'Virtual biopsy' device to detect skin tumors

Using sound vibrations and pulses of near-infrared light, a Rutgers University scientist has developed a new "virtual biopsy" device that can quickly determine a skin lesion's depth and potential malignancy without using a scalpel.

The ability to analyze a skin tumor non-invasively could make biopsies much less risky and distressing to patients, according to a report in Wiley Online Library. Currently, physicians who perform surgical biopsies often don't know the extent of a lesion and whether it will be necessary to refer the patient to a specialist for extensive tissue removal or plastic surgery until surgery has already begun.

The first-of-its-kind experimental procedure, called vibrational optical coherence tomography (VOCT), creates a 3-D map of the legion's width and depth under the skin with a tiny laser diode. It also uses soundwaves to test the lesion's density and stiffness since cancer cells are stiffer than healthy cells. An inch-long speaker applies audible soundwaves against the skin to measure the skin's vibrations and determine whether the lesion is malignant.

"This procedure can be completed in 15 minutes with no discomfort to the patient, who feels no sensation from the light or the nearly inaudible sound. It's a significant improvement over surgical biopsies, which are invasive, expensive and time consuming," said Frederick Silver, a professor of pathology and laboratory at Rutgers Robert Wood Johnson Medical School.

The study found that a prototype VOCT device, which awaits FDA approval for large-scale testing, is able to accurately distinguish between healthy skin and different types of skin lesions and carcinomas. The researchers tested the device over six months on four skin excisions and on eight volunteers without skin lesions. Further studies are needed to fine-tune the device's ability to identify a lesion's borders and areas of greatest density and stiffness, which would allow physicians to remove tumors with minimally invasive surgery.

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Source: https://www.sciencedaily.com/releases/2019/06/190613103129.htm

New genes out of nothing

 

One key question in evolutionary biology is how novel genes arise and develop. Swedish researchers now show how new genes and functions that are advantageous to bacteria can be selected from random DNA sequences. The results are presented in the scientific journal mBio.

How do new genes and functional proteins arise and develop? This is one of the most fundamental issues in evolutionary biology. Two different types of mechanism have been proposed: (1) new genes with novel functions arise from existing genes, and (2) new genes and proteins evolve from random DNA sequences with no similarity to existing genes and proteins.

In the present study, the researchers explored the latter type of mechanism: evolution of new genes and proteins from randomised DNA sequences as its called as de novo evolution. It is fairly easy to understand that when a gene already exists, it can be modified and acquire a new function. But how does "nothing" turn into a function affording a small advantage that is favoured by natural selection?

The raw material for the experiment was an big library of some 500 million randomised gene sequences, from which peptide sequences with a biological function were identified. In the experiment, random gene sequences were placed on a plasmid and overexpressed. The scientists then investigated whether they could give bacteria a specific, defined property. Were they, for example, able to give the bacteria antibiotic resistance? They identified several short peptides (22-25 amino acids long) that could give the bacteria a high degree of resistance to aminoglycosides, an important class of antibiotics used for severe infections.

"When the project started, we had low expectations. We were amazed when we found peptides able to confer a resistance level 48 times higher," says Dr Michael Knopp, the study's lead author.

Through a combination of genetic and functional experiments, the scientists were able to demonstrate that the peptides cause resistance by attaching themselves to bacterial cell membranes and affecting the proton potential across the membrane. The disruption of the proton potential causes a decrease in antibiotic uptake, rendering the bacteria resistant.

"This study is important because it shows that completely random sequences of amino acids can give rise to new, advantageous functions, and that this process of de novo evolution can be studied experimentally in the laboratory," says Dan I. Andersson, Professor of Medical Bacteriology, who is chiefly responsible for the study.

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Source of the article: https://www.sciencedaily.com/releases/2019/06/190604131214.htm

How prostate cancer cells mimic bone when they metastasize

Prostate cancer often becomes lethal as it spreads to the bones, and the process behind this deadly feature could potentially be turned against it as a target for bone-targeting radiation and potential new therapies.

Study published online in the journal PLOS ONE, Duke Cancer Institute researchers describe how prostate cancer cells develop the ability to mimic bone-forming cells called osteoblasts, enabling them to proliferate in the bone microenvironment.

Attacking these cells with radium-233, a radioactive isotope that selectively targets cells in these bone metastases, has been shown to prolong patients' lives. But a better understanding of how radium works in the bone was needed.

The mapping of this mimicking process could lead to a more effective use of radium-233 and to the development of new therapies to treat or prevent the spread of prostate cancer to bone.

"Given that most men who die of prostate cancer have bone metastases, this work is critical to helping understand this process," said lead author Andrew Armstrong, Director of Research at the Duke Cancer Institute Center for Prostate and Urologic Cancers.

The research team enrolled a small study group of 20 men with symptomatic bone-metastatic prostate cancer. When analyzing the circulating tumor cells from study participants, they found that bone-forming enzymes appeared to be expressed commonly, and that genetic alterations in bone forming pathways were also common in these prostate cancer cells.

They validated these new genetic findings in a separate multicenter trial involving a larger group of more than 40 men with prostate cancer and bone metastases.

Following treatment with radium-223, the researchers found that the radioactive isotope was concentrated in bone metastases, but tumor cells still circulated and cancer progressed within six months of therapy. The researchers found a range of complex genetic alterations in these tumor cells that likely enabled them to persist and develop resistance to the radiation over time.

"Osteomimicry may contribute in part to how prostate cancer spreads to bone, but also to the uptake of radium-223 within bone metastases and may thereby enhance the therapeutic benefit of this bone targeting radiotherapy," Armstrong said.

He said by mapping this lethal pathway of prostate cancer bone metastasis, the study points to new targets and thus critical areas of research into designing better tumor-targeting therapies.

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