Cuirasse skin metastases secondary to gastric adenocarcinoma

Skin metastases are infrequent manifestations of solid tumours. However, it is important to recognize them since they may be the first evidence of a neoplasia, or a sign of tumour progression or recurrence. Skin metastases from gastric adenocarcinomas are particularly rare, and represent 6% of the total in males and 1% in females. We report, here, the case of a patient diagnosed with gastric adenocarcinoma with extensive subcutaneous infiltration of the abdominal wall, resulting in an abdominal cuirass.     

Severe skin reaction secondary to concomitant radiotherapy plus cetuximab

Background

Late effects after radiotherapy in childhood and adolescence have mainly been characterized retrospectively with small patient numbers. However, these analyses are limited due to little information regarding organ dose levels in many cases. To overcome this limitation, the German Group of Paediatric Radiation Oncology (APRO) established the ?Registry for the evaluation of late side effects after radiation in childhood and adolescence” (RiSK). The study protocol and the documentation forms are given in this publication.

Methods/Design

Radiation parameters including detailed organ doses as well as toxicity evaluations are collected prospectively from centres all over Germany. Standardized documentation forms are used. These forms are given in an English and German version as additional files to this publication. Documentation is planned for all children who receive radiotherapy in one of the therapy trials of the "German Society of Paediatric Oncology and Haematology (GPOH)". The study started in a pilot phase in June 2001 in few centres. Since 2004 documentation has been performed all over Germany and is still on-going.

Discussion

To our knowledge, "RiSK" is the only multi-centre study that evaluates radiation associated side effects prospectively with detailed information about organ dose levels. With ongoing recruitment and prolongation of follow-up powerful data will be obtained in a few years. A broad use and international cooperation are welcome.     

Staphylococcus aureus bacteremia secondary to severe erlotinib skin toxicity

Epidermal growth factor receptor (EGFR) inhibitors are associated with unique and dramatic dermatologic side effects. Skin rash is the dose-limiting factor for all EGFR inhibitors and is usually dose related and reversible. Microbiologic stains and cultures from skin rash usually do not show an infectious cause. We report on a patient with known non-small-cell lung cancer who developed Staphylococcus aureus bacteremia secondary to severe erlotinib skin toxicity.     

Quality of life implications as a consequence of surgery: limb salvage, primary and secondary amputation

Purpose. We investigated self-reported quality of life (QoL), body image and daily competence of patients as a consequence of limb salvage surgery (LSS), primary or secondary amputation, and the views of patients following secondary amputation.Patients. Patients (n=37) had all been treated for osteosarcoma or Ewing's sarcoma in the lower limb.Methods. QoL was measured by questionnaire. A separate interview to determine satisfaction with decision-making was conducted with those treated for secondary amputation.Results. For the total group, QoL was below that expected from population norms. There were no differences in QoL between those undergoing LSS surgery compared with amputation. However, LSS reported better daily competence and were less likely to use a walking aid. For the total group, body image and daily competence were associated with better QoL.Discussion. All these patients are at risk of compromised QoL following surgery. Our data are in line with previous work suggesting outcomes may be better for LSS compared with amputation. Following secondary amputation, most patients (80%) did not regret initial LSS treatment, but felt that the time gained allowed them to come to terms with subsequent surgery.     

IKKalpha is required to maintain skin homeostasis and prevent skin cancer

It has long been known that excessive mitotic activity due to H-Ras can block keratinocyte differentiation and cause skin cancer. It is not clear whether there are any innate surveillants that are able to ensure that keratinocytes undergo terminal differentiation, preventing the disease. IKKalpha induces keratinocyte terminal differentiation, and its downregulation promotes skin tumor development. However, its intrinsic function in skin cancer is unknown. Here, we found that mice with IKKalpha deletion in keratinocytes develop a thickened epidermis and spontaneous squamous cell-like carcinomas. Inactivation of epidermal growth factor receptor (EGFR) or reintroduction of IKKalpha inhibits excessive mitosis, induces terminal differentiation, and prevents skin cancer through repressing an EGFR-driven autocrine loop. Thus, IKKalpha serves as an innate surveillant.     

Breast cancer-associated metastasis is significantly increased in a model of autoimmune arthritis

Introduction  

Sites of chronic inflammation are often associated with the establishment and growth of various malignancies including breast cancer. A common inflammatory condition in humans is autoimmune arthritis (AA) that causes inflammation and deformity of the joints. Other systemic effects associated with arthritis include increased cellular infiltration and inflammation of the lungs. Several studies have reported statistically significant risk ratios between AA and breast cancer. Despite this knowledge, available for a decade, it has never been questioned if the site of chronic inflammation linked to AA creates a milieu that attracts tumor cells to home and grow in the inflamed bones and lungs which are frequent sites of breast cancer metastasis.     

Selenium supplementation and secondary prevention of nonmelanoma skin cancer in a randomized trial

The Nutritional Prevention of Cancer Trial was a double-blind, randomized, placebo-controlled clinical trial designed to test whether selenium as selenized yeast (200 microg daily) could prevent nonmelanoma skin cancer among 1312 patients from the Eastern United States who had previously had this disease. Results from September 15, 1983, through December 31, 1993, showed no association between treatment and the incidence of basal and squamous cell carcinomas of the skin. This report summarizes the entire blinded treatment period, which ended on January 31, 1996. The association between treatment and time to first nonmelanoma skin cancer diagnosis and between treatment and time to multiple skin tumors overall and within subgroups, defined by baseline characteristics, was evaluated. Although results through the entire blinded period continued to show that selenium supplementation was not statistically significantly associated with the risk of basal cell carcinoma (hazard ratio [HR] = 1.09, 95% confidence interval [CI] = 0.94 to 1.26), selenium supplementation was associated with statistically significantly elevated risk of squamous cell carcinoma (HR = 1.25, 95% CI = 1.03 to 1.51) and of total nonmelanoma skin cancer (HR = 1.17, 95% CI = 1.02 to 1.34). Results from the Nutritional Prevention of Cancer Trial conducted among individuals at high risk of nonmelanoma skin cancer continue to demonstrate that selenium supplementation is ineffective at preventing basal cell carcinoma and that it increases the risk of squamous cell carcinoma and total nonmelanoma skin cancer.     

Vitamin E is a complete tumor promoter in mouse skin

The dorsal skins of 6–8 week old female SENCAR mice wereinitiated with a single application of 10 nmol of 7,12-dimethylbenz[a]anthracene(DMBA) and subsequently promoted twice/week with topical applicationsof vitamin E (dl-     

The hiv tat gene is a promoter of epidermal skin tumors

Human immunodeficiency virus (HIV) infected patients have a very high incidence (>90%) of neoplastic and non-neoplastic skin disorders. The proliferative lesions frequently involve the epidermis and include squamous and basal cell carcinomas, and the papulosquamous diseases of seborrheic dermatitis and psoriasis. Although the role played by HIV in the development of these proliferative skin lesions is not clear, there are several lines of evidence suggesting that HIV may play a causative role. We show that transgenic mice carrying the HIV tat gene under the control of the viral LTR constitutively express the tnt gene in keratinocytes. When a single subthreshold dose of a carcinogen initiator is topically applied to these mice, tumor promoters are no longer required to induce the development of epidermal skin tumors, suggesting that Tat expression in keratinocytes is capable of substituting for phorbol ester tumor promoters in the two-step carcinogenesis skin cancer model. Together, Tat and phorbol ester have additive effects in promoting tumors in transgenic mice first initiated with carcinogens. We conclude that although Tat alone is insufficient to cause epidermal tumors, it functions as a tumor promoter and predisposes these mice to develop tumors following an initiating event.     

Retinoyl-phorbol-acetate is a complete skin tumor promoter in SENCAR mice

The semi-synthetic phorbol ester 12-O-retinoyl phorbol 13-acetate (RPA) was tested for activity as a complete tumor promoter, as well as for first or second stage promotion activity, in the skin of SENCAR mice. Unlike in NMRI mice where RPA has been reported to act only as a second stage promoter, in SENCAR mice it has moderate complete promoting activity as well as second stage activity. RPA also induces epidermal hyperplasia and an increase in the number of dark basal keratinocytes.     

Response of mouse skin tumors to doxorubicin is dependent on carcinogen exposure

To investigate the role of carcinogenesis in determining the response of tumors to anticancer drugs, we have used the in vivo model of multistage carcinogenesis of the mouse skin. Mice were initiated with Harvey murine sarcoma virus or single and repeated applications of dimethylbenzanthracene (DMBA). The papillomas which developed as a result of these initiation protocols were monitored quantitatively for their response to the anticancer drug doxorubicin. A single dose of 10 mg/kg doxorubicin is relatively inefficient at reducing the frequency of papillomas arising as a result of either single or repeated applications of the chemical DMBA. However, virally initiated papillomas are sensitive to the single 10-mg/kg dose of doxorubicin and are reduced in frequency by greater than 80%. Repeat treatment with four doses of 5 mg/kg doxorubicin over a 4-week period also reveals differences in the responses of the papillomas to doxorubicin. As with the single dose of doxorubicin, papillomas initiated with multiple applications of DMBA showed only a limited response to four 5-mg/kg doses of doxorubicin. In comparison both the virally initiated and the single DMBA initiated papillomas responded to the four doses of doxorubicin and are reduced in frequency by about 80%. These data show that the response of papillomas to doxorubicin is related to the initiating event. Papillomas derived by viral initiation are most sensitive to doxorubicin while increasing the level of exposure to the chemical carcinogen DMBA increases the proportion of papillomas which do not respond to treatment with doxorubicin. There was no obvious relationship between the method of initiation or the treatment of the mice with doxorubicin and the levels of P-glycoprotein expression observed in the papillomas. All the papillomas expressed detectable levels of P-glycoprotein approaching that of the multidrug resistant cell line, CHRC5.