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Tomasz Tuziak

Publications and source records attributed to Tomasz Tuziak.

7 recordsLinked to original sources
PubMed2006

Evidence for alternative candidate genes near RB1 involved in clonal expansion of in situ urothelial neoplasia.

In this paper, we present whole-organ histologic and genetic mapping studies using hypervariable DNA markers on chromosome 13 and then integrate the recombination- and single-nucleotide polymorphic sites (SNPs)-based deletion maps with the annotated genome sequence. Using bladders resected from patients with invasive urothelial carcinoma, we studied allelic patterns of 40 microsatellite markers mapping to all regions of chromosome 13 and 79 SNPs located within the 13q14 region containing the RB1 gene. A whole-organ histologic and genetic mapping strategy was used to identify the evolution of allelic losses on chromosome 13 during the progression of bladder neoplasia. Markers mapping to chromosomal regions involved in clonal expansion of preneoplastic intraurothelial lesions were subsequently tested in 25 tumors and 21 voided urine samples of patients with bladder cancer. Four clusters of allelic losses mapping to distinct regions of chromosome 13 were identified. Markers mapping to the 13q14 region that is flanked by D13S263 and D13S276, which contains the RB1 gene, showed allelic losses associated with early clonal expansion of intraurothelial neoplasia. Such losses could be identified in approximately 32% bladder tumor tissue samples and 38% of voided urines from patients with bladder cancer. The integration of distribution patterns of clonal allelic losses revealed by the microsatellite markers with those obtained by genotyping of SNPs disclosed that the loss within an approximately 4-Mb segment centered around RB1 may represent an incipient event in bladder neoplasia. However, the inactivation of RB1 occurred later and was associated with the onset of severe dysplasia/carcinoma in situ. Our studies provide evidence for the presence of critical alternative candidate genes mapping to the 13q14 region that are involved in clonal expansion of neoplasia within the bladder antecedent to the inactivation of the RB1 gene.

Aged↗
PubMed2005

Malignant mesothelioma of the tunica vaginalis.

OBJECTIVES: To review our experience with the management of malignant mesothelioma of the tunica vaginalis with emphasis on disease-related outcomes. METHODS: A retrospective chart review of patients seen during the past 25 years at our cancer center identified 5 cases of malignant mesothelioma of the tunica vaginalis. RESULTS: The mean age of patients at presentation was 61.2 years (range 57 to 83). Asbestos exposure was identified in 4 patients. Three patients presented with clinical symptoms suggestive of a hydrocele and two presented with clinical signs of an inguinal hernia. The final diagnosis was established intraoperatively in 1 patient and postoperatively in the remaining 4. Radical orchiectomy or hernia sac with spermatic cord excision was the primary treatment modality. Although radical surgical treatment achieved negative resection margins in 4 cases, 4 of 5 patients died of the disease, with a mean disease-specific survival of only 29 months (range 5 to 68). Regional inguinal lymph node metastasis developed in 3 of 5 patients. Salvage therapy did not prove curative in the 2 patients who received it. CONCLUSIONS: Malignant mesothelioma of the tunica vaginalis constitutes a rare but often fatal malignancy of the male genitalia. This diagnosis should be suspected in patients exposed to asbestos and presenting with clinical symptoms of either hydrocele or inguinal hernia. Frequent inguinal lymph node involvement indicates a potential role of inguinal lymphadenectomy in the primary treatment.

Aged↗
PubMed2005

Alterations in transcription clusters underlie development of bladder cancer along papillary and nonpapillary pathways.

Bladder cancer develops in the urothelial lining from intraurothelial preneoplasia via two pathways, papillary and nonpapillary, which correspond to nonaggressive and aggressive forms of the disease. Because these two forms of cancer may develop via distinct molecular events, we examined the gene expression patterns in the development of bladder cancer from preneoplasia along papillary and nonpapillary pathways. The expression profiles of 19 pairs of RNA samples from adjacent urothelium and tumors were analyzed using cDNA microarrays. For selected genes their expressions were verified on a cohort of 251 bladder cancer patients using tissue microarray and immunohistochemistry and were related to clinicopathological parameters including follow-up data. We identified alterations in seven gene clusters controlling proliferation, differentiation, and programmed cell death that were common for papillary and nonpapillary cancer. In contrast, genes controlling cellular and stromal interactions were altered in the nonpapillary cancer. The expression levels of only two genes from this group could be used to define an aggressive form of the disease. Tumors characterized by the low expression of e-cadherin and the high expression of DNA alpha-topoisomerase II had a high propensity for distant metastasis and were associated with poor survival.

DNA, Complementary↗
PubMed2005

High-resolution whole-organ mapping with SNPs and its significance to early events of carcinogenesis.

We attempted to identify deleted segments in two model tumor suppressor gene loci on chromosomes 13q14 and 17p13 that were associated with clonal expansion of in situ bladder preneoplasia using single nucleotide polymorphisms (SNPs)-based whole-organ histologic and genetic mapping. For mapping with SNPs, the sequence-based maps spanning approximately 27 and 5 Mb centered around RB1 and p53, respectively, were assembled. The integrated gene and SNP maps of the regions were used to select 661 and 960 SNPs, which were genotyped by pyrosequencing. Genotyping of SNPs was performed on DNA samples corresponding to histologic maps of the entire bladder mucosa in human cystectomy specimens with invasive urothelial carcinoma. By using this approach, we have identified deleted regions associated with clonal expansion of intraurothelial neoplasia; which ranged from 0.001 to 4.3 Mb (average 0.67 Mb) and formed clusters of discontinuous deleted segments. The high resolution of such maps is a prerequisite for future positional targeting of genes involved in early phases of bladder neoplasia. This approach also permits analysis of the overall genomic landscape of the involved region and discloses that a unique composition of noncoding DNA characterized by a high concentration of repetitive sequences may predispose to deletions.

Carcinoma in Situ↗
PubMedDate not supplied

Multilocular cystadenoma and cystadenocarcinoma of the prostate.

BACKGROUND: Multicystic prostatic tumors are rare, with only a few reported cases of prostatic cystadenoma and cystadenocarcinoma in the scientific literature. METHODS: A retrospective review of our tumor registry over the last 25 years identified 2 rare cystic tumors of the prostate: 1 multilocular cystadenoma and 1 multilocular cystadenocarcinoma. RESULTS: The first case illustrates the clinical and pathologic features of prostatic multilocular cystadenoma. A 42-year-old man presented with a 16-cm suprapubic mass causing displacement of adjacent visceral organs. Pathologic examination after prostatectomy confirmed it to be a multilocular cystadenoma of the prostate. The patient's postoperative course was uneventful, and his serum prostate-specific antigen level remained at < or =0.04 ng/ml throughout the course of his disease. In the second case, we present an 80-year-old male presenting with a 12-cm cystic mass of the prostate. His serum prostate-specific antigen level remained at > or =9.0 ng/ml throughout the course of his disease. The tumor had an aggressive local growth pattern, with invasion into perirectal adipose tissue. This patient underwent a pelvic exenteration, followed by adjuvant systemic chemotherapy and complete androgen blockade. Despite aggressive treatment, he had 3 recurrences over 4 months but remains alive with disease at 23-month follow-up. CONCLUSIONS: Cystadenocarcinoma of the prostate is locally aggressive and should be included in the differential diagnosis of cystic lesions of the prostate.

Adult↗
PubMedDate not supplied

Review of the M.D. Anderson experience in the treatment of bladder sarcoma.

OBJECTIVE: To assess the histologic subtypes, clinical presentations, treatment approaches, and treatment-related outcomes of patients with bladder sarcoma. METHODS: Between January 1985 and July 2004, 19 patients (12 men and 7 women) with primary bladder sarcoma were evaluated at the University of Texas M.D. Anderson Cancer Center. Median follow-up duration was 72 months (range 3-141). RESULTS: The median age of patients at presentation was 57 years (range 22-94). The histologic subtypes of bladder sarcoma were leiomyosarcoma (N = 14), angiosarcoma (N = 3), and unclassified sarcoma (N = 2). The clinical presentation consisted of gross, painless hematuria in 79% of patients, lower urinary tract symptoms in 16%, and microhematuria in 5%. The primary treatment modalities used were surgery in 16 (84%) patients, chemotherapy in 2 (11%), and palliation in 1 (5%). The rate of local and distal recurrence was 16% and 53%, respectively. The most common sites of distant metastases were the lungs, bone, brain, and liver. The 5-year disease-specific survival rate was 59%, with a median survival duration of 6 years. There was no statistically significant difference in disease-specific survival between patients with bladder leiomyosarcoma compared to other sarcoma subtypes (P = 0.149). Lymphovascular invasion (P = 0.03) and lymphatic metastasis (P = 0.03) were associated with disease-specific survival, and surgical margin status was associated with recurrence-free (P = 0.04), disease-specific (P = 0.03), and overall survival (P = 0.005). CONCLUSIONS: Bladder sarcoma is a highly aggressive malignancy, regardless of its histologic subtype. Surgical margin status is an important determinant of survival.

Adult↗