DNA alterations in the tumor genome and their associations with clinical outcome in prostate cancer

Although most prostate cancer （PCa） cases are not life-threatening, approximately 293 000 men worldwide die annually due to PCa. These lethal cases are thought to be caused by coordinated genomic alterations that accumulate over time. Recent genome-wide analyses of DNA from subjects with PCa have revealed most, if not all, genetic changes in both germline and PCa tumor genomes. In this article, I first review the major, somatically acquired genomic characteristics of various subtypes of PCa. I then recap key findings on the relationships between genomic alterations and clinical parameters, such as biochemical recurrence or clinical relapse, metastasis and cancer-specific mortality. Finally, I outline the need for, and challenges with, validation of recent findings in prospective studies for clinical utility. It is clearer now than ever before that the landscape of somatically acquired aberrations in PCa is highlighted by DNA copy number alterations （CNAs） and TMPRSS2-ERG fusion derived from complex rearrangements, numerous single nucleotide variations or mutations, tremendous heterogeneity, and continuously punctuated evolution. Genome-wide CNAs, PTEN loss, MYC gain in primary tumors, and TP53 loss/mutation and AR amplification/mutation in advanced metastatic PCa have consistently been associated with worse cancer prognosis. With this recently gained knowledge, it is now an opportune time to develop DNA-based tests that provide more accurate patient stratification for prediction of clinical outcome, which will ultimately lead to more personalized cancer care than is possible at present.

Detection of chromosomal imbalance in oligodendroglial tumors by comparative genomic hybridization

Objective To investigate the relationship between genomic DNA imbalance in oligodendroglial tumors and its different classification. Methods 16 oligodendrogliomas and 17 anaplastic oligodendrogliomas were investigated by comparative genomic hybridization on Paraffin-Embedded tissue samples,and the chromosomal genomic DNA imbalances were analyzed. Results Chromosome DNA imbalance rates in oligodendrogliomas

The 150 most important questions in cancer research and clinical oncology series: questions 86-93

Since the beginning of 2017,Chinese Journal of Cancer has published a series of important questions in cancer research and clinical oncology,which spark diverse thoughts,interesting communications,and potential collabora-tions among researchers all over the world.In this article,8 more questions are presented as follows.Question 86.In which circumstances is good supportive care associated with a survival advantage in patients with cancer?Question 87.Can we develop animal models to mimic immunotherapy response of cancer patients?Question 88.What are the mechanisms underlying hepatitis B virus-associated non-hepatocellular cancers?Question 89.Can we more pre-cisely target tumor metabolism by identifying individual patients who would benefit from the treatment?Question 90.What type of cranial irradiation-based prophylactic therapy combination can dramatically improve the survival of patients with extensive small-cell lung cancer?Question 91.How can postoperative radiotherapy prolong overall survival of the patients with resected pIIIA-N2 non-small cell lung cancer?Question 92.What are the key molecular events that drive oral leukoplakia or erythroplakia into oral cancer?Question 93.How could we track the chemothera-peutics-driven evolution of tumor genome in non-small cell lung cancer for more effective treatment?

Identification of chromosomal imbalances in pancreatic carcinoma using comparative genomic hybridization

Objective To identify genetic abnormalities in primary pancreatic carcinoma in humans.Methods Comparative genomic hybridization (CGH) was used to investigate genomic imbalances in 27 cases of pancreatic carcinomas. Multiple deletions and gains were observed in all tumor specimens.Results Losses affecting chromosomes 9p,17p,4q and 6p and gains involving 8q,7q,3q and 1q were commonly observed.Conclusions There are multiple regions of chromosomes with changes copy number in pancreatic carcinoma. The altered chromosomal regions may contain several candidate genes which are involved in the development and progress of pancreatic carcinogenesis.