With the improvement of high-throughput genomic technology such as microarray and next-generation sequencing over the last ten to twenty year, we have come to know that the portion of the genome responsible for protein coding constitutes just approximately 1.5%. The remaining 98.5% of the genome not responsible for protein coding have been regarded as 'junk DNA'. More recently, however, 'Encyclopedia of DNA elements project' revealed that most of the junk DNA were transcribed to RNA regardless of being translated into proteins. In addition, many reports support that a lot of these non-coding RNAs play a role in gene regulation. In fact, there are various functioning short non-coding RNAs including rRNA, tRNA, small interfering RNA, and micro RNA. Mechanisms of these RNAs are relatively well-known. Until recently, however, little is known about long non-coding RNAs which consist of 200 nucleotides or more. In this article, we will review the representative long non-coding RNAs which have been reported to be related to gastrointestinal cancers and to play a certain role in its pathogenesis.
Gastrointestinal Neoplasms/*genetics/*metabolism/pathology ; Humans ; Liver Neoplasms/genetics/metabolism/pathology ; RNA, Long Noncoding/genetics/*metabolism

With the improvement of high-throughput genomic technology such as microarray and next-generation sequencing over the last ten to twenty year, we have come to know that the portion of the genome responsible for protein coding constitutes just approximately 1.5%. The remaining 98.5% of the genome not responsible for protein coding have been regarded as 'junk DNA'. More recently, however, 'Encyclopedia of DNA elements project' revealed that most of the junk DNA were transcribed to RNA regardless of being translated into proteins. In addition, many reports support that a lot of these non-coding RNAs play a role in gene regulation. In fact, there are various functioning short non-coding RNAs including rRNA, tRNA, small interfering RNA, and micro RNA. Mechanisms of these RNAs are relatively well-known. Until recently, however, little is known about long non-coding RNAs which consist of 200 nucleotides or more. In this article, we will review the representative long non-coding RNAs which have been reported to be related to gastrointestinal cancers and to play a certain role in its pathogenesis.
Gastrointestinal Neoplasms/*genetics/*metabolism/pathology ; Humans ; Liver Neoplasms/genetics/metabolism/pathology ; RNA, Long Noncoding/genetics/*metabolism

Cancer remains an outstanding cause of global morbidity and mortality, despite intensive research and unprecedented insights into the basic mechanisms of cancer development. A plethora of clinical and experimental evidence suggests that cancers from individual patients are likely to be molecularly heterogeneous in their use of distinct oncogenic pathways and biological programs. Efforts to significantly impact cancer patient outcomes will almost certainly require the development of robust strategies to subdivide such heterogeneous panels of cancers into biologically and clinically homogenous subgroups, for the purposes of personalizing treatment protocols and identifying optimal drug targets. In this review, I describe recent progress in the development of both targeted and genome-wide approaches for the molecular stratification of cancers, drawing examples from both the haematopoietic and solid tumor malignancies.
Animals ; Genomics ; Humans ; Neoplasms/*genetics/*metabolism/pathology

Cancer remains an outstanding cause of global morbidity and mortality, despite intensive research and unprecedented insights into the basic mechanisms of cancer development. A plethora of clinical and experimental evidence suggests that cancers from individual patients are likely to be molecularly heterogeneous in their use of distinct oncogenic pathways and biological programs. Efforts to significantly impact cancer patient outcomes will almost certainly require the development of robust strategies to subdivide such heterogeneous panels of cancers into biologically and clinically homogenous subgroups, for the purposes of personalizing treatment protocols and identifying optimal drug targets. In this review, I describe recent progress in the development of both targeted and genome-wide approaches for the molecular stratification of cancers, drawing examples from both the haematopoietic and solid tumor malignancies.
Animals ; Genomics ; Humans ; Neoplasms/*genetics/*metabolism/pathology

Adenocarcinoma, Follicular ; genetics ; metabolism ; pathology ; Carcinoma, Papillary ; genetics ; metabolism ; pathology ; Carcinoma, Renal Cell ; genetics ; metabolism ; pathology ; Diagnosis, Differential ; Humans ; Immunohistochemistry ; Kidney Diseases, Cystic ; genetics ; metabolism ; pathology ; Kidney Neoplasms ; genetics ; metabolism ; pathology ; Thyroid Neoplasms ; genetics ; metabolism ; pathology ; Translocation, Genetic

OBJECTIVE: To observe expression of stathmin gene in laryngeal squamous cell carcinoma (LSCC) and relation between expression of stathmin gene and occurrence and development of LSCC. METHOD: The expression of the stathmin gene was determined in 35 LSCC of specimens and 18 normal laryngeal tissues (NLT) of specimens by in situ hybridization with Digoxigenin labeled probe of stathmin mRNA. RESULT: Expression of stathmin gene was observed in 35 cases of laryngeal squamous cell carcinoma tissue (positive rate, 69%) and positive signal was observed in both cytoplasm and nuclear. Among 18 cases of normal tissue, only 6 showed weak positive signal. There was significant difference in expression of stathmin gene between laryngeal squamous cell carcinoma tissue and normal tissue. CONCLUSION Expression of stathmin gene may play a key role in the pathogenesis and development of laryngeal squamous cell carcinoma. It may be a very important biotherapy target in the treatment of laryngeal squamous cell carcinoma.
Carcinoma, Squamous Cell ; genetics ; metabolism ; pathology ; Gene Expression ; Humans ; Laryngeal Neoplasms ; genetics ; metabolism ; pathology ; RNA, Messenger ; genetics ; Stathmin ; genetics ; metabolism

Carcinoma, Hepatocellular ; metabolism ; pathology ; DNA-Binding Proteins ; genetics ; metabolism ; Humans ; Liver Neoplasms ; metabolism ; pathology ; Phosphoproteins ; genetics ; metabolism ; RNA, Messenger ; genetics

Cancer stem cells (CSCs), a subpopulation of cancer cells with ability of initiating tumorigenesis, exist in many kinds of tumors including breast cancer. Cancer stem cells contribute to treatment resistance and relapse. Conventional treatments only kill differentiated cancer cells, but spare CSCs. Combining conventional treatments with therapeutic drugs targeting to CSCs will eradicate cancer cells more efficiently. Studying the molecular mechanisms of CSCs regulation is essential for developing new therapeutic strategies. Growing evidences showed CSCs are regulated by non-coding RNA (ncRNA) including microRNAs and long non-coding RNAs (lncRNAs), and histone-modifiers, such as let-7, miR-93, miR-100, HOTAIR, Bmi-1 and EZH2. Herein we review the roles of microRNAs, lncRNAs and histone-modifiers especially Polycomb family proteins in regulating breast cancer stem cells (BCSCs).
Breast Neoplasms ; genetics ; metabolism ; pathology ; Histones ; metabolism ; Humans ; Neoplastic Stem Cells ; metabolism ; RNA, Untranslated ; genetics ; metabolism

OBJECTIVETo study the clinicopathologic features of small cell carcinoma of ovary, hypercalcemic type (SCCOHT) and to evaluate the diagnostic significance of loss of SMARCA4 expression.

METHODSThe clinicopathologic characteristics of 5 cases of SCCOHT were reviewed. The expression of SMARCA4 protein was detected by immunohistochemistry in the cases of SCCOHT and 240 cases of other primary malignant tumors of ovary and peritoneum.

RESULTSThe mean and medium age of these patients was 30 years and 28 years, respectively. The presenting symptoms included abdominal pain, distention and a pelvic mass. Hypercalcemia was found in 3 patients. The maximum diameter of tumors ranged from 13.5 to 22.0 cm. Extraovarian spread was demonstrated in all of the patients on presentation. Histologically, the tumors were composed of closely packed small round cells with scanty cytoplasm, hyperchromatic nuclei and irregular chromatin clumps. The tumor cells grew in sheets, nests, cords or trabecular pattern. Follicle-like spaces were observed in 4 cases. Three of the tumors contained large cells with abundant eosinophilic cytoplasm. Spindle cell morphology was found in 1 case. There were 2 cases with myxoid or hyaline stroma. Four out of five of SCCOHT cases showed loss of SMARCA4 protein while only 6.3% (15/240) of the other primary malignant tumors of ovary and peritoneum , including undifferentiated carcinoma (1/5), high-grade serous carcinoma (4.6%, 5/109), endometrioid carcinoma (7.7%, 2/26), clear cell carcinoma (1/9), mucinous carcinoma (1/5), mixed carcinoma (4.9%, 3/61), carcinosarcoma (1/9) and high-grade serous carcinoma of peritoneum (1/9), were negative.

CONCLUSIONSSCCOHT is a rare malignant tumor and often misdiagnosed as other types of ovarian small cell tumor. Loss expression of SMARCA4 protein is characteristic and facilitates the diagnosis and differential diagnosis of SCCOHT.

Adenocarcinoma, Mucinous ; Adult ; Carcinoma, Small Cell ; genetics ; metabolism ; pathology ; DNA Helicases ; genetics ; metabolism ; Female ; Humans ; Hypercalcemia ; pathology ; Immunohistochemistry ; Neoplasms, Glandular and Epithelial ; genetics ; metabolism ; pathology ; Nuclear Proteins ; genetics ; metabolism ; Ovarian Neoplasms ; genetics ; metabolism ; pathology ; Transcription Factors ; genetics ; metabolism

Animals ; Carrier Proteins ; genetics ; metabolism ; Cell Line, Tumor ; Insulinoma ; genetics ; metabolism ; pathology ; Mice ; Neoplasm Proteins ; genetics ; metabolism ; Pancreatic Neoplasms ; genetics ; metabolism ; pathology ; Phosphoproteins ; genetics ; metabolism