Introduction: Placental metastasis from maternal malignancies is a rare occurrence with a significantly adverse prognosis on the mother with no known effect or established risk factors for the newborn. As such, characterization of these lesions is necessary to serve as a stepping stone for more exhaustive studies regarding this presentation. Case Summary : This is a case of a metastatic breast carcinoma in a mature singleton placenta in a 39 year old woman diagnosed with invasive breast carcinoma of no special type/invasive ductal carcinoma, not otherwise specified, during the second trimester of pregnancy. Also discussed are the immunohistochemistry studies done to confirm the origin of the tumor. A comparison of the ER, PR, and HER2/neu receptor status between the primary lesion and the placental metastasis was also done. Conclusion Pregnancy-associated breast cancer is a lesion that carries adverse prognosis for the mother because of the delay in diagnosis attributable to confusion of symptomatology. The pertinent problem in pregnancy-associated breast cancer with placental metastasis is the deficiency of the placenta to induce tumor metastasis away from itself.
Immunohistochemistry

INTRODUCTION Primary peritoneal serous carcinoma is a rare, malignant, epithelial tumor arising from the peritoneum and associated tissues, that presents commonly with diffuse peritoneal involvement and ascites. Carsinomas that morphologically resemble papillary serous carcinoma of the ovary, with uninvolved and minimally involved ovaries, with lesion of the peritoneum larger than other primary ovarian lesions, and with no other identifiable primary tumor, are categorized under such. The aim of this report is to contribute to the fund of knowledge pertinent to this rare lesion with a relatively poor prognosis.

Carcinosarcoma ex pleomorphic adenoma of the salivary gland is an extremely rare tumor of the
major and minor salivary glands that is composed of a mixture of both carcinomatous and sarcomatous
elements with an identifiable benign epithelial and mesenchymal tumor counterpart.

This report describes a rare case of carcinosarcoma ex pleomorphic adenoma involving the left parotid
gland in a 61-year-old female with no history of a long-standing pleomorphic adenoma, nor a recurrent
pleomorphic adenoma, and describes its morphology and important immunohistochemistry findings.
Carcinosarcoma ex pleomorphic adenoma contains features of the two tumors under malignant mixed
tumors, which are carcinosarcoma and carcinoma ex pleomorphic adenoma. Immunohistochemistry
studies were done to document the epithelial and mesenchymal areas from both the malignant and
benign sections of the tumor and to classify the carcinoma and sarcoma component, consisting of
adenocarcinoma, not otherwise specified for the carcinoma component, and myxoid chondrosarcoma
and mesenchymal chondrosarcoma for the sarcoma component.

The paucity of documented cases of carcinosarcoma ex pleomorphic adenoma in prior scientific
publications requires reporting cases such as this. Furthermore, the report provides an insight into
the more complex molecular and structural changes that manifest as cancer behavior in the tumors
of the salivary gland. The case contributes to the fund of knowledge for diagnosis and improvement
of quality of care.

Human ; Adenoma ; Carcinoma ; Carcinosarcoma

Introduction: Chronic traumatic encephalopathy (CTE) is a progressive neurodegenerative disorder that is defined, neuropathologically, by the presence of aggregated hyperphosphorylated tau in the neurons and astrocytes of the perivascular area that is located deep in the cerebral sulci. The lesion is associated with repetitive brain trauma, from the spectrum of asymptomatic subconcussive head injury to grossly identifiable features of concussion. Although the diagnostic neuropathology of CTE is well-characterized, the precise mechanism that causes this to occur in CTE is not yet clearly elucidated. The features of hyperphosphorylated tau in CTE is quite similar with Alzheimer’s Disease (AD), as is the reduced expression of certain genes that are required to dephosphorylate tau, which is the putative culprit in the generation of amyloid aggregates and hyperphosphorylated tau.1 In comparison, Parkinson’s Disease (PD) is a neurodegenerative disease that is caused by accumulation of misfolded alpha-synuclein (α-syn) that causes the formation of intraneuronal Lewy Body aggregates. The pattern of accumulation for α-syn involves the olfactory bulb and the gut with progressive involvement of the posterior part of the brain.2 Despite establishing the presence of two different intraneuronal inclusions for CTE and PD, contact sports associated with the clinical spectrum of CTE has been shown to present with Parkinsonian features along with dementia. Mood disorders has been reported to occur in patients with these neurologic conditions. Several studies have documented that patients had a previous experience of traumatic brain injury prior to the diagnosis of Bipolar Disorder (BD). A review of electronic literature suggested that having an earlier diagnosis of BD increased the likelihood of having a diagnosis of PD in the future. Objectives: This research aimed to compare the over- and underexpressed genes in cases with Parkinson's Disease (PD), cases with Bipolar Disorder (BD), and cases with Chronic Traumatic Encephalopathy (CTE) versus normal controls. This was done to determine if parallel overexpression in certain genes may indicate the possible association at the level of gene expression. Identifying similar RNA sequence establishing gene expression may provide an insight to the relationship of the diseases in terms of pathobiological behavior. Determining the similar over- or underexpression pattern may provide an insight on the common pathobiologic mechanisms that may be the reason for the three disorders being associated by way of pre-morbid or co-morbid condition. Methodology: Transcripts from the public domain archive of the NCBI SRA were identified for the RNA sequence (RNAseq) of interest using the search string “Chronic Traumatic Encephalopathy”, “Bipolar Disorder”, and “Parkinson”. Only public domain transcriptome files of post-mortem brain samples labeled as RNAseq data extracted thru the Illumina platform that have a paired normal control were selected. A total of ten (10) cases for each disorder and thirty (30) normal subjects for control in the NCBI SRA RNAseq database with a whole exome sequence file that was available for public domain use was utilized for differential gene expression analysis. Results and Discussion: Among 21,122 identified genes from the RNAseq, the analysis was able to identify 26 genes exhibiting increased expression of up to >15 log2 fold change among cases with CTE, PD, and BD compared with normal controls. In contradistinction, only 6 well-described genes exhibited a decreased expression among cases with CTE and BD compared to normal controls. However, there were no identified genes that exhibited underexpression in cases with PD compared with normal controls. The identification of parallel gene overexpression among the CTE, BD, and PD groups with respect to structural integrity, cellular metabolism, homeo-stasis, and apoptosis may indicate a common pathway that have been initiated as part of the response to maintain tissue function or as a consequence of the underlying pathobiologic mechanism that caused the primary lesion. In comparison, the underexpressed genes detected in the CTE and BD cases compared to the normal controls and the PD cases may indicate the lack of genes that have a role in repressing the mRNA for protein coding. Conclusion The overexpression of genes responsible for homeostasis, regulation of inflammation, balance of apoptosis and anti-apoptosis, and maintenance of structural integrity among the CTE, BD, and PD groups indicate that there is an interrelated mechanism that serves converging pathways as part of the response to lesional- forming structures in the brain. The goal of studies such as this is to have a better understanding on the common pathways that explain the interrelatedness of brain disorders and the putative mechanism for being co-morbid and pre-morbid conditions of each other.
Chronic Traumatic Encephalopathy