Over the years, increasing information has been asked of the pathologist: we have moved from a purely morphological diagnosis to biomolecular and genetic studies, which have made it possible to implement the use of molecular targeted therapies, such as anti-epidermal growth factor receptor (EGFR) molecules in EGFR-mutated lung cancer, for example. Today, next generation sequencing (NGS) has changed the approach to neoplasms, to the extent that, in a short time, it has gained a place of absolute importance and diagnostic, prognostic and therapeutic utility. In this scenario, formaldehyde-fixed and paraffin-embedded (FFPE) biological tissue samples are a source of clinical and molecular information. However, problems can arise in the genetic material (DNA and RNA) for use in NGS due to fixation, and work is being devoted to possible strategies to reduce its effects. In this paper, we discuss the applications of FFPE tissue samples in the execution of NGS, we focus on the problems arising with the use of this type of material for nucleic acid extraction and, finally, we consider the most useful strategies to prevent and reduce single nucleotide polymorphisms (SNV) and other fixation artifacts.

Acne vulgaris is a chronic dermatological disorder that affects the majority of teenagers in the Western world. Topical therapy is widely used to treat mild-moderate acne and is known as well-tolerated thanks to its low systemic toxicity, although associated to skin adverse effects. Acne seems to be associated also to an intrinsic alteration of the epidermal barrier, regarding both the upper and the follicular stratum corneum that promotes the onset of such local side effects. The commonest one is irritant contact dermatitis, an event of frequent observation occurring with erythema, burning, dryness, scaling, and itching, usually characterized by low severity and limited duration. Among topical acne drugs, retinoids are the most irritating ones. Another side effect is allergic contact dermatitis: it is rare and mainly associated to benzoyl peroxide.

Chemical leukoderma, often clinically mimicking idiopathic vitiligo and other congenital and acquired hypopigmentation, is an acquired form of cutaneous pigment loss caused by exposure to a variety of chemicals that act through selective melanocytotoxicity. Most of these chemicals are phenols and aromatic or aliphatic catechols derivatives. These chemicals, however, are harmful for melanocytes in individuals with an individual susceptibility. Nowadays, chemical leukoderma is fairly common, caused by common domestic products. The presence of numerous acquired confetti- or pea-sized macules is clinically characteristic of chemical leukoderma, albeit not diagnostic. Other relevant diagnostic elements are a history of repeated exposure to a known or suspected depigmenting agent at the sites of onset and a macules distribution corresponding to sites of chemical exposure. Spontaneous repigmentation has been reported when the causative agent is avoided; the repigmentation process is perifollicular and gradual, taking place for a variable period of weeks to months.