•Meat quality parameters of the wild and farm-raised fallow deer were analyzed.•Our findings may suggest that meat from wild fallow deer has more desirable properties.•Further research is needed to ...validate this hypothesis.
The objective of the present study was to determine the chemical composition as well as the physicochemical and sensory properties of meat (Longissimus lumborum muscle) from wild fallow deer (Dama dama L.) bucks shot during a hunt in forests of north-eastern Poland (n=11) and farm-raised fallow deer bucks (n=14) slaughtered on a farm in north-eastern Poland. It was found that the number of samples with pHu higher than 6.0 accounted for 57% of all samples collected in the group of farmed-raised fallow deer. Meat samples with pH>6.0 were not taken into consideration while evaluating meat quality. Meat from wild fallow deer, compared with farmed animals, was characterized by a higher (P≤0.01) content of fat, a higher (P≤0.01) calorific value, a more desirable fatty acid profile, including higher (P≤0.05) concentrations of unsaturated fatty acids, lower (P≤0.01) average pHu values, lower (P≤0.05) lightness (L*) and higher (P≤0.01) color saturation resulting from a higher contribution of redness (P≤0.01) and yellowness (P>0.05). Meat from wild fallow deer received also higher scores for aroma desirability (P≤0.01), taste desirability (P≤0.05), juiciness (P≤0.05) and lower (P≤0.01) scores for tenderness.
Abstract
Introduction/Objective
Blinatumomab is a monoclonal antibody directed against CD19/CD3 utilized for the treatment of relapsed or refractory B-cell precursor acute lymphoblastic leukemia ...(ALL) and for the treatment of B-cell precursor ALL in first or second complete remission with minimal residual disease (MRD) ≥0.1%. Although Blinatumomab treatment has shown better overall survival, progression-free survival, and complete remission when compared to chemotherapy, most patients have a relapse and ultimately succumb to the disease. Interestingly, there are a number of cases reporting relapse in extramedullary places. The mechanisms for relapse in these unusual extramedullary sites are not well-understood. We herein report a case of a 20-year-old African American male with primary refractory Philadelphia-negative (Ph-) precursor B cell ALL with MLL rearrangement, who received treatment with Blinatumomab after achieving morphological remission with a pediatric-inspired regimen but found to be MRD +.
Methods/Case Report
A 20 year old African American male was found to have B cell precursor ALL. It was found to be Ph-. While initally receiving vincristine, prednisone, and aspariginase, the ALL proved to be refractory to treatment. Blinatumomab was used as second line therapy after the first failed remission. The patient remained with morphological response; however, remained MRD+ after three cycles of Blinatumomab. During the fourth cycle, the patient presented with back pain and lower extremity weakness. A spine MRI revealed an extradural mass in the thoracic spine causing cord compression. A thoracic laminectomy with partial removal of the mass, followed by radiation, was performed with improvement of symptoms. Pathology results of the extradural mass revealed a myeloid sarcoma with MLL rearrangement.
Results (if a Case Study enter NA)
NA
Conclusion
This case report demonstrates how patients treated with blinatumomab can have relapse in unusual extramedullary places. The possibility of leukemia manifesting in extramedullary sites should always be kept in mind by clinicians treating patients with Blinatumomab. The mechanisms of resistance against Blinatumomab are not well- understood and need further elucidation.
Abstract
Introduction/Objective
Hodgkins lymphoma is a B cell lymphoproliferative disease, with most cases showing PAX5 positivity. Very few PAX5 negative hodgkins lymphoma cases have been described. ...We describe four PAX5 negative nodular sclerosing hodgkins lymphoma cases. All received standard chemotherapy, three received additional chemotherapeutic agents. Exploring these rare cases can be invaluable in characterizing and later treating his atypical presentation.
Methods/Case Report
Four cases of Hodgkins Lymphoma were diagnosed between 2017 and 2020. Two males and two females between 31 and 80 year old. Case 1 was a 31 year old male with a left neck lymphadenopathy that revealed nodular sclerosing Hodgkins lymphoma without bone marrow involvement. IHC staining revealed CD15, CD30, fascin and MUM-1 positivity, and PAX5 negativity. He received Doxorubicin, Vinblastine, Dacarbazine (AVD) and Brentuximab with radiation, and later brentuximab with bendamutine. Follow up PET-CT and left axillary node excisional biopsy found nodular sclerosing classic hodgkins. He received Ifosfamide, Carboplatin, and Etoposide.
Case 2 was a 37 year old male with bilateral mediastinal lymphadenopathy that demonstrated nodular sclerosing Hodgkins lymphoma on biopsy. The cells were CD15, CD30 positive, and PAX5 negative. He received AVD with bleomycin (ABVD), and field radiation with excellent response and is currently under surveillance. Case 3 was a 31 year old female with a left chest mass that demonstrated nodular sclerosing Hodgkins lymphoma. The cells were positive for MUM1, CD30 and fascin and negatively for CD15 and PAX5. She received ABVD. Case 4 was an 80 year old female with prior stage IV gastric diffuse large B cell lymphoma treated with Rituximab, Cyclophophamide, Vincristine, and Prednisone and achieved remission. She later developed neck masses that were biopsied revealing classic Hodgkins lymphoma. The cells stained for CD30, for CD15, and were negative for PAX5. She was started on AVD and is on palliative care.
Results (if a Case Study enter NA)
NA
Conclusion
Most hodgkins lymphomas are PAX5 positive. We found four cases of PAX5 negative Hodgkins lymphoma. Incidentally, all were of the nodular sclerosing subtype. All cases were treated with recommended chemotherapy and/or radiation. All four cases had good response with reduction in disease burden. This finding suggests that PAX5 negativity still allows the nodular sclerosing hodgkins lymphoma to be responsive to standard treatment modalties.
Abstract
Introduction/Objective
Adrenal Cortical Carcinoma (ACC) is a rare malignant neoplasms originating from adrenal cortical tissue with an annual incidence rate of 1 to 2 cases per million ...individuals. These tumors have poor prognosis with 5-year disease free survival being 30% after complete resection in Stage I to Stage III patients. Hence, there is a need for identifying prognostic markers for effective management of disease in these patients.
Methods
We analyzed the data in The Cancer Genome Atlas of 1141 ACC individuals, using cbioportal.org, a web- based platform for analysis of large-scale cancer genomics data sets, and derived correlation between prognosis and genetic alterations in approximately 51,309 genes.
Results
We identified 15 signature genes (NOTCH1, TP53, ZNRF3, LRP1, KIF5A, MDM2, LETMD1, MTOR, NOTCH3, RERE, SMARCC2, LDLR, HRNR, AVPR1A and PCDH15), alterations in which indicated a poor prognosis for ACC individuals. Analysis of 15 signature genes demonstrated that disease specific median survival for the patients with ACC, was reduced to 39.5 months (p value < 8 x 10 -9 and sensitivity of 93%) when any one or more of these genes was altered. Whereas, disease specific median survival was greater than 180 months (90% survival being 180 months) with no alteration in our signature genes. In addition, our analysis of our signature genes demonstrates reduced overall survival, disease free survival and progression free survival in individuals having alterations in our signature genes. Moreover, our set of 15 genes belonged mainly to MDM2-TP53, NOTCH and mTOR pathways, and small molecule modulators of these pathways are in process of development.
Conclusion
Our 15 gene signature was not only able to predict poor prognosis in ACC, but also has the potential to serve as a molecular marker set for initiation of NOTCH and mTOR specific targeted therapies in these patients.
Abstract
Introduction/Objective
The anaplastic lymphoma kinase (ALK) gene is a receptor tyrosine kinase gene located in the 2p23.2 region. Normally, dimerization of ALK receptor by binding to its ...ligand activates the ALK receptor by autophosphorylation of c-termius and activates downstream PI3K, MAPK and JAK3 pathways. The ALK gene is abnormally hyperactivated by fusion of the 3’ half containing the kinase domain with 5’ portion of other genes, resulting in the ligand independent dimerization and activation of the ALK receptor. The tumors harboring these translocations are termed as ALK-positive tumors and can be treated with ALK inhibitors.
Methods
We analyzed the status of clinically relevant ALK fusion driver mutations in 230 different cancer studies, containing tumors from 79222 different individuals, in The Cancer Genome Atlas database (TCGA) using the cbioportal web browser.
Results
We observed that, as expected ALK-positive mutations are predominantly present in NSCLC, with EML4- ALK being the most common. In addition, we were able to identify ALK positive mutations in colorectal carcinomas, papillary thyroid carcinomas, papillary renal cell carcinomas, sarcomas and invasive ductal carcinomas of the breast. Most important, our analysis identified extremely rare ALK positive cases in salivary duct carcinomas, urothelial carcinomas, cutaneous melanomas and prostatic adenocarcinomas.
Conclusion
Our analysis identified ALK positive cases were predominant in adenocarcinoma of lung with EML4-ALK being the most common ALK positive mutation, which is also consistent with the literature. However, the ALK positive mutations were at a lower prevalence rate than that described in the literature. We attribute the lower prevalence rate to underrepresentation of the Asian population in the TCGA database. In addition, we identified extremely rare ALK positive cases in salivary duct carcinomas, melanomas and prostate cancers, thus highlighting the need for testing for these mutations in these cancers.
ABSTRACT
During hypoxia, a cellular adaptive response activates hypoxia‐inducible factors (HIFs; HIF‐1 and HIF‐2) that respond to low tissue‐oxygen levels and induce the expression of a number of ...genes that promote angiogenesis, energy metabolism, and cell survival. HIF‐1 and HIF‐2 regulate endothelial cell (EC) adaptation by activating genesignaling cascades that promote endothelial migration, growth, and differentiation. An HIF‐1 to HIF‐2 transition or switch governs this process from acute to prolonged hypoxia. In the present study, we evaluated the mechanisms governing the HIF switch in 10 different primary human ECs from different vascular beds during the early stages of hypoxia. The studies demonstrate that the switch from HIF‐1 to HIF‐2 constitutes a universal mechanism of cellular adaptation to hypoxic stress and that HIF1A and HIF2A mRNA stability differences contribute to HIF switch. Furthermore, using 4 genome‐wide mRNA expression arrays of HUVECs during normoxia and after 2, 8, and 16 h of hypoxia, we show using bioinformatics analyses that, although a number of genes appeared to be regulated exclusively by HIF‐1 or HIF‐2, the largest number of genes appeared to be regulated by both.—Bartoszewski, R., Moszynska, A., Serocki, M., Cabaj, A., Polten, A., Ochocka, R., Dell'Italia, L., Bartoszewska, S., Króliczewski, J., Dabrowski, M., Collawn, J. F. Primary endothelial cell–specific regulation of hypoxia‐inducible factor (HIF)‐1 and HIF‐2 and their target gene expression profiles during hypoxia. FASEB J. 33, 7929–7941 (2019). www.fasebj.org
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