Trans-sacral (Kraske) approach for gastrointestinal stromal tumour of the lower rectum: old procedure for a new disease.

Gastrointestinal stromal tumours (GISTs) of the lower rectum are rare cancers from mesenchymatous origin, which are characterized by; 1) the absence of metastases in loco-regional lymph nodes; and 2) a tendency to grow opposite to the intestinal lumen. Thus, the two preferred surgical approaches for rectal adenocarcinomas (i.e. abdominal and transanal) are inappropriate for GISTs, due to: 1) the uselessness of total mesorectal excision; and 2) to the difficulty to locate the tumour with a transanal approach. We report here a case of a large GIST of the lower rectum which was successfully treated with a posterior trans-sacral approach. Lower rectum GISTs are good indications for the Kraske procedure, and this relatively new disease entity may contribute to the reintroduction of an old procedure into the armamentarium of 21(st) century colorectal surgeons.

[Supportive care in oncology: a concept of rehabilitation]. / Soins de support en oncologie: un concept de réhabilitation.

The prevalence and prognosis of cancer are changing. The number of diagnosed cancers is rising in Western countries. These diseases often become chronic illnesses and necessitate major efforts of adjustment and coping for patients and families, but also for health professionals. This paper focuses on the question of the follow-up of cancer patients and highlights some of the difficulties faced by professionals and institutions when attempting to improve the quality of care in this field. We describe how the divisions of general medical rehabilitation and of oncology of the Geneva university hospitals promote the implementation of supportive oncological care practice in a rehabilitation centre.

Topography of mammalian connexins in human skin.

We have explored the expression of gap junction proteins in normal human skin by immunostaining cryostat sections (indirect immunofluorescence) or lyophilized epidermis (Western blotting) with antibodies against four mammalian connexins Cx26, Cx32, Cx40, Cx43; and by hybridizing total epidermal RNA (Northern blotting) with cRNA probes for Cx26, Cx32, and Cx43. We found that epidermal keratinocytes express Cx43 but not Cx26, Cx32, or Cx40. This expression was minimal in the basal layer, much higher in the spinous layer, reduced in the granular layer, and absent in the stratum corneum. Immunostaining for Cx43 was also observed in sebaceous glands, hairs, and eccrine sweat ducts. The two latter epidermal adnexae were also markedly labeled by antibodies against Cx26, a gap junction protein that was undetectable by immunofluorescence in interfollicular keratinocytes. Immunoblots of polyacrylamide gel electrophoresis-separated epidermal proteins and hybridization of epidermal RNA confirmed the presence of Cx43 in epidermis. These observations indicate that 1) Cx43 and Cx26 are components of human keratinocyte gap junctions; 2) these two proteins are differentially expressed in the interfollicular epidermis and the skin adnexae; 3) in interfollicular epidermis, Cx43 is a predominant gap junction protein, mostly expressed by the differentiating spinous cells; 4) Cx43 distribution is in accordance with the extensive dye coupling previously observed in this epidermal compartment.

Tumor necrosis factor alpha inhibits the hormonal response of the pituitary gland to hypothalamic releasing factors.

Tumor necrosis factor alpha (TNF alpha), a monokine produced by activated macrophages and monocytes, may be an essential mediator of the pathogenesis and of the hormonal response to endotoxic shock. It has been suggested that an elevated level of TNF alpha is a marker for morbidity and mortality during septic shock, and that treatment with antibodies against TNF alpha decreases mortality. Because monokines have been shown to interact at the hypothalamic-pituitary level, we have studied the effect of TNF alpha on basal and stimulated hormone release from normal rat anterior pituitary cells. After 3 days of incubation, primary cultures of rat anterior pituitary cells were stimulated with either 0.5 ng/ml CRF, 3 ng/ml AVP, 10 ng/ml angiotensin II (AII), 10(-6) M TRF, 10(-8) M LHRH, or 10(-8) M GHRH, alone or in the presence of 20 or 50 ng/ml human or murine recombinant TNF alpha. The culture media were analyzed for ACTH, GH, LH, and PRL content. Each experiment was performed in triplicate and was repeated 3 to 8 times. Time-course experiments (n = 3) demonstrated that TNF alpha inhibited CRF-stimulated ACTH production over a period of 8, 16, and 24 h, but had no effect before a period of 4 h. At doses ranging from 1 to 100 ng/ml, TNF alpha did not affect basal ACTH secretion but inhibited CRF-stimulated ACTH release in a dose-dependent manner (ED50 approximately 10 ng/ml). At a dose of 50 ng/ml, TNF alpha inhibited AVP-stimulated ACTH release by 30% and blocked the effect of AII. TNF alpha (20 and 50 ng/ml) completely prevented the CRF-AVP potentiation of ACTH release. Similarly, TNF alpha inhibited the stimulated release of GH (100% inhibition), LH (35% inhibition), and PRL (100% inhibition). TNF alpha had no effect on the basal secretion of GH or LH but inhibited basal PRL in a dose-dependent manner. The administration of the monokine did not cause any cellular damage because 48 h after removal of the TNF alpha treatment the cells showed normal basal and stimulated hormone levels in response to their specific stimuli. Incubation of TNF alpha solutions with antibody to TNF alpha reversed all TNF alpha actions. These data suggest that TNF alpha inhibits the secretion of pituitary hormones and particularly suppresses the response of the corticotroph cells. This inhibitory effect may contribute to the increased mortality observed in cases of severe septic shock with high circulating TNF alpha levels.

[Epidermoid cancer of the esophagus: overview]. / Cancer épidermoïde de l'oesophage: mise au point.

Numerous extrinsic factors are involved in the pathogenesis of esophageal cancer. The disease exhibits clinical symptoms only at the advanced stage, often when no further curative possibilities exist; this delay is one of the main causes of the poor prognosis still associated with esophageal cancer. To secure early diagnosis, contrast GI series and endoscopy should be performed immediately whenever esophageal symptoms are present. Initial assessment of esophageal cancer should in any case include thoraco-abdominal scan. Bronchoscopy is indicated when the tumor is localized in the middle third of the organ. Surgery has long been considered the only valid treatment for esophageal cancer. However, the rule today is a multidisciplinary approach which offers either curative or palliative treatment designed to optimize therapy and minimize side effects. Promising results have recently been obtained with a combination of radiotherapy-chemotherapy followed by esophagectomy.

[The toxicity/efficacy relationship in polychemotherapy of lung neoplasms]. / Etude de la relation toxicité/efficacité dans la polychimiothérapie des cancers pulmonaires.

Although it is generally accepted that anti-cancer chemotherapy should be administered at the maximum tolerable dose, it is not clearly established that the therapeutic results at dosage levels involving maximum tolerable toxicity are really superior to those with lower, better tolerated doses. 392 patients with advanced primary lung cancer were treated with 5 chemotherapy regimens including cyclophosphamide, methotrexate, vincristine, procarbazine, hydroxyurea, adriamycin and CCNU, in combinations of 3 to 7 agents. Response rates of 50% and over were registered after 8 weeks of treatment. During the same time the intensity of leukopenia, thrombocytopenia, vomiting, other digestive toxicity, neurologic disorders and alopecia was graded according to the worst observation from 0 to 4. The results show that there is no correlation between the grade of toxicity and the rate of response either for the whole group or for subgroups of patients as defined by cell type, degree of dissemination, age, or performance status. They demonstrate that the search for maximum tolerable toxicity is not a sine qua non for the best possible response to chemotherapy in primary lung cancer.