Over-expression of tissue specific transplantation antigen P35B in human endometrial cancer.

Gynecologic cancers including cancers of the endometrium are a clinical problem (1-4). We mined published microarray data (5, 6) to discover genes associated with endometrial cancers by comparing transcriptomes of the normal endometrium and endometrial tumors from humans. We identified tissue specific transplantation antigen P35B, encoded by TSTA3, as among the most differentially expressed genes, transcriptome-wide, in cancers of the endometrium. TSTA3 was expressed at significantly higher levels in endometrial tumor tissues as compared to the endometrium. Importantly, in human endometrial cancer, primary tumor expression of TSTA3 was correlated with recurrence-free survival in white patients with low mutational burden. TSTA3 may be a molecule of interest in understanding the etiology or progression of human endometrial cancer.

TSTA3 is a differentially expressed gene in human metastatic breast cancer, in the brain and in the lymph nodes.

Metastasis to the brain is a clinical problem in patients with breast cancer (1-3). We mined published microarray data (4, 5) to compare primary and metastatic tumor transcriptomes for the discovery of genes associated with brain metastasis in humans with metastatic breast cancer. We found that GDP-L-fucose synthetase, encoded by TSTA3 (tissue specific transplantation antigen P35B), was among the genes whose expression was most different in the brain and lymph node metastases of patients with metastatic breast cancer. TSTA3 mRNA was present at increased quantities in brain metastatic tissues as compared to primary tumors of the breast. Importantly, expression of TSTA3 in primary tumors was significantly correlated with patient overall survival in patients with breast cancer. Modulation of TSTA3 expression may be relevant to the biology by which tumor cells metastasize from the breast to the brain while evading immune clearance in the lymph nodes in humans with metastatic breast cancer. These data are one piece of evidence suggesting a common ancestor or tumor clone for brain and lymph node metastases that originate from the primary tumor, alluding to patterns in developmental origin and migratory pathways through the lymph node in human brain metastatic breast cancer.

Effects of Radiotherapy on Ehrlich’s Ascetic Carcinoma in Swiss Albino Mice: An Experimental Study

Background: Experimental tumors have great importance in modeling, and Ehrlich ascites carcinoma (EAC) is one of the most common tumors. EAC is referred to as an undifferentiated carcinoma and is originally hyperdiploid, has high transplantable capability, no-regression, rapid proliferation, shorter life span, 100% malignancy, and also does not have tumor-specific transplantation antigen. The current concepts that radiotherapy alone or with cancer chemotherapy is administered at a dose to the maximum a patient can tolerate before the onset of severe and even life-threatening toxicity is still in wide clinical use. This study was conducted to evaluate the response of radiotherapy in the treatment of EAC. Materials and Methods: A mouse bearing the tumor strain was taken from our laboratory in the Department of Pathology, IPGMER, Kolkata, where the strain was being maintained serially by inoculation of malignant cells into healthy mice every 8–10 days. In our work, altogether 25 mice were taken for each set of experimental work. They were divided in four groups of 5–10 mice in each group. The various parameters to assess the response of various therapeutic schedules were regression of tumor by decrease in body weight of mice and decrease in abdominal girth; cell count of ascetic fluid and morphological changes of tumor cells after treatment with drugs and to study the percentage viability of the cells. Results: All the mice in Group I gained weight steadily. Mice of Group II were unaffected by single dose whole body radiation and they behaved as mice of Group I. All mice of Group III died within 20–25 days. Conclusion: Cell changes were observed but not as marked. Cell viability was as high as 65% after treatment as compared to tumor control which showed a viability of about 75%.

P53 and The Immune Response: 40 Years of Exploration—A Plan for the Future

The p53 field was born from a marriage of the techniques of cancer virus research and immunology. Over the past 40 years, it has followed the path of cancer research. Now cancer treatments are turning to immunotherapy, and there are many hints of the role of the p53 protein in both the regulation of the innate immune system and as an antigen in adaptive immune responses. The p53 gene and protein are part of the innate immune system, and play an important role in infectious diseases, senescence, aging, and the surveillance of repetitive DNA and RNAs. The mutant form of the p53 protein in cancers elicits both a B-cell antibody response (a tumor antigen) and a CD-8 killer T-cell response (a tumor-specific transplantation antigen). The future will take the p53-immune response field of research into cancer immunotherapy, autoimmunity, inflammatory responses, neuro-degeneration, aging, and life span, and the regulation of epigenetic stability and tissue regeneration. The next 40 years will bring the p53 gene and its proteins out of a cancer focus and into an organismic and environmental focus.

Matching for the nonconventional MHC-I MICA gene significantly reduces the incidence of acute and chronic GVHD

Key Points Matching for MICA significantly reduces the incidence of acute and chronic GVHD in otherwise HLA 10/10-matched unrelated-donor HCT. Our results formally define MICA as a novel major histocompatibility complex-encoded human transplantation antigen.