Biomarkers have become a potential tool in the diagnosis of cancer patients, allowing a more accurate diagnosis and treatment. Prostate cancer is the second most common type of cancer in men worldwide. In prostate cancer, it is important to identify which patients would benefit from early treatment. Here we report the combination of phosphorylation of the retinoblastoma protein (Rb) on serine 249 (Rb S249) wit with p39 expression as biomarkers for predicting prostate cancer. We performed an immunohistochemical analysis of Rb S249 and p39 expression. Our results indicate that there is an inverse relationship between Rb S249 and prostate adenocarcinoma. Hence, Rb S249 could help in determining a more accurate prognosis for prostate cancer patients.Support or Funding InformationFunded by NIH‐NIGMS #2R25GM096955This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Mitosis is required to grow and develop from a single cell to a multicellular organism. However, this process can often lead to cancer when its regulation is lost. The Highly Express in Cancer 1 (Hec1) protein is one of the four subunits of the Nuclear Division Cycle (Ndc80) complex present in mitosis. The function of this complex is required for robust kinetochore‐microtubule (kMT) attachment and is regulated by Aurora B Kinase phosphorylation of Hec1. Given that Hec1 protein binds directly to spindle microtubules, it certainly plays a critical role in chromosome alignment and segregation. To assess how Hec1 leads to defects in cell division cycle in human cells and induce cancer, we expressed a non‐phosphorylatable version of Hec1 (Hec1‐9A) in MDA‐MB‐436 (breast cancer) cells. We observed how mitosis was modified by the Hec1‐9A mutant by employing immunofluorescence microscopy to mark the chromosomes and the mitotic spindle in our Hec1‐9A positive and control cells. The Hec1‐9A satisfied the genome surveillance mechanism, thus, allowing cells that presented erroneous chromosome alignment and segregation to exit mitosis. Further studies will be aimed to investigate whether spindle checkpoint is defective at erroneous kMT attachments and whether Hec1 plays a role in other steps of mitosis.Support or Funding InformationFunded by NIH‐NIGMS #2R25GM096955Funded by NIH #R00CA178188This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Lung cancer is the leading cause of cancer death in both men and women in the United States. Lung cancer is divided into non‐small cell lung cancer (NSCLC) and small cell lung cancer (SCLC). NSCLC accounts for 80% of all primary lung cancers and subdivided into adenocarcinoma (ADC), squamous cell carcinoma (SCC), and large cell carcinoma (LCC). Due to late diagnosis, only 16% of diagnosed patients live beyond 5 years, but this survival rate increases if the cancer has not yet metastasized. Recent developments in lung cancer therapies depend on precise histological subtyping of NSCLC. Accurate discrimination of SCC from the remaining NSCLCs is crucial for understanding the outcome and metastatic dissemination of lung cancer. The epithelial‐to‐mesenchymal transition (EMT) has been associated with an early proclivity for metastasis in lung cancer. We want to identify if N‐cadherin and E‐cadherin expression in tumor samples can be of clinical value for discriminating between SCC and ADC and in predicting the development of lung cancer metastasis. We performed immunohistochemistry analysis in two tissue microarrays that contained 24 lung cancer patients. An EMT phenotype was defined as a low expression of E‐cadherin and high expression of N‐cadherin. An EMT phenotype was observed in 58% cases of SCC and carried prognostic utility for lymph node metastasis. The EMT phenotype observed in SCC can be suggested as potential markers of malignant transformation.Support or Funding InformationR25GM096955, 2R25GM082406, 2U54CA163071‐06This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
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