Adenocarcinoma in ectopic prostatic tissue at dome of bladder: a case report of a patient with urothelial carcinoma of the bladder and adenocarcinoma of the prostate.

We report a case of ectopic prostate tissue with an associated prostatic adenocarcinoma occurring in the dome of the urinary bladder. A 62-year-old man presented with a 4-month history of persistent microscopic hematuria following a urinary tract infection. Other complaints included frequent urination, but there was neither dysuria nor gross hematuria.

Mismatch repair expression in testicular cancer predicts recurrence and survival.

We investigated mismatch repair (MMR) gene expression in testicular cancer as a molecular marker for clinical outcome (recurrence, response to chemotherapy and death) using protein expression and specific genetic alterations associated with the presence or absence of MMR activity. One hundred sixty-two cases of paraffin-embedded testis cancer specimens were subjected to immunohistochemical analysis using monoclonal antibody for MLH1 and MSH2 MMR proteins and genetic analysis using specific polymorphic markers. The degree of MMR immunoreactivity and genetic instability in the form of loss of heterozygosity (LOH) and/or microsatellite instability (MSI) were determined by comparing matched normal and tumor tissue.

CDC4 gene expression as potential biomarker for targeted therapy in prostate cancer.

Targeted therapy of proteasome regulated gene expression has potential utility in cancer treatment since components of ubiquitin-mediated proteolysis are altered in human malignancy. Specific regulators of proteasome degradation such as F-box proteins of the SCF E3 ligase complex are ideal biomarkers for assessing therapeutic efficacy since these components determine substrate specificity. An F-box protein that appears to be important in this process is human Cdc4 (Fbw7) since expression is detected in a variety of human cancers including breast, colon, pancreas and uterus.

Tissue microarray analysis of hMSH2 expression predicts outcome in men with prostate cancer.

Purpose: Mismatch repair genes are responsible for the coordinated correction of misincorporated nucleotides formed during DNA replication. Mismatch repair expression is altered in a subset of prostate cancers (PCs) and a recent study suggested that time to biochemical recurrence following prostatectomy correlated with the degree of hMSH2 immunohistochemical staining. We compared hMSH2 expression and survival in clinically organ confined PC.

Prostate specific antigen as a clinical biomarker for prostate cancer: what's the take home message?

Prostate specific antigen (PSA) continues to be challenged as a legitimate clinical biomarker in early detection of prostate cancer due to lack of specificity for malignant transformation. Skepticism surrounding the utility of serum PSA as a clinical marker is not new and many questioned its initial use in widespread prostate cancer screening due to non-specific expression and low predictive value for cancer detection. Despite these initial concerns, serum PSA measurement along with digital rectal examination (DRE) is currently the accepted practice for prostate cancer screening in the United States with hundreds of thousands of men undergoing serum PSA measurement annually.

Microsatellite instability and loss of heterozygosity have distinct prognostic value for testicular germ cell tumor recurrence.

Germ cell tumor (GCT) is the most common genitourinary malignancy of men between the ages of 18 and 35 years. Therapy is ultimately successful in over 90% of patients, however significant morbidity and mortality can be associated with adjuvant treatment and relapse. Molecular markers that predict treatment response and/or poor outcome would have immediate clinical benefit since adjuvant treatment could be selectively reserved for patients at higher risk for relapse and those patients most likely to respond to treatment.

Mismatch repair gene expression and genetic instability in testicular germ cell tumor.

Human mismatch repair (MMR) genes encode highly conserved interacting proteins that correct replication errors predisposing to hereditary gastrointestinal and genitourinary malignancies. A subset of sporadic genitourinary tumors also exhibits MMR deficiency and can be identified by measuring the frequency of microsatellite instability (MSI) in cancer cell DNA. We investigated expression of the two most commonly mutated MMR genes, MSH2 and MLH1, in sporadic testicular germ cell tumor (GCT) in order to: (1) determine the expression pattern of MSH2 and MLH1 proteins in normal seminiferous tubules and histologically distinct GCT subtypes, (2) correlate MMR gene expression with genetic instability in GCT and (3) develop a panel of molecular markers that can identify genetically distinct subsets of GCT for prognostic assessment.

Linking human genetics with molecular medicine: will hereditary renal cancer play a major role?

An inherited or familial predisposition to form kidney tumors represents less than 4% of all renal malignancies. However, hereditary renal cancer (HRC) syndromes offer important opportunities for gene discovery and function. Basic and clinical HRC investigation often provides unique insight into regulation of cell growth, cell proliferation, tumor invasion and metastasis.

Decreased expression of bone morphogenetic protein (BMP) receptor type II correlates with insensitivity to BMP-6 in human renal cell carcinoma cells.

Purpose: Bone morphogenetic proteins (BMPs) are members of a family of pleiotropic growth factors that play a critical role during renal development as well as maintaining kidney homeostasis. In the present study, we investigated the potential role of BMP receptors (BMPRs) in renal cell carcinoma (RCC) cells.

Experimental Design: Immunohistochemistry was used to investigate the expression of BMPRs in human RCC tissues.

Mismatch repair gene mutations in renal cell carcinoma.

We investigated the spectrum and genetic basis for mismatch repair (MMR) deficiency in renal cell carcinoma (RCC) by examining expression of four MMR genes important for hereditary and sporadic carcinogenesis. MMR deficiency was assessed using microsatellite instability (MSI) and genetic analyses of 25 cell lines derived from renal tumors. MMR gene alterations were detected using reverse transcription of RNA coupled with polymerase chain reaction (RT-PCR) and DNA sequencing.

Clinicopathologic implications of hMSH2 gene expression and microsatellite instability in prostate cancer.

Human mismatch repair (MMR) genes encode highly conserved interacting proteins that correct replication errors predisposing to hereditary gastrointestinal and genitourinary malignancies. We previously investigated expression of the prototype MMR gene hMSH2 in normal, benign prostatic hyperplasia and malignant prostate tissues (Velasco et al., Cancer 94:690-699, 2002).

Microsatellite instability and prostate cancer: clinical and pathological implications.

Purpose Of Review: The purpose of this review is to discuss early and recent reports investigating microsatellite instability and mismatch repair expression in prostate cancer.

Recent Findings: Human mismatch repair genes encode highly conserved interacting proteins that suppress genetic instability by correcting misincorporated nucleotides and insertion/deletion mispairs formed during DNA replication. Mismatch repair deficiency causes genetic instability at microsatellite sequences because of the cell's inability to correct errors caused by DNA polymerase slippage at repetitive sequences.

Differential expression of the mismatch repair gene hMSH2 in malignant prostate tissue is associated with cancer recurrence.

Background: Mismatch repair (MMR) genes are responsible for coordinated correction of misincorporated nucleotides formed during DNA replication. Inactivating mutations in MMR genes have been described in sporadic cancers and a hereditary cancer predisposition syndrome. Mismatch repair deficiency causes instability at microsatellites and increased mutation rates.