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Abstract Background Hepatocellular carcinoma (HCC) is the most common type of liver cancer that occurs predominantly in patients with previous liver conditions. In the absence of an ideal screening modality, HCC is usually diagnosed at an advanced stage. Recent studies show that loss or gain of genomic materials can activate the oncogenes or inactivate the tumor suppressor genes to predispose cells toward carcinogenesis. Here, we evaluated both the copy number alteration (CNA) and RNA sequencing data of 361 HCC samples in order to locate the frequently altered chromosomal regions and identify the affected genes. Results Our data show that the chr1q and chr8p are two hotspot regions for genomic amplifications and deletions respectively. Among the amplified genes, YY1AP1 (chr1q22) possessed the largest correlation between CNA and gene expression. Moreover, it showed a positive correlation between CNA and tumor grade. Regarding deleted genes, CHMP 7 (chr8p21.3) possessed the largest correlation between CNA and gene expression. Protein products of both genes interact with other cellular proteins to carry out various functional roles. These include ASH1L, ZNF496, YY1, ZMYM4, CHMP4A, CHMP5, CHMP2A and CHMP3, some of which are well-known cancer-related genes. Conclusions Our in-silico analysis demonstrates the importance of copy number alterations in the pathology of HCC. These findings open a door for future studies that evaluate our results by performing additional experiments.

Multiple myeloma (MM) is an incurable plasma cell malignancy with a heterogeneous genetic background. Each MM subtype may have its own therapeutic vulnerabilities, and tailored therapy could improve outcomes. However, the cumulative frequency of druggable targets across patients is very low, which has precluded the widespread adoption of precision therapy for patients with MM. Amplification of the long arm of chromosome 1 (Amp1q) is one of the most frequent genetic alterations observed in patients with MM, and its presence predicts inferior outcomes in the era of proteasome inhibitors and immunomodulatory agents. Therefore, establishing precision medicine for MM patients with Amp1q stands to benefit a large portion of patients who are otherwise at higher risk of relapse. In this article, we review the prevalence and clinical significance of Amp1q in patients with MM, its pathogenesis and therapeutic vulnerabilities, and discuss the opportunities and challenges for Amp1q-targeted therapy. [ABSTRACT FROM AUTHOR]

Multiple myeloma (MM) is an incurable plasma cell malignancy with a heterogeneous genetic background. Each MM subtype may have its own therapeutic vulnerabilities, and tailored therapy could improve outcomes. However, the cumulative frequency of druggable targets across patients is very low, which has precluded the widespread adoption of precision therapy for patients with MM. Amplification of the long arm of chromosome 1 (Amp1q) is one of the most frequent genetic alterations observed in patients with MM, and its presence predicts inferior outcomes in the era of proteasome inhibitors and immunomodulatory agents. Therefore, establishing precision medicine for MM patients with Amp1q stands to benefit a large portion of patients who are otherwise at higher risk of relapse. In this article, we review the prevalence and clinical significance of Amp1q in patients with MM, its pathogenesis and therapeutic vulnerabilities, and discuss the opportunities and challenges for Amp1q-targeted therapy.

Background: Hepatocellular carcinoma (HCC) is the most common type of liver cancer that occurs predominantly in patients with previous liver conditions. In the absence of an ideal screening modality, HCC is usually diagnosed at an advanced stage. Recent studies show that loss or gain of genomic materials can activate the oncogenes or inactivate the tumor suppressor genes to predispose cells toward carcinogenesis. Here, we evaluated both the copy number alteration (CNA) and RNA sequencing data of 361 HCC samples in order to locate the frequently altered chromosomal regions and identify the affected genes. Results: Our data show that the chr1q and chr8p are two hotspot regions for genomic amplifications and deletions respectively. Among the amplified genes, YY1AP1 (chr1q22) possessed the largest correlation between CNA and gene expression. Moreover, it showed a positive correlation between CNA and tumor grade. Regarding deleted genes, CHMP7 (chr8p21.3) possessed the largest correlation between CNA and gene expression. Protein products of both genes interact with other cellular proteins to carry out various functional roles. These include ASH1L, ZNF496, YY1, ZMYM4, CHMP4A, CHMP5, CHMP2A and CHMP3, some of which are well-known cancer-related genes. Conclusions: Our in-silico analysis demonstrates the importance of copy number alterations in the pathology of HCC. These findings open a door for future studies that evaluate our results by performing additional experiments. [ABSTRACT FROM AUTHOR]