This topic review will provide an overview of the incidence and specific patterns of lung toxicity seen with cytotoxic chemotherapy agents. Separate monographs are available for many of the drugs that are most commonly associated with pulmonary toxicity. (See "Bleomycin-induced lung injury" and "Busulfan-induced pulmonary injury" and "Chlorambucil-induced pulmonary injury" and "Cyclophosphamide pulmonary toxicity" and "Methotrexate-induced lung injury" and "Mitomycin-C pulmonary toxicity" and "Nitrosourea-induced pulmonary injury" and "Taxane-induced pulmonary toxicity" .)
Genetic loss on chromosomes 1p/19q (co-deletion or loss of heterozygosity [LOH] 1p/19q) is a consequence of a chromosomal translocation and describes a distinct tumour entity characterised by a prolonged natural history irrespective of treatment, and increased sensitivity both to radiotherapy (RT) and to chemotherapy ( Jenkins 2006) . LOH 1p/19q should be evaluated to support a diagnosis of oligodendroglioma.
The incidence of either 1p or 19q chromosomal deletions in OD is approximately 75%, the combined loss of 1p and 19q is observed in 25% to 48% of all ODs ( van den Bent 2013b; Cairncross 2013) . Additional chromosomal deletions, such as loss of heterozygosity for 9p, deletion of CDKN2A gene, deletions on chromosome 10 and chromosome 7 amplification, occur less frequently in anaplastic OD ( Bigner 1999; Jeuken 1999) . Oligodendroglial tumours with a classical histological appearance (perinuclear halo, chicken-wire vascular pattern) show 1p/19q co-deletions, whereas in tumours with an atypical appearance, other chromosomal abnormalities are often found (., TP53 mutations) ( Sasaki 2002; van den Bent 2003) . In AOD both the loss of 10q and the amplification of EGFR were found inversely related to 1p/19q loss, and were associated with poor chemosensitivity and short survival ( Hoang-Xuan 2001) . The mutually exclusive occurrence of 1p/19q loss and TP53 mutations, EGFR amplification, 10q loss, or PTEN mutations suggests that these tumours are in fact derived from different precursor cells. This hypothesis is supported by the marked differences in outcome and prognosis.
Recent genome sequencing of high-grade gliomas has identified mutations of the isocitrate dehydrogenase gene (IDH) as an early event in glioma genesis ( Yan 2009) . IDH1 mutations are present in 55% to 80% of grade III oligodendrogliomas and astrocytomas ( Sanson 2009) . Less frequently, glial tumours show mutations of the IDH2.
The presence of IDH 1 or 2 mutations is characteristic of a high-grade glioma developing from a lower grade precursor lesion ( Sturm 2012; Hartmann 2013) .
MGMT promoter methylation is highly associated with LOH 1p/19q and IDH mutations ( Sanson 2009) . Conversely, IDH1 was correlated with an absence of EGFR, absence of chromosome 7 polisomy, or absence of loss of chromosome 10.
Chronic rhinosinusitis represents a multifactorial inflammatory disorder, rather than simply a persistent bacterial infection.  The medical management of chronic rhinosinusitis is now focused upon controlling the inflammation that predisposes patients to obstruction, reducing the incidence of infections. However, all forms of chronic rhinosinusitis are associated with impaired sinus drainage and secondary bacterial infections. Most individuals require initial antibiotics to clear any infection and intermittently afterwards to treat acute exacerbations of chronic rhinosinusitis.