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SummaryBackgroundIn the era of improving overall survival rates of malignant diseases, the impact of a previous malignancy (PM) on treatment and outcome of lung cancer (LC) remains unclear.MethodsWe reviewed all LC patients from our institution that were treated from 2004 to 2006 for the occurrence of LC with PM excluding patients with multiple primary LC.ResultsA total of 444 and 2698 LC patients with and without a history of a PM were identified (prevalence of 14.1%). PM were most often located in breast (15.5%), prostate (14.9%), bladder (9.0%) and kidney (8.8%). Compared to never smokers, patients with nicotine consumption had more often a cancer history of prostate, gastrointestinal, and the head-neck region. The median interval until diagnosis of LC was 72.2 months (range 0–537 months) with most LC diagnosed 5 years after PM diagnosis. With a similar distribution of histology, stage and localization compared to controls, NSCLC patients with PM and stage IV disease showed a favorable overall survival (p

Patients with lung cancer are at risk of developing a second primary lung cancer (SPLC). However, the characteristics of patients at risk remain largely speculative. We reviewed 2816 lung cancer patients from our institution for the occurrence of SPLC. Any SPLC was categorised as synchronous when diagnosed within 2 years of the first primary lung cancer (FPLC) and after direct histological comparison of both tumours. All other SPLCs were considered as metachronous. 139 patients developed a second malignancy including 69 nonsmall cell lung cancer (NSCLC) and 9 small cell lung cancer. The median interval for diagnosis of metachronous SPLC (n=59) after FPLC occurrence was 72 months. SPLC detected within 5 years of FPLC diagnosis had a more favourable stage distribution (p=0.02). After diagnosis of SPLC, patients had a superior median overall survival compared to controls (57.7 versus 18.1 months; p

To complete the process of comprehensive growth-oriented brand management, this chapter deals with the unanswered questions addressed in Chap. 3 – how to develop your marketing and sales plan, calculate your return on marketing investment and monitor success. It also presents checklists and questions for successful use of the BGB model.

Before looking at the Brand Growth Barrier Model and its advantages, we need to understand the flaws in today’s popular approaches to brand management. This will help us identify the key requirements a model for growth-oriented brand management must meet. Several ideas presented in this chapter will strike you as new and inspiring. Some you may have thought about already, but not found a satisfying solution yet. If you come away from this chapter with the impression that your brand management challenges are even bigger than you thought – that’s fine. You will find answers to your (new) questions in the next chapter.

There are only three ways a company or its brand can go: up – growth; down – decline; neither nor – stagnation. And only one way satisfies everyone involved, especially owners and shareholders: going up, i.e. achieving growth. Theoretically, the sky’s the limit in terms of growth – you can always grow more. Even in economically hard times, you need to strive for growth because, sooner or later, you’ll have cut all the costs you can. The only other lever with which to increase profits is growth. So it’s all the more important to use that lever and create new growth – especially with the help of your brand. Even in a period of crisis when many potential customers focus on price, a strong brand can overcome that barrier and revive sales, turnover and profits.

We present the clinical and laboratory features of a boy with a new syndrome of mitochondrial depletion syndrome and T cell immunodeficiency. The child suffered from severe recurrent infectious diseases, anemia, and thrombocytopenia. Clinically, he presented with severe psychomotor retardation, axial hypotonia, and a disturbed pain perception leading to debilitating biting of the thumb, lower lip, and tongue. Brain imaging showed hypoplasia of corpus callosum and an impaired myelinization of the temporo-occipital region with consecutive supratentorial hydrocephalus. Histologic examination of a skeletal muscle biopsy was normal. Biochemical investigation showed combined deficiency of respiratory chain complexes II+III and IV. MtDNA depletion was found by real-time PCR. No pathogenic mutations were identified in the TK2, SUCLA2, DGUOK, and ECGF1 genes. A heterozygous missense mutation was found in POLG1. The pathogenic relevance of this mutation is unclear. Interestingly, a lack of CD8(+) T lymphocytes as well as NK cells was also observed. The percentage of CD45RO-expressing cells was decreased in activated CD8(+) T lymphocytes. Activation of T lymphocytes via IL-2 was diminished. The occurrence of the immunologic deficiency in our patient with mtDNA depletion is a rare finding, implying that cells of the immune system might also be affected by mitochondrial disease.