Immune cell analysis has become a heightened priority in the development of novel therapeutic medicines. The complexity of cell interactions makes evaluation inherently difficult, requiring in vitro analysis of each cell type. There have been significant strides in research to support large-scale immune interaction of various cells such as CTen (Cell Type Enrichment) and GSEA (Gene Set Enrichment Analysis), however, these methods calculate enrichment scores according to the presence of a gene query over predefined gene set and don’t account for expression information as they are qualitative in nature. This tactic is beneficial for research surrounding single cell activation during treatment and isn’t necessarily representative to mixed typing from a tissue derived sample.

When working on targeted therapeutic drug development in oncology, tumor mutation heterogeneity makes it difficult to treat all patients. However, there is one biomarker that has been found to affect 30% of all tumor cases- the RAS mutation. The abundance of this genomic abnormality was discovered via the ongoing investigations into targeted RAS cancer therapies. Researchers thus have been working to find a method to block the RAS pathway in all tumors, with the desired outcome to treat all patients regardless of differing cancer subtype.

Glioblastomas — the most common and aggressive brain tumors in adults — can be difficult to treat because therapies only affect a proportion of tumor cells, which in turn leads to a poor survival rate in the patient population. It is hypothesized that a subgroup of cells within these tumors, identified as Glioblastoma Stem Cells (GSCs), reproduce making identical drug-resistant copies of themselves.

With an incident rate of 55,000 diagnosed cases per year, thyroid cancer is becoming the fastest-growing cancer type in the United States. Like other tumor classifications, genetic abnormalities and mutations play a key role in the proliferation of cancer cells; and although previously identified point mutations are observed in 90% of thyroid cancers, driver mutation intricacies have an opportunity for exploration. For example, the insulin-like growth factor 2 mRNA-binding protein 3’s (IGF2BP3) activation is still not fully understood.

Telomeres are regions of highly repetitive DNA at the end of a chromosome that assists in cellular duplication and rejuvenation. This physiological function has been historically associated with biological aging as the length of the telomere shortens after division and subsequently alters the effectiveness of DNA replication. However, a team of researchers at the Jackson Laboratory at the University of Texas MD Anderson Cancer Center (UTMD) have found that the length is also impactful in genetic alterations in 31 different types of metastatic tumors.

Huge strides are being made in the realm of Immuno-Oncology by a team of scientists at Sichuan University in West China. Nature reports that for the first time — as part of a clinical trial — an individual with aggressive lung cancer has been injected with their own cells engineered to express edited genes leveraging the CRISPR-Cas9 technique and targeting the PD-1 encoding gene. PD-1, which upon T-cell activation blocks the recognition of cancer cells as a foreign entity, impedes the immune responses innate ability to disrupt tumor cell proliferation. The CRISPR-Cas9 strategy combines a DNA-cutting enzyme along with molecular guide that can identify targets (such as PD-1) and replace the removed sequence with stretches of non-coding DNA.

A professor at the University of Limerick has identified a gap in the classification of a portion of the digestive system. The mesentery, which connects the intestine to the abdomen, has for hundreds of years been mistakenly considered a fragmented structure made of separate parts. However, the Professor or Surgery at UL’s Medical School, J Calvin Coffey, challenged this ideology and found that the mesentery is one continuous structure. By acknowledging this differentiation, it allows researchers to target abnormalities and diseases as well as could lead to improved health outcomes.

It is widely accepted that the presentation and course of Crohn’s disease (CD) is highly variable. A new study conducted by the University of North Carolina at Chapel Hill and Cedars-Sinai Medical Center sought to conceptualize the cellular mechanisms behind CD and characterize the processes associated with disease phenotypes (http://gut.bmj.com/content/early/2016/10/13/gutjnl-2016-312518.abstract).

It’s imperative in clinical trials, exploratory studies, proof of concept analysis, and research & development to attain samples which are best suited for desired outcomes. Both processing types preserve specimens well, but which to leverage is contingent upon intended application.

Research has found that KRAS mutations are present in 30 percent of non-small cell lung cancers (NSLC) and in 40 to 50 percent of colorectal cancers. This mutation prevalence has been linked to poor survival rates and chemotherapy resistance within the impacted oncology cohorts. In an attempt to remedy this known issue, researchers at University of California, San Diego screened KRAS mutant cells for synthetic lethal interactions (https://www.genomeweb.com/cancer/kras-driven-tumor-growth-inhibited-microrna). Results concluded that the miR-1298 gene when inhibited is lethal to the growth of KRAS-mutated cells, both in vitro and in vivo through a combination of microarray analyses.