A Case of Synchronous Primary Tumors of the Left Ovary and Uterus.

BACKGROUND Synchronous tumors occur when 2 separate primary tumors are diagnosed within 6 months. They can originate from the same site or different locations. For example, synchronous primary tumors of uterine and ovarian origin are a common type. Diagnosis can be challenging, however is critical to determine whether a patient has multiple primary tumors or a single tumor with metastasis to guide effective treatment. Compared with endometrial cancer that has spread to the ovary, synchronous primary tumors of the uterus and ovaries typically require less aggressive treatment. CASE REPORT A 45-year-old woman with nonspecific symptoms of headache and confusion had imaging studies that revealed a neoplasm in her brain, which was likely causing her symptoms. The masses were metastatic lesions, and the primary cancer was determined to be synchronous endometrial ovarian cancer (SEOC). She underwent bilateral frontal craniotomy for tumor resection and diagnostic tests. She had an exploratory laparotomy, total abdominal hysterectomy, bilateral salpingo-oophorectomy, and omentectomy. She was stable during hospitalization but lost to follow-up after discharge. CONCLUSIONS Regular gynecologic examinations, including bimanual palpation of the ovaries during cervical cancer screenings, are essential for detecting cancer early and improving chances of recovery. This case also highlights the indolent growth and high risk of metastasis associated with SEOC. Although this type of cancer is rare, patients with it can be at increased risk of developing metastatic lesions in other parts of their bodies. To manage synchronous tumors effectively, a multidisciplinary approach and close collaboration between medical professionals are necessary to ensure best patient outcomes.

Diagnosis of the Primary Tumor Site in the Case of Liver Metastatic Carcinoma.

Immunohistochemical markers have been frequently utilized as a diagnostic tool in pathology to help in diagnosing malignancy of unknown primary sites. In previous cases, the immunohistological expression of cytokeratin 7 (CK7), Napsin A, and thyroid transcription factor-1 (TTF-1) has helped identify and diagnose primary malignancy as originating from the lung. This case report describes an elderly woman with a liver metastasis consistent with a lung primary and illustrates the utility and importance of tissue-specific markers as a diagnostic tool in the evaluation of unknown primary tumors.

Promoter hypermethylation of ARID1A gene is responsible for its low mRNA expression in many invasive breast cancers.

ARID1A (AT-rich interactive domain 1A) has recently been identified as a tumor suppressor gene. Its mRNA expression is significantly low in many breast cancers; this is often associated with more aggressive phenotypes. However, the underlying molecular mechanism for its low expression has not been fully understood. This study was undertaken to evaluate the contribution of gene copy number variation, mutations, promoter methylation and histone modification to ARID1A's low expression. 38 pairs of breast invasive ductal carcinomas and their normal breast tissue counterparts from the same patients were randomly selected for gene expression and copy number variation detection. Promoter methylation and histone modification levels were evaluated by MeDIP-qPCR and ChIP-qPCR, respectively. PCR product Sanger sequencing was carried out to detect the exon mutation rate. Twenty-two out of 38 invasive ductal carcinomas in the study (57.9%) revealed ARID1A mRNA low expression by realtime RT-PCR. The relative promoter methylation level was, significantly higher in ARID1A mRNA low expression group compared with its high expression group (p<0.001). In the low expression group, nineteen out of 22 invasive ductal carcinomas (86.4%) exhibited ARID1A promoter hypermthylation. In addition, the promoter hypermethylation was accompanied with repressive histone modification (H3K27Me3). Although five out of 38 invasive ductal carcinomas (13.2%) exhibited loss of ARID1A gene copy number by realtime PCR and nine exon novel mutations are seen from eight out of 33 invasive ductal carcinomas (24.2%), there was no statistically significant difference in both ARID1A mRNA low and high expression groups (p=0.25,and p=0.68, respectively). We demonstrate that promoter hypermethylation was the main culprit for ARID1A mRNA low expression in invasive ductal carcinomas. The influence of mutation and copy number variation on the expression were statistically insignificant at mRNA level, and were, therefore, not considered the main causes for ARID1A mRNA low expression in invasive breast cancer.