Purpose of review To discuss the recent developments of multimodal treatment for patients with local advanced rectal cancer, including incorporation of new chemotherapeutic and targeted agents, and the optimal sequence and timing of treatment components. Recent findings Five randomized trials have been completed to determine whether the addition of oxaliplatin to preoperative, fluorouracil-based chemoradiotherapy (CRT) offers an advantage compared to single-agent fluorouracil CRT. Early results from the ACCORD 12, STAR-01, and NSAPB R-04 trials did not confirm a significant improvement of early efficacy endpoints with the addition of oxaliplatin, whereas the German CAO/ARO/AIO-04 did. Most of the phase II trials incorporating cetuximab into CRT reported disappointingly low rates of pathologic complete response (pCR); the combination of CRT with VEGF inhibition showed encouraging pCR rates; however, it was associated with increased surgical complications. Novel clinical trials address the role of induction chemotherapy, of delayed, minimal or omitted surgery following CRT, or the omission of radiotherapy for selected patients. Summary At this time, the use of oxaliplatin or targeted agents as component of multimodality treatment for rectal cancer outside of a clinical trial is not recommended. The inclusion of different treatment options, according to tumor stage, location, imaging features, and response, will render the multimodal treatment approach of rectal cancer more risk-adapted.
Gastrointestinal stromal tumours (GISTs) are the most common group of mesenchymal tumours affecting the gastrointestinal tract. Despite this, GISTs are relatively rare, since all mesenchymal tumours constitute just 1 percent of all primary GI cancers. Most often, GISTs affect the stomach and proximal small intestine but can be found in any section of the alimentary tract, including, occasionally, the omentum, mesentery and peritoneum. Virtually all GISTs (especially those larger than 1 cm) have malignant potential. Malignant potential of a tumour increases with its size and its mitotic rate, and it also depends on its anatomic location: intestinal GISTs are more aggressive than gastric tumours. Treatment of GISTs was revolutionized when it was discovered that mutational activation of KIT or PDGFRA stimulates the growth of these cancer cells. Mutational activation of KIT or PDGFRA led to abnormal activation of receptor tyrosine kinase and uncontrolled oncogenic signalling. This uncontrolled oncogenic signalling can be specifically targeted therapeutically with small molecule inhibitors of the receptor tyrosine kinase (imatinib, sunitinib). All GISTs > or = 2 cm in size should be resected. To reduce disease recurrence, adjuvant imatinib therapy is recommended for all high-risk patients after resection. Neoadjuvant therapy is recommended for primarily unresectable tumours or a limited amount of potentially resectable metastatic disease. The goal of treatment is to reduce tumour size, thus facilitating complete surgical resection and increasing the likelihood of organ preservation.
This chapter contains sections titled: Diagnosis Treatment Prognosis and follow-up References
This chapter contains sections titled: Diagnosis Staging of esophageal cancer Treatment Prognosis and follow-up References
The incidence of hepatocellular carcinoma (HCC) has increased both due to the worldwide increase on the virus C infection and to the increase on the survival rate of patients with chronic liver disease. It usually is an aggressive tumor with survival rate directly associated with the hepatic residual liver function as well as the size of the tumor at the diagnosis.
