCR on der(9)t(9;22)(q34;q11.2)inv(9)(p22q34) in 67.5% of bone marrow cells in the AML patient, but did not detect the deletion of the sequence of ASS/9q34 in these four patients. Reverse transcriptase–polymerase chain reaction revealed a b3a2 type of <em>BCR/ABL1</em> fusion transcript in all of them, proving their disease to be Ph-positive leukemia. On reviewing the literature, only two solitary Ph-positive leukemia patients have been noticed to have the inv(9)(p22q34) anomaly. These two patients, together with our four documented patients, indicate that inv(9)(p22q34) is a novel, rare, but recurrent secondary chromosomal abnormality for Ph-positive leukemia. Despite receiving hydroxyurea therapy (<em>n</em> = 3 patients), combined chemotherapy (<em>n</em> = 2), even imatinib treatment (<em>n</em> = 1), three patients, including one with AML and two with CML (one of whom progressed into the lymphoblastic blast phase), died with survival times of 28 days, 13 months, and 34 months, respectively. Only one patient with CML remained alive for 5.5 months. Their negative outcome implies that inv(9)(p22q34) has an unfavorable impact on prognosis. Presently, no firm conclusions can be drawn from this study. Because the case number reported here is very small, more patients with this anomaly need to be investigated to elucidate its true prognostic significance.</p></div>","PeriodicalId":55596,"journal":{"name":"Cancer Genetics and Cytogenetics","volume":"203 2","pages":"Pages 333-340"},"PeriodicalIF":0.0,"publicationDate":"2010-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.cancergencyto.2010.05.009","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"29534505","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Response to the letter by Najfeld regarding the article “Chromosome abnormalities additional to the Philadelphia chromosome at the diagnosis of chronic myelogenous leukemia: pathogenetic and prognostic implications”","authors":"Alfonso Zaccaria","doi":"10.1016/j.cancergencyto.2010.09.008","DOIUrl":"https://doi.org/10.1016/j.cancergencyto.2010.09.008","url":null,"abstract":"","PeriodicalId":55596,"journal":{"name":"Cancer Genetics and Cytogenetics","volume":"203 2","pages":"Page 357"},"PeriodicalIF":0.0,"publicationDate":"2010-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.cancergencyto.2010.09.008","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"136856804","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Germline mutations of BRCA1 and BRCA2 genes in Turkish breast, ovarian, and prostate cancer patients","authors":"Esra Manguoğlu ,&nbsp;Şefik Güran ,&nbsp;Deniz Yamaç ,&nbsp;Taner Çolak ,&nbsp;Mehmet Şimşek ,&nbsp;Mehmet Baykara ,&nbsp;Mustafa Akaydın ,&nbsp;Güven Lüleci","doi":"10.1016/j.cancergencyto.2010.07.125","DOIUrl":"10.1016/j.cancergencyto.2010.07.125","url":null,"abstract":"<div><p>Distribution and prevalence of germline mutations in <em>BRCA1</em> and <em>BRCA2</em> differ among different populations. For the Turkish population, several studies have addressed high-risk breast cancer and ovarian cancer (BC–OC) patients. In most studies, both genes were analyzed in part, and a quite heterogeneous mutation spectrum was observed. For high-risk Turkish prostate cancer (PCa) patients, however, there are no data available about mutations of germline <em>BRCA</em> genes. To accurately determine the contribution of germline mutations in <em>BRCA1</em> and <em>BRCA2</em> in Turkish BC, OC, and PCa high-risk patients, 106 high-risk BC–OC patients, 50 high-risk PCa patients, and 50 control subjects were recruited. The study represents the only full screening, to date, of a large series of Turkish high-risk BC–OC patients and the only study in Turkish high-risk PCa patients. Mutation screenings were performed on coding exons of both genes with either denaturing gradient gel electrophoresis or denaturing high performance liquid chromatography, or with both techniques. Three deleterious mutations in <em>BRCA1</em> and three deleterious mutations in <em>BRCA2</em> were detected in different BC–OC patients, and one truncating mutation was detected in a high-risk PCa patient. In addition, 28 different unclassified and mostly novel variants were detected in both genes, as well as several silent polymorphisms. These findings reflect the genetic heterogeneity of the Turkish population and are relevant to genetic counseling and clinical management.</p></div>","PeriodicalId":55596,"journal":{"name":"Cancer Genetics and Cytogenetics","volume":"203 2","pages":"Pages 230-237"},"PeriodicalIF":0.0,"publicationDate":"2010-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.cancergencyto.2010.07.125","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"29533579","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cytogenetics and genetics of human cancer: methods and accomplishments","authors":"Avery A. Sandberg ,&nbsp;Aurelia M. Meloni-Ehrig","doi":"10.1016/j.cancergencyto.2010.10.004","DOIUrl":"10.1016/j.cancergencyto.2010.10.004","url":null,"abstract":"<div><p>Cytogenetic and related changes in human cancer constitute part of a constantly developing and enlarging continuum of known genetic alterations associated with cancer development and biology. The cytogenetic component of this continuum has fulfilled much of its pioneering role and now constitutes a small but dynamic segment of the vast literature on cancer genetics, in which it has played an important if not initiating role. The goals of this article are (a) to address historical and methodological aspects of cancer cytogenetics; (b) to present information on diagnostic translocations in leukemias, lymphomas, bone and soft tissue tumors, and carcinomas; (c) to connect some of these chromosomal aberrations with their molecular equivalents; and (d) to describe anomalies in some solid tumors indicative of the complexity of the genomic alterations in cancer. We also look at a few of the more recent genomic developments in cancer and offer an opinion as to what all these findings add up to.</p></div>","PeriodicalId":55596,"journal":{"name":"Cancer Genetics and Cytogenetics","volume":"203 2","pages":"Pages 102-126"},"PeriodicalIF":0.0,"publicationDate":"2010-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.cancergencyto.2010.10.004","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"29533664","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correlation of cytomorphology, immunophenotyping, and interphase fluorescence in situ hybridization in 381 patients with monoclonal gammopathy of undetermined significance and 301 patients with plasma cell myeloma","authors":"Ulrike Bacher ,&nbsp;Torsten Haferlach ,&nbsp;Wolfgang Kern ,&nbsp;Tamara Alpermann ,&nbsp;Susanne Schnittger ,&nbsp;Claudia Haferlach","doi":"10.1016/j.cancergencyto.2010.08.006","DOIUrl":"10.1016/j.cancergencyto.2010.08.006","url":null,"abstract":"<div><p>To further clarify the transformation from monoclonal gammopathy of undetermined significance (MGUS) to plasma cell myeloma (PCM), we compared interphase fluorescence in situ hybridization (FISH) patterns in 381 MGUS and 301 PCM patients. According to the World Health Organization and the International Myeloma Working Group, a threshold of 10% of bone marrow plasma cells separated MGUS from PCM. After magnetic activated cell sorting for CD138⁺ cells, FISH succeeded in 272 of 301 (90.4%) PCM, but in only 302 of 381 (79.3%) MGUS cases (<em>P</em> &lt; 0.001). Cytogenetic alterations were more frequent in PCM (237 of 272; 87.1%) than MGUS (169 of 302; 56.0%; <em>P</em> = 0.0002). PCM showed a median of two cytogenetic alterations (range, 0–9) and MGUS one (range, 0–6). Considering only cases with a yield of plasma cells allowing five or more FISH probes, del(13)(q14) was found in 99 of 251 (39.3%) PCM but in only 59 of 267 (22.1%) MGUS (<em>P</em> = 0.0001), del(17p) in 15 PCM (6.0%) and in 6 MGUS (2.2%) patients (<em>P</em> = 0.029). A t(4;14)/<em>IGH-FGFR3</em> was detected in 28 PCM (11.1%) and 5 MGUS (1.9%; <em>P</em> &lt; 0.001). The t(11;14)/<em>IGH-CCND1</em> and the t(14;16)/<em>IGH-MAF</em> showed no significant differences. Cytomorphology detected higher numbers of plasma cells than multiparameter flow cytometry (median ratio 4.25). This study underlines the genetic heterogeneity of MGUS similar to PCM. Genetic analysis might contribute to more diversified monitoring strategies for MGUS patients.</p></div>","PeriodicalId":55596,"journal":{"name":"Cancer Genetics and Cytogenetics","volume":"203 2","pages":"Pages 169-175"},"PeriodicalIF":0.0,"publicationDate":"2010-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.cancergencyto.2010.08.006","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"29533669","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Acute myeloid leukemia associated with t(1;3)(p36;q21) and extreme thrombocytosis: a clinical study with literature review","authors":"Gayoung Lim ,&nbsp;Min Jin Kim ,&nbsp;Seung Hwan Oh ,&nbsp;Sun Young Cho ,&nbsp;Hee Joo Lee ,&nbsp;Jin-Tae Suh ,&nbsp;Juhie Lee ,&nbsp;Woo-In Lee ,&nbsp;Kyung Sam Cho ,&nbsp;Tae Sung Park","doi":"10.1016/j.cancergencyto.2010.08.001","DOIUrl":"10.1016/j.cancergencyto.2010.08.001","url":null,"abstract":"<div><p>We present an unusual case study on acute myeloid leukemia associated with t(1;3) and extreme thrombocytosis, along with a thorough review on relevant literature of t(1;3) cases (58 patients). On the basis of this study and literature review, thrombocytosis (&gt;400,000/μL) is a relatively common finding in one third of patients with t(1;3), whereas increase of platelet count by more than 1,000,000/μL is an extremely rare phenomenon, even among patients with t(1;3). To our knowledge, this study is the only documented case that recorded more than 2,000,000/μL of extreme thrombocytosis in a de novo acute myeloid leukemia patient with t(1;3) at initial diagnosis. Because only a few patients with t(1;3) responded to conventional chemotherapy, more aggressive therapy such as stem-cell transplantation should be considered to improve patient survival in t(1;3) cases.</p></div>","PeriodicalId":55596,"journal":{"name":"Cancer Genetics and Cytogenetics","volume":"203 2","pages":"Pages 187-192"},"PeriodicalIF":0.0,"publicationDate":"2010-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.cancergencyto.2010.08.001","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"29533573","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Stimulation of chronic lymphocytic leukemia cells with CpG oligodeoxynucleotide gives consistent karyotypic results among laboratories: a CLL Research Consortium (CRC) Study","authors":"Nyla A. Heerema ,&nbsp;John C. Byrd ,&nbsp;Paola S. Dal Cin ,&nbsp;Marie L. Dell’ Aquila ,&nbsp;Prasad R.K. Koduru ,&nbsp;Ayala Aviram ,&nbsp;Stephanie A. Smoley ,&nbsp;Laura Z. Rassenti ,&nbsp;Andrew W. Greaves ,&nbsp;Jennifer R. Brown ,&nbsp;Kanti R. Rai ,&nbsp;Thomas J. Kipps ,&nbsp;Neil E. Kay ,&nbsp;Daniel L. Van Dyke ,&nbsp;Chronic Lymphocytic Leukemia Research Consortium","doi":"10.1016/j.cancergencyto.2010.07.128","DOIUrl":"10.1016/j.cancergencyto.2010.07.128","url":null,"abstract":"<div><p>Cytogenetic abnormalities are important prognostic indicators in CLL. Historically, only interphase cytogenetics was clinically useful in CLL, because traditional mitogens are not effective mitotic stimulants. Recently, CpG-oligodeoxynucleotide (ODN) stimulation has shown effectiveness in CLL cells. The CLL Research Consortium tested the effectiveness and reproducibility of CpG-ODN stimulation for detecting chromosomally abnormal clones by five laboratories. More clonal abnormalities were observed after culture of CLL cells with CpG-ODN than with the traditional pokeweed mitogen plus 12-<em>O</em>-tetradecanoylphorbol-13-acetate (PWM+TPA). All clonal abnormalities in PWM+TPA cultures were observed in CpG-ODN cultures, whereas CpG-ODN identified some clones not found by PWM+TPA. CpG-ODN stimulation of one normal control sample and 12 CLL samples showed that, excepting clones of del(13q) in low frequencies and one translocation, results in all five laboratories were consistent, and all abnormalities were concordant with FISH. Abnormal clones in CLL were more readily detected with CpG-ODN stimulation than with traditional B-cell mitogens. With CpG-ODN stimulation, abnormalities were reproducible among cytogenetic laboratories. CpG-ODN did not appear to induce aberrations in cell culture, but did enhance detection of abnormalities and complexity in CLL. Because karyotypic complexity is prognostic and is not detectable by standard FISH analyses, stimulation with CpG-ODN is useful for identifying this additional prognostic factor in CLL.</p></div>","PeriodicalId":55596,"journal":{"name":"Cancer Genetics and Cytogenetics","volume":"203 2","pages":"Pages 134-140"},"PeriodicalIF":0.0,"publicationDate":"2010-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.cancergencyto.2010.07.128","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"29533666","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Progressive but previously untreated CLL patients with greater array CGH complexity exhibit a less durable response to chemoimmunotherapy","authors":"Neil E. Kay ,&nbsp;Jeanette E. Eckel-Passow ,&nbsp;Esteban Braggio ,&nbsp;Scott VanWier ,&nbsp;Tait D. Shanafelt ,&nbsp;Daniel L. Van Dyke ,&nbsp;Diane F. Jelinek ,&nbsp;Renee C. Tschumper ,&nbsp;Thomas Kipps ,&nbsp;John C. Byrd ,&nbsp;Rafael Fonseca","doi":"10.1016/j.cancergencyto.2010.09.003","DOIUrl":"10.1016/j.cancergencyto.2010.09.003","url":null,"abstract":"<div><p>To better understand the implications of genomic instability and outcome in B-cell chronic lymphocytic leukemia (CLL), we sought to address genomic complexity as a predictor of chemosensitivity and ultimately clinical outcome in this disease. We used array-based comparative genomic hybridization (aCGH) with a one-million probe array and identified gains and losses of genetic material in 48 patients treated on a chemoimmunotherapy clinical trial. We identified chromosomal gain or loss in ≥6% of the patients on chromosomes 3, 8, 9, 10, 11, 12, 13, 14, and 17. Higher genomic complexity, as a mechanism favoring clonal selection, was associated with shorter progression-free survival, and predicted a poor response to treatment. Of interest, CLL cases with loss of p53 surveillance showed more complex genomic features and were found both in patients with a 17p13.1 deletion and in the more favorable genetic subtype characterized by the presence of 13q14.1 deletion. This aCGH study adds information on the association between poor trial response and increasing genetic complexity as CLL progresses.</p></div>","PeriodicalId":55596,"journal":{"name":"Cancer Genetics and Cytogenetics","volume":"203 2","pages":"Pages 161-168"},"PeriodicalIF":0.0,"publicationDate":"2010-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.cancergencyto.2010.09.003","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"29533670","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Role of TP53 Arg72Pro polymorphism in urinary bladder cancer predisposition and predictive impact of proline related genotype in advanced tumors in an ethnic Kashmiri population","authors":"Arshad A. Pandith ,&nbsp;Zafar A. Shah ,&nbsp;Nighat P. Khan ,&nbsp;Roohi Rasool ,&nbsp;Dil Afroze ,&nbsp;Adfar Yousuf ,&nbsp;Saleem Wani ,&nbsp;Mushtaq Siddiqi","doi":"10.1016/j.cancergencyto.2010.08.010","DOIUrl":"10.1016/j.cancergencyto.2010.08.010","url":null,"abstract":"<div><p>Among various polymorphic variants of <em>TP53</em> gene, codon 72 polymorphism (Arg72Pro) has been found to be associated with cancer susceptibility, but only few studies have investigated their effect on bladder cancer risk. A case–control study was conducted and we observed the genotype distribution of <em>TP53</em><span> Arg72Pro SNP, to elucidate the possible role of this SNP as risk factor in urinary bladder cancer (UBC) development and to examine its correlation with the clinicopathologic variables of UBC cases. Using the polymerase chain reaction-restriction fragment length polymorphism approach, we tested the genotype distribution of 108 bladder cancer patients in comparison with 138 cancer-free controls from the same geographical region. We observed significant differences between the control and bladder cancer patients with odds ratio = 2.9 and 95% confidence interval = 1.5–4.5 (</span><em>P</em><span> = 0.00001). Interestingly, the proline form was abundantly observed in advanced tumors (</span><em>P</em> &lt; 0.05). We also found a significant association of the variant allele (GC+CC) with male subjects and ever smokers (<em>P</em> = 0.001). Thus, it is evident from our study that Arg72Pro SNP is implicated in bladder cancer, and that the rare, proline-related allele is connected with higher susceptibility to bladder cancer.</p></div>","PeriodicalId":55596,"journal":{"name":"Cancer Genetics and Cytogenetics","volume":"203 2","pages":"Pages 263-268"},"PeriodicalIF":0.0,"publicationDate":"2010-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.cancergencyto.2010.08.010","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"29534050","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}