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Restoration of natural processes via the reintroduction of locally extinct species is a key component of the rewilding process. In Ireland, the Eurasian lynx (Lynx lynx), an indigenous medium-sized felid, is no longer extant, possibly due to increasing human pressures over the course of the Holocene. With increased afforestation levels and subsequent range expansion in the populations of both native and exotic deer species, the potential for the Irish landscape to support a viable lynx population was examined. Four sequential steps were undertaken: (1) identifying the extent of available habitat using GIS software, (2) assessing the connectivity between habitat patches using a least-cost path analysis, (3) estimating the number of lynx which could be supported by the available habitat, and (4) investigating the long-term viability of a reintroduced lynx population under differing scenarios, using Rangeshifter software. Overall, a total of 4,488 km2of suitable habitat was identified, spread between 4 habitat networks and 3 isolated patches. Under current habitat availability, a lynx population was found to have a low chance of persistence after 100 years under varying densities, with some improvement seen when habitat availability was increased. For Ireland to be capable of sustaining a viable population of lynx, there must be enhancement of both habitat availability and connectivity, through coherent landscape-scale woodland restoration. The results also highlight the importance of an evidence-based approach in species reintroduction planning, allowing for the likelihood of success to be rapidly quantified.

Mutations in the mitochondrial genome have been reported as biomarkers for the detection of cancer. Hallmarks of cancer development include the accumulation of genetic alterations in the mitochondrial and nuclear genomes. Damage to mitochondria affects energy metabolism, generation of reactive oxygen species, apoptosis, cell growth and other processes that contribute to the neoplastic process. Furthermore, mitochondrial DNA mutations occur frequently in cancer. Little work has been done to link a pathway between mitochondrial mutations and cancer etiology. Volumes of work have been reported on the association of mitochondrial mutations and almost all types of cancer including the use of body fluids for early detection. This review examines the measurement of mitochondrial mutations for the application of detecting human tumor tissue.

The recent surge in mitochondrial research has been driven by the identification of mitochondria-associated diseases and the role of mitochondria in apoptosis. Both of these aspects have identified mitochondrial analysis as a vital component of medical research. Moreover, mitochondria have been implicated in the process of carcinogenesis because of their vital role in energy production, nuclear-cytoplasmic signal integration and control of metabolic pathways. Interestingly, at some point during neoplastic transformation, there is an increase in reactive oxygen species, which damage the mitochondrial genome. This accelerates the somatic mutation rate of mitochondrial DNA. It has been proposed that these mutations may serve as an early indication of potential cancer development and may represent a means for tracking tumour progression. The purpose of this review is to explore the potential utility that these mutations may afford for the identification and monitoring of neoplasia and malignant transformation where appropriate body fluids or non-invasive tissue access is available for mitochondrial DNA recovery. Specifically, prostate, breast, colorectal, skin and lung cancers are discussed.

Studies of somatic mitochondrial DNA mutations have become an important aspect of cancer research because these mutations might have functional significance and/or serve as a biosensor for tumor detection. Here we report somatic mitochondrial DNA mutations from three specific tissue types (tumor, adjacent benign, and distant benign) recovered from 24 prostatectomy samples. Needle biopsy tissue from 12 individuals referred for prostate biopsy, yet histologically benign (symptomatic benign), were used as among individual control samples. We also sampled blood (germplasm tissue) from each patient to serve as within individual controls relative to the somatic tissues sampled (malignant, adjacent, and distant benign). Complete mitochondrial genome sequencing was attempted on each sample. In contrast to both control groups [within patient (blood) and among patient (symptomatic benign)], all of the tissue types recovered from the malignant group harbored significantly different mitochondrial DNA (mtDNA) mutations. We conclude that mitochondrial genome mutations are an early indicator of malignant transformation in prostate tissue. These muta-tions occur well before changes in tissue histo-pathology, indicative of prostate cancer, are evident to the pathologist.

Developing early detection biosensors for disease has been the long‒held goal of the Human Genome Project, but with little success. Conversely, the biological properties of the mitochondrion coupled with the relative simplicity of the mitochondrial genome give this organelle extraordinary functionality as a biosensor and places the field of mitochondrial genomics in a position of strategic advantage to launch significant advances in personalized medicine. Numerous factors make the mitochondrion organelle uniquely suited to be an early detection biosensor with applications in oncology as well as many other aspects of human health and disease. Early detection of disease translates into more effective, less expensive treatments for disease and overall better prognoses for those at greater risk for developing diseases.