Intraperitoneal chemotherapy is associated with a significant pharmacokinetic and pharmacodynamic benefit and can, alone or in combination with systemic chemotherapy (bidirectional chemotherapy), be used for treating primary and secondary peritoneal surface malignancies. Due to the peritoneal–plasma barrier, high intraperitoneal drug concentration can be achieved by intraperitoneal chemotherapy, whereas systemic concentration remains low. Bidirectional chemotherapy may provide in addition adequate drug concentrations from the side of the subperitoneal space to the peritoneal tumour nodules. Major pharmacological problems of intraperitoneal chemotherapy are limited tissue penetration and poor homogeneity of drug distribution to the entire seroperitoneal surface. Significant pharmacological determinants of intraperitoneal chemotherapy are choice of drug, drug dosage, solution volume, carrier solution, intra-abdominal pressure, temperature, duration, mode of administration, extent of peritonectomy and interindividual variability. Drugs most commonly applied for intraperitoneal chemotherapy include mitomycin C, cisplatin, carboplatin, oxaliplatin, irinotecan, 5-fluoruracil, gemcitabine, paclitaxel, docetaxel, doxorubicin, premetrexed and melphalan. The drugs and their doses that are used vary widely among centres. While the adequate drug choice for intraperitoneal and bidirectional chemotherapy is essential, randomized clinical trials to determine the most optimal drug or drug combination are lacking, and only eight retrospective comparative clinical studies are available. Further clinical pharmacological studies are required to determine the most effective drug regimen for intraperitoneal and bidirectional chemotherapy in various indications. In the future, reliable drug sensitivity testing and genetic profiling of peritoneal metastases will be needed for enabling patient-specific therapy.

Desmoid tumor, also known as aggressive fibromatosis or desmoid-type fibromatosis, is a rare monoclonal, fibroblastic proliferation arising in musculoaponeurotic structures. Although histologically benign, desmoids are often locally invasive and associated with a high local recurrence rate after resection. Since it is a heterogeneous disease, in particular regarding clinical presentation, anatomic location and biological behavior, treatment should be individualized to reduce local tumor control failure with concurrently acceptable morbidity and preservation of quality of life. Many issues regarding optimal treatment of desmoids remain controversial. However, wide surgical excision remains the treatment of choice, except when surgery is mutilating and is associated with considerable function loss or major morbidity. Involvement of surgical margins is probably associated with an increased risk of local recurrence. Postoperative radiotherapy results in a significant reduction of the local recurrence rate, but only in the case of involved surgical margins. Radiotherapy for gross disease is considerably effective, but is associated with a relatively high rate of complications, which are usually mild or moderate and radiation dose dependent. Radiotherapy should only be applied where anatomic constraints preclude complete resection and radiotherapy is not too toxic. Risk factors for local tumor control failure include young age, large size, presentation as recurrent disease, limb/girdle or intra-abdominal location, involved surgical margins, omission of radiotherapy, radiation dose less than 50 Gy and insufficient radiation field size. Increased comprehension of the pathogenesis and biological behavior of desmoids resulted in the emerging applicability of systemic therapies and a wait-and-see policy. Systemic treatment may be indicated in patients that have anatomic barriers to effective surgery or radiotherapy. Considering the significant morbidity of surgery and/or radiotherapy for certain locations, especially mutilation and loss of function, and the tumor's natural history, which is often characterized by prolonged periods of stability or even regression, a period of watchful waiting may compose the most appropriate management in selected asymptomatic patients. Attempts to complete eradication of the disease may be worse than the disease itself.

Chronic stress is thought to be involved in the occurrence and progression of multiple diseases, via mechanisms that still remain largely unknown. Interestingly, key regulators of the stress response, such as members of the corticotropin-releasing-hormone (CRH) family of neuropeptides and receptors, are now known to be implicated in the regulation of chronic inflammation, one of the predisposing factors for oncogenesis and disease progression. However, an interrelationship between stress, inflammation, and malignancy, at least at the molecular level, still remains unclear. Here, we attempt to summarize the current knowledge that supports the inseparable link between chronic stress, inflammation, and colorectal cancer (CRC), by modulation of a cascade of molecular signaling pathways, which are under the regulation of CRH-family members expressed in the brain and periphery. The understanding of the molecular basis of the link among these processes may provide a step forward towards personalized medicine in terms of CRC diagnosis, prognosis and therapeutic targeting.