In recent news, there have been two great discoveries – similar in theory, but very different in appearance and use – for delivering drugs. Both use remote control mechanisms, the first invention describes how a remote control pill can release its contents once it reaches the area at which the drugs need to be delivered (see:Remote-control Nanoparticles Deliver Drugs Directly Into Tumors). The second discovery takes place at the nano-level – here, Remote-control Nanoparticles Deliver Drugs Directly Into Tumors; the drugs are released by an electromagnetic field once the nanoparticles get in the vicinity of the tumorigenic cells. This therapy works well for attacking primary tumor sites; however, this therapy won’t be very robust when trying to eliminate metastatic colonies, or rogue cells that may have broken off from originating tumors. I am still bullish on an approach to cancer therapy that includes the programming of one’s own immune system to identify tumorigenic cells and destroy them.
Cancer is able to evade the immune system, and grow within our bodies in a number of ways. Tumours are able to accomplish this feat in hundreds, if not thousands of different ways.
Researchers at USC mentioned that you could then take these “immune signatures” generated by the immune response against a tumour — and target them with whichever drugs or therapy is best suited. This builds on personalized medicine, here’s why: lets say two tumours exist, A + B, where A is a breast tumour and B is a prostate tumour. Generally tumours A + B will have different biochemistry for reasons including: (1) different cell of origin; and (2) different prepotency for specific mutations thus causing cancers in the different cells. Traditionally, drugs have either tries to poison these cells, or hijack an intracellular process associated with a specific mutation found in one cancer. By looking at the immune response signature, you could generate immune-specific drugs that could target tumour illiciting similar immune signatures. Therefore, it could be found for one drug commonly used for tumour A to work perfectly in tumour B if the immune response signatures are in alignment.
In the article, the researchers generated signatures using real-time PCR on 14 pro-immunity genes, and 11 anti-immunity genes from 5 different mouse tumour models. This is merely a start to what seems to be the tip of the iceburg here. It will be excited to see future developments.
MIT scientists just discovered the function of 14-3-3 sigma protein, and also, what happens if it isn’t present in cells. This is a HUGE discovery toward preventative measures in cancer screening technology. It won’t be long before there are a new set of diagnostics out that screeen for a wide range of cancer precursor biomarkers that increase risk of cancer to a give tissue.
So, what do scientists propose that 14-3-3 sigma does? It plays a role in cell division. Specifically, it helps cells finish cytokinesis and separate into two distinct cells, right at the end of cell division. Michael Yaffe, an associate professor of biology and biological engineering and leader of the research team said “The cells try to divide and try to divide, and they just give up. They can’t finish cytokinesis.” This results in a single cell with two nuclei.
Key information not to be missed from the article:
- Fused, or binucleate, cells have recently been shown to be precursors to cancer cells. They are often found in so-called “dysplastic” tissue, which consists of cells that are not fully normal but are not cancerous. Comparing tumors to weeds, Yaffe explained that those tissues act as fertile “soil” for tumor development. “Tumors grow in epithelial tissues that are already deranged for some reason, and something about that soil makes it better able to grow weeds.”
- Loss of 14-3-3 sigma in dysplastic tissue could serve as a marker to help doctors predict whether tumors will develop. “Our hope is that it will be possible to monitor 14-3-3 expression in these ‘benign’ conditions, a subset of which may not be so benign,” said Yaffe.
- The researchers were initially intrigued by the fact that 14-3-3 sigma is missing in normal tissue that surrounds tumors, which suggested that its function is lost very early in tumor development. Once the researchers started investigating the protein, they eventually unraveled a complex signaling pathway whose disruption leads to the failure of cell division.
- They discovered that 14-3-3 sigma is most active during mitosis, when it helps control production of proteins necessary for division.
- 14-3-3 sigma interacts with a translation factor known as eIF4B, whichforms part of an enzyme that allows mRNA to unwind so the ribosome can read its sequence.
- When 14-3-3 sigma is knocked out, eIF4B is not produced, and mRNA for the protein p58 cannot be translated. p58 plays a critical role in the final splitting of one cell into two during mitosis, so when it is missing, the cells cannot fully divide.
- When p58 function is restored, the cells resume normal division.
The story was orginally issued by MIT, and covered by ScienceDaily under the title: MIT Identifies Role Of Key Protein In Tumor Growth
Two recent articles discuss diagnostic and medical imaging technologies that help researchers to identify cancers and look deep within. Another discusses some “preventitive medicine” that has no prevention, only costs.
Headlines indicate that Holographic Images Use Shimmer To Show Cellular Response To Anticancer Drug, and another study demonstrates that PET Imaging Identifies Aggressive Kidney Cancers That Require Surgery. The Holographic imaging research is at the cutting edge of technology, specifically, it is “the first time holography has been used to study the effects of a drug on living tissue,” mentions David D. Nolte. He is the leader of the research group from Purdue.
Some smokers and/or lung cancer candidates have been screened for presence of tumours or micro-tumours in the lungs by multi-detector CT scanners. While the technology found 3 times the amount of tumours than expected, earlier treatments for these patients didn’t yield better results as the mortality rate remained the same. Dr. Peter Bach, who is a lung physician and epidemiologist, and the study’s first author said, “Early detection and additional treatment did not save lives but did subject patients to invasive and possibly unnecessary treatments.”
But, Dr. Bach … you should focus on the fact that you were able to find 3 TIMES the amount of tumours originally predicted. Right now, current treatment regiments don’t allow for an increase in the number of lives saved, but as technology improves and more clinical trials come to market, many of these micro-tumours will be stopped in their tracks by new therapeutics, chemotherapies, cancer-targeting viruses, or perhaps nanoparticles linked to toxins which target tumorigenic tissues. Maybe the process of surgical excision should be rethought; maybe only certain tumours that have a certain genetic profile should be removed early. Genotype the tumour, and THEN deploy the necessary tactics. Don’t just cut out anything that looks like it “could” be fatal, surgeries often have complications and implications for the patient’s health.