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Older cancer patients are underrepresented in clinical trials. We aimed to evaluate the enrollment of older women aged 70 years old (yo) or over with metastatic breast cancer (MBC) in clinical trials.We used the national Epidemio-Strategy and Medical Economics MBC Data Platform, a French multi-center real-life database. We selected MBC women over 70yo, without central nervous system metastases, with at least one line of systemic treatment, between January 1st, 2008 and December 31st, 2016, and had no other cancer in the 5 years before MBC. The primary objective was to evaluate the proportion of patients enrolled in clinical trials according to their age. Secondary objective was to identify variables associated with enrollment in older ones.5552 women were aged ≥ 70 (median 74yo; IQR 72-77). 14,611 were less than 70. Of the older ones, 239 (4%) were enrolled in a clinical trial during first line of treatment, compared with 1529 (10.5%) for younger ones. Multivariable analysis of variables predicting for enrollment during first line of treatment in older patients were younger age (OR 0.50 [95%CI 0.33-0.76] for the 80-85yo class; OR 0.17 [95%CI 0.06-0.39] for the 85yo and more class), good ECOG Performance Status (PS 0-1) (OR 0.15 [95%CI 0.08-0.27] for the PS 2-4 class), HER2 + disease (OR 1.78 [95%CI 1.27-2.48]), type of treatment (chemotherapy/targeted therapy/immunotherapy OR 5.01 [95%CI 3.13-8.18]), and period (OR 1.65 [95%CI 1.22-2.26] for 2012-2016, compared to 2008-2011).In this large database, few older MBC patients were enrolled in a trial compared with younger ones.

International audience; Bone is the most common metastatic site for breast cancer. Estrogen-related-receptor alpha (ERRα) has been implicated in cancer cell invasiveness. Here, we established that ERRα promotes spontaneous metastatic dissemination of breast cancer cells from primary mammary tumors to the skeleton. We carried out cohort studies, pharmacological inhibition, gain-of-function analyses in vivo and cellular and molecular studies in vitro to identify new biomarkers in breast cancer metastases. Meta-analysis of human primary breast tumors revealed that high ERRα expression levels were associated with bone but not lung metastases. ERRα expression was also detected in circulating tumor cells from metastatic breast cancer patients. ERRα overexpression in murine 4T1 breast cancer cells promoted spontaneous bone micro-metastases formation when tumor cells were inoculated orthotopically, whereas lung metastases occurred irrespective of ERRα expression level. In vivo, Rank was identified as a target for ERRα. That was confirmed in vitro in Rankl stimulated tumor cell invasion, in mTOR/pS6K phosphorylation, by transactivation assay, ChIP and bioinformatics analyses. Moreover, pharmacological inhibition of ERRα reduced primary tumor growth, bone micro-metastases formation and Rank expression in vitro and in vivo. Transcriptomic studies and meta-analysis confirmed a positive association between metastases and ERRα/RANK in breast cancer patients and also revealed a positive correlation between ERRα and BRCA1 mut carriers. Taken together, our results reveal a novel ERRα/RANK axis by which ERRα in primary breast cancer promotes early dissemination of cancer cells to bone. These findings suggest that ERRα may be a useful therapeutic target to prevent bone metastases.

Background We aimed to describe, among a population of women with intellectual disabilities (ID) living in institutions in France, the characteristics in whom breast cancer (BC) was diagnosed and of those who participated in BC screening. Methods Study was performed in 2009 among a random, representative sample of women with ID living in institutions in France. Participants answered a questionnaire either directly by themselves, or with the help of an intermediary. Results In total, 978 women with ID aged over 18 years were included, and 14 were diagnosed with BC. The incidence observed in this sample of women with ID is similar to that of the general population (standardised incidence ratio, SIR 0.857, 95% confidence interval (CI) 0.42–1.53). Average age at diagnosis was 47.8 years, and the risk of developing BC before the age of 50 was 2.03% (0.4–3.66). This risk was not significantly different from that of the general population (2.4%, 1.0–3.78). Obesity was almost twice as frequent in women who had BC as compared to those without BC (43% vs. 22.5%, P = 0.0196). Among the 310 women aged >50 years and eligible for the national BC screening programme, 238 (77%) had already had at least one mammogram, and 199 had had it within the previous 2 years. Adherence to the screening programme was 64.2% (199/310) in the participating institutions. This rate was slightly higher than the national average of 62% for the same period. Conclusions The results of this study show that BC is equally as frequent among women with ID living in institutions as in the general population, and occurs at around the same age. Obesity was significantly more frequent among women in whom BC was diagnosed in our study. Participation in BC screening is slightly higher among women with ID living in institutions than among the general population.

Breast cancer treatment decision-making has been radically changed by the discovery of biomarkers that enable the prescription of stratified therapies according to the cancer genomic subtype. First, estrogen (ER) and progesterone receptors played an important role in the selection of patients for anti-hormonal therapy. Then, human epidermal growth factor receptor 2 (HER2) was validated as predictor of breast cancer response to anti-HER2 therapies. Now, molecular profiling to classify ER-positive breast cancers in luminal A and B types is carried out routinely and triple negative breast cancers tend to be categorized according to their different outcome. Prognostic and predictive biomarkers of the response to hormone/chemotherapy are also needed to identify patients who will benefit from the currently available adjuvant therapies. Several genomic signatures have been described that should outperform these traditional markers, but few are available on the market and their cost-benefit has not been thoroughly assessed yet. New protein biomarkers that can be more easily tested in clinical laboratories are also available. Particularly, uPA and PAI-1 are the only biomarkers validated with the highest level of evidence and recommended by ASCO. Moreover, IHC4 could be used as a surrogate marker at the place of molecular classifiers for ER-positive HER2-negative breast cancers. This review focuses on new protein biomarkers used to refine early-stage breast cancer taxonomy in view of personalized medicine decision-making.

Resume Le cancer du sein reste, malgre les progres des traitements et l’apparition des therapies ciblees, la premiere cause de mortalite par cancer chez la femme. C’est aussi le premier cancer a avoir beneficie d’un ciblage therapeutique avec les recepteurs hormonaux (RH) et aujourd’hui HER2. La classification anatomoclinique utilisee pour optimiser la therapeutique est prise en defaut dans un certain nombre de cas, ce qui est source de surtraitements ou de traitements inappropries. L’etude des alterations genomiques des cellules tumorales a mis en evidence leur relation avec le pronostic et l’efficacite des traitements. La classification moleculaire qui en decoule a permis l’emergence de nombreux tests diagnostiques utilisant des approches technologiques et cliniques tres differentes qui devraient permettre de mieux classer les tumeurs pour aboutir a une therapie personnalisee. Dans cette revue, huit tests moleculaires sont evalues en regard de leur validation scientifique et de leur utilite clinique. Des approches proteiques sont egalement envisagees avec la presentation de uPA/PAI-1, le seul marqueur pronostique actuellement valide avec un niveau de preuve 1.

Resume La chimiotherapie des cancers bronchiques non a petites cellules au stade avance est fondee sur le cisplatine. Elle permet de prolonger la survie. Cependant, la toxicite elevee des associations de type doublets incluant le cisplatine impose la recherche d’alternatives. Les nouveaux cytotoxiques anti-cancereux ont un meilleur rapport efficacite : toxicite. Les doublets sans cisplatine, fondes sur de nouvelles molecules, constituent un espoir d’ameliorer la survie des malades sans deteriorer leur qualite de vie. Plusieurs etudes randomisees, a ce jour publiees ou presentees dans la maturite de leurs resultats, suggerent que certains doublets de nouveaux cytostatiques soient une alternative aux classiques doublets fondes sur le cisplatine. Les modifications recentes des recommandations de l’ American Association of Clinical Oncology tiennent comptent de ces recents resultats en admettant que “les chimiotherapies ne contenant pas de platine puissent etre utilisees comme une alternative aux chimiotherapies fondees sur le platine, en premiere ligne”. Cette breve revue de la litterature aborde les questions methodologiques soulevees par les publications des etudes randomisees evaluant essentiellement les doublets gemcitabine-vinorelbine ou gemcitabine-taxane, en les confrontant soit a des mono-chimiotherapies, soit a des chimiotherapies de reference fondees sur le cisplatine. Les criteres de jugement choisis dans de telles etudes sont discutes.

Asthma has been associated with an exaggerated T-helper type 2 (Th2) over Th1 responses to allergic and nonallergic stimuli, which leads to chronic airway inflammation and airway remodeling. In the present article, we propose that many of the genes involved in IgE synthesis and airways (re)modeling in asthma are persistent or reminiscent fetal genes which may not be silenced during early infancy (or late pregnancy). Genes of the embryologic differentiation of ectodermic and endodermic tissues may explain some of the patterns of airway remodeling in asthma. In utero programming leads to gene expression, the persistence of which may be associated with epigenetic inheritance phenomena induced by nonspecific environmental factors. Clear delineation of these issues may yield new information on the mechanisms of asthma and new targets for therapeutic intervention and primary prevention.

Background: PIK3CA mutations frequently occur in breast cancer (BC), being present in ∼40% of estrogen receptor (ER)-positive, HER2-negative breast tumors. PIK3CA mutations promote growth and proliferation of tumors and mediate resistance to endocrine therapies in BC. Taselisib is a potent and selective PI3-kinase (PI3K) inhibitor that displays greater selectivity for mutant PI3Kα than wild-type PI3Kα through a unique mechanism. In cell studies, taselisib preferentially degraded mutant compared with wild-type PI3Kα, which was not seen with alpelisib and pictilisib. Taselisib has enhanced activity against PIK3CA-mutant BC cell lines, and clinical data include confirmed partial responses in patients with PIK3CA-mutant BC treated with taselisib either as a single agent or in combination with fulvestrant. Trial design: SANDPIPER is a double-blinded, placebo-controlled, randomized, phase III study, designed to evaluate efficacy and safety of taselisib plus fulvestrant in patients with ER-positive, HER2-negative locally advanced or metastatic BC. Patients will be randomized 2:1 to receive either taselisib (4 mg daily) or placebo plus fulvestrant (500 mg intramuscular on Days 1 and 15 of Cycle 1, and on Day 1 of each subsequent 28-day cycle). Randomization will be stratified by visceral disease, endocrine sensitivity, and geographic region. The study enriches for patients with PIK3CA-mutant tumors who will be randomized separately from those with non-mutant tumors. Eligibility: Postmenopausal women with ER-positive, HER2-negative, locally advanced or metastatic BC are eligible if they have disease recurrence or progression during or after aromatase inhibitor treatment. A valid cobas® PIK3CA Mutation Test result via central assessment is required prior to enrollment. Aims: The primary efficacy endpoint is investigator-assessed progression-free survival (PFS) in patients with PIK3CA-mutant tumors. Additional endpoints include overall survival (OS), objective response rate (ORR), clinical benefit rate (CBR), duration of objective response, safety, pharmacokinetics, and patient-reported outcomes. Statistical methods: The primary efficacy analysis population will include all randomized patients with PIK3CA-mutant tumors. Patients will be grouped according to randomized treatment arm. Median PFS and OS will be estimated using Kaplan–Meier methodology. Cox proportional-hazards models, stratified by the stratification factors, will be used to estimate the hazard ratio with 95% confidence intervals (CIs). ORR, CBR, and their 95% CIs will be estimated. Duration of objective response will be estimated using Kaplan–Meier methodology. Quality of life will be analyzed and summarized. Safety will be analyzed for all treated patients according to actual treatment received. Accrual: Target enrollment is 600 patients. The study is open for enrollment and, as at April 2016, over 200 patients have been enrolled. Clinicaltrials.gov ID: NCT02340221. Contact information: For more information or to refer a patient, email global.rochegenentechtrials@roche.com or call 1-888-662-6728 (USA only). Citation Format: Baselga J, Cortés J, De Laurentiis M, Dent S, Diéras V, Harbeck N, Hsu J, Jin H, Schimmoller F, Wilson TR, Im Y-H, Jacot W, Krop IE, Verma S. SANDPIPER: Phase III study of the PI3-kinase inhibitor taselisib (GDC-0032) plus fulvestrant in patients with estrogen receptor-positive, HER2-negative locally advanced or metastatic breast cancer enriched for patients with PIK3CA-mutant tumors [abstract]. In: Proceedings of the 2016 San Antonio Breast Cancer Symposium; 2016 Dec 6-10; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2017;77(4 Suppl):Abstract nr OT2-01-01.

uPA et PAI-1 ont ete valides comme des facteurs pronostiques de niveau de preuve 1 par l’ASCO, l’INCa et la SFSPM dans le cadre de la prise en charge adjuvante du cancer du sein localise (CSL) [1]. Leur elevation predit de plus un benefice augmente a une chimiotherapie adjuvante contenant des anthracyclines [2]. Leur association avec certains marqueurs pronostiques, ainsi que l’impact de leur utilisation meritent d’etre precises.

During the last French radiation oncology society annual congress, the therapeutic options for the management of brain metastases were presented. The indications and limits of surgery, stereotactic radiotherapy and whole brain radiotherapy, as well as their benefit in terms of overall survival, local control and improvement of the functional and neurocognitive status were discussed. The prognosis significance of the different phenotypes of breast cancer on the risk for BM as well as their roles in the treatment of brain metastases were also described. Surgery improves overall survival for patients with a single brain metastase and should be considered in the case of symptomatic lesions. The overall survival of patients treated with stereotactic radiotherapy do not differ from that of patients treated with surgery. These treatments should be mainly considered for patients with good performance status, one to three small brain metastases (3cm) and limited extracranial disease. Whole brain radiotherapy is more and more discussed in adjuvant setting due to potential late neurocognitive toxicity. This toxicity could be improved with the development of techniques sparing the hippocampus. HER2+ and triple-negative breast cancer patients are at increased risk for brain metastases. Prognosis of these patients differs as the overall survival of HER2+ patients has improved with anti-HER2 therapies. The optimal combination of local and systemic therapies remain to be determined.

Les cancers bronchiques a petites cellules (anciens anaplasiques) (1) sont des cancers de differenciation neuroendocrine. Les malades qui en sont atteints presentent souvent une maladie metastatique declaree lorsque le diagnostic est porte. Dans les 20 a 30 % des cas ou ce cancer semble localise au thorax, il est frequent que la maladie metastatique existe a un stade occulte. Des les annees 1970, l’observation de la grande chimiosensibilite de ce type histologique a suscite l’interet de nombreux oncologues convaincus qu’il y aurait une proportionnalite de cette sensibilite et de la curabilite, mais les problemes devaient rapidement s’averer plus complexes.

The several options for therapy in breast cancer underline the difficulties to determine the reliable population which can be treated by a specific adjuvant therapy, and the population in which that therapy could generate morbidity, mortality, "medical surcharge" without prognosis improvement. This problem is particularly accurate in node-negative breast cancer patients. Adjuvant therapy has been proved to be more efficient, so a better definition of the prognosis and the response to adjuvant treatments could allow the selection of a sub-group of patients who can be spared chemotherapy. The quantification of the uPA/PAI-1 tumor content is one of the most relevant prognostic factors in this clinical setting. The integration of the uPA/PAI-1 prognostic information gathered in the multidisciplinary medical consensus meetings could be used to select the node-negative good/prognosis population in which chemotherapy could be avoided. This review will focus on the uPA/PAI-1 system, its biological role and its clinical implications in breast oncology. The different ways to analyse the uPA and PAI-1 content in tumor cells will be also presented and commented.

Adjuvant hormono-radiotherapy applied to breast cancers have been published for many years as an efficient neo-adjuvant treatment. Given the common hormonal dependence of breast cancer and the potential synergistic effect of these two treatment modalities, this strategy has been increasing in the adjuvant setting. Indeed, two strategies are used in daily clinical practice: upfront aromatase inhibitors or sequentially after a variable delay of tamoxifen (TAM). These molecules may thus interact with radiotherapy (RT). Retrospectives studies did not show any differences in terms of loco-regional recurrences between concurrent or sequential radio-hormono-therapy. Lung and skin fibroses due to concurrent treatment are still under debate. Nevertheless, late side-effects appeared to be increased particularly in hypersensitive patients identified by the lymphocyte predictive test. Preliminary results from the phase II randomized study (CO-HO-RT trial) evaluating the impact of concurrent or sequential letrozole and RT on toxicities has recently confirmed the need to identify hypersensitive patients before delivering concurrent systemic therapy with RT.

Combined radiation and hormone therapies have become common clinical practice in recent years for locally-advanced prostate cancers. The use of such concomitant therapy in the treatment of breast disease has been infrequently reported in the literature, but seems justified given the common hormonal dependence of breast cancer and the potential synergistic effect of these two treatment modalities. As adjuvant therapy, two strategies are used in daily clinical practice: upfront aromatase inhibitors or sequentially after a variable delay of tamoxifen. These molecules may, thus, interact with radiotherapy. Retrospectives studies recently published did not show any differences in terms of locoregional recurrences between concurrent or sequential radiohormonotherapy. Lung and skin fibroses due to concurrent treatment are still under debate. Nevertheless, late side effects appeared to be increased by such a treatment, particularly in hypersensitive patients identified at risk by the lymphocyte predictive test. Concurrent radiohormonotherapy should, thus, be delivered cautiously at least for these patients. This article details the potent advantages and risks of concurrent use of adjuvant hormonotherapy and radiotherapy in localized breast cancers.

Small cell bronchial carcinoma holds a prominent position among malignant tumours on account of its high incidence and the problems of its treatment. The diagnostic approach is dictated by the concern not to overlook any metastatic sites. Small cell bronchial carcinoma is often metastatic at the time of diagnosis and should be considered an actual or potential systemic disease. Chemotherapy is therefore the basis of treatment. It should consist of at least a two drug regime combining cisplatin and etoposide. In extensive disease, that is when all the disease cannot be contained within one irradiation field, chemotherapy alone is recommended. In limited disease combined simultaneous radiotherapy and chemotherapy is recommended. Prophylactic cranial irradiation is indicated in patients in complete remission after chemotherapy. The therapeutic armamentarium has recently been enlarged by the development of new antineoplastic drugs and the development of non-toxic targeted agents including those influencing angiogenesis. The understanding of the specific mechanisms of drug resistance and the study of the tumour phenotypes and genotypes will allow, in the future, the development of treatments adapted for each patient.

Thymic epithelial tumours (TET) are rare. Their optimal management is still not well defined on account of their rarity and the consequent difficulty of clinical research into the subject. This review presents the current clinical and therapeutic data, emphasising the need for a multidisciplinary management of advanced stage TET.Three situations may be defined: localised tumours requiring radical surgery following a careful search for associated paraneoplastic syndromes; tumours with capsular invasion requiring surgery and adjuvent radiotherapy; advanced stage TET where only multimodal treatment is capable of improving the prognosis by increasing the percentage of complete resections while optimising local control with adjuvent radiotherapy.An evaluation of the multimodal strategies for the treatment of advanced stage TET requires the establishment of multidisciplinary collaborative trials. The contribution of new therapies, somatostatin analogues and targeted therapies needs to be defined.The management of advanced stage TET should rest upon a multidisciplinary dialogue between a team of specialists, ideally in the framework of collaborative trials.

Chemotherapy of advanced non-small cell lung cancers is based on cisplatin, which prolongs survival. However, the high toxicity of double-type combinations including cisplatin warrants the search for alternatives. New anti-cancer cytotoxic agents exhibit improved efficacy-toxicity ratio. Bitherapy, without cisplatin and with new molecules, provides hope of improvement in survival without deterioration in quality of life. Several randomised trials, already published or presented with mature results, suggest that certain bitherapies with new cytostatic agents are an alternative to the classical cisplatin-based bitherapies. The recent modifications in the guidelines of the American Association of Clinical Oncology take into account these recent results by admitting that "chemotherapy without cisplatin can be used as an alternative to the first-line platin-based chemotherapies". This brief review of the literature underlines the methodological questions raised by the publication of randomised studies essentially assessing gemcitabine-vinorelbine or gemcitabine-taxane combinations, by confronting them with either mono-chemotherapies or reference chemotherapy based on cisplatin. The assessment criteria selected in such studies are discussed.

Lung cancer is the leading cause of cancer mortality for men and its incidence is increasing for women (Greenlee et al. 2001). The WHO pathologic description of malignant tumours classifies lung cancers into four groups (WHO, 1999): small cell lung cancer, squamous cell carcinoma, primary adenocarcinoma, and large cell carcinoma. Small cell lung cancer has neuroendocrine properties which confer to this tumour specific biological and clinical features. From a prognostic and therapeutic point of view, squamous cell carcinomas, adenocarcinomas, and large cell carcinomas are pooled in a non-small cell lung cancer group. This oversimplified concept has been changed recently by the results of pathological studies demonstrating that mixed small cell and non-small cell lung cancers are frequent (Breteron et al. 1978; Yesner and Carter, 1982). The study of serum markers in non-small cell lung cancer should take into account this lung cancer heterogeneity.

In the setting of reduced-intensity conditioning (RIC) regimens for allogeneic stem cell transplantation (allo-SCT), the epidemiology of transplant-related infections is still poorly defined. In 101 high-risk patients who received an HLA-identical sibling allo-SCT after RIC, including fludarabine, busulfan and antithymocyte globulin (ATG), we report during the first 6 months a cumulative incidence of positive CMV antigenemia of 42% (95% CI 32-52%), developing at a median of 37 (range 7-116) days without evidence of CMV disease (median follow-up, 434 days). The cumulative incidence of bacteremia was 25% (95% CI 17-33%), occurring at a median of 67 (range 7-172) days, while patients had recovered a full neutrophil count. In all, 65% of the bacteremia (95% CI 49-81%) were gram negative. The cumulative incidence of fungal infections was 8% (95% CI 3-13%), with a median onset of 89 (range 7-170) days. In multivariate analysis, stem cell source (bone marrow; P=0.0002) was significantly associated with the risk of positive CMV antigenemia, while higher doses of prednisone (2 mg/kg) represented the major risk factor for bacteremia (P=0.0001). Infectious-related mortality was 5% (95% CI 1-9%), with aspergillosis being the principal cause. Collectively, these results suggest that prospective efforts are warranted to develop optimal antimicrobial preventive strategies after RIC allo-SCT.

Non small cell lung cancer (NSCLC) is the leading cause of cancer death among the world. The incidence of adenocarcinoma is rising while squamous cell carcinoma decreases. The biology of NSCLC is characterized by a multistep carcinogenesis. During the last years, changing in the management of NSCLC have occurred. The lobectomy and mediastinal lymph node dissection are now the references. Postoperative radiotherapy has failed to improve survival, but hyperfractionated radiotherapy seems to be interesting for inoperable patients. The platin-based chemotherapy is now considered as standard treatment for stage IV. Gene therapy and angiogenesis inhibitors are currently under development.

Among a number of biochemical and morphological criteria, alveolar type-II epithelial cells are defined by the synthesis of surfactant proteins. These molecules are implicated in numerous human diseases such as neonatal respiratory distress syndrome 1 and possibly acute respiratory distress syndrome (ARDS) 2, where a better understanding could lead to new therapeutic modalities via a targeted induction of surfactant synthesis. The synthesis of surfactant proteins (SPs) is under the control of a variety of potential developmental and hormonal regulators, however, two transcription factors, thyroid transcription factor (TTF)‐1 and hepatocyte nuclear factor (HNF)‐3, have a crucial role in mediating the expression of SPs 3. The promoter region of the SP‐B gene has been studied extensively 4. In the human SP‐B gene, a region located at the immediate 5′ flanking region of the basal promoter TATA box between 80–110 contains two cis-acting elements for TTF‐1 and HNF‐3 binding 4. These two elements are important for the specificity and activation of SPs gene expression in the lung. SP‐B is a 79-amino acid peptide critical to postnatal respiratory adaptation. SP‐B is the only surfactant-associated protein required for postnatal lung function and survival. Complete deficiency of SP‐B in mice and humans results in lethal neonatal respiratory distress syndrome and is characterised by a virtual absence of lung compliance, highly disorganised lamellar bodies, and greatly diminished levels of SP‐C mature …

A 72-year-old man with hormone refractory prostate cancer presented with spontaneous cutaneous petechiae and bleeding at incision foci. He had been receiving leuprolide for more than 7 years for prostate cancer with bone metastases, which had been diagnosed when biopsy demonstrated liver involvement with classic prostate adenocarcinoma cells. At presentation serum prostate specific antigen (PSA) was 44 ng./ml. and neuron specific enolase (NSE) was 86 ng./ml. (normal less than 15). Platelet count was 19,000/ml. (normal 150,000 to 300,000), hemoglobin 12 gm./dl. (normal 12 to 14), fibrinogen 0.7 gm./l. (normal 2 to 4) and D-dimer test was positive. The patient was administered 75 mg./m. 2 docetaxel intravenously and 70 mg./m. 2 cisplatin intravenously on day 1. Platelet count increased to 70,000/ml., fibrinogen increased to 1.2 gm./l. and hemorrhagic diathesis was controlled by day 3 after treatment. Coagulase tests normalized within 1 week. The patient was subsequently treated every 3 weeks for a total of 4 cycles. PSA nadir was 2.8 ng./ml. immediately after the last cycle of chemotherapy, while serum NSE decreased to below normal after the first cycle. At 12 months of followup the patient had a good performance status with normal hematological parameters but PSA had increased to 9.6 ng./ml. DISCUSSION The cornerstone of management of disseminated intravascular coagulation is treatment of the underlying condition. Unfortunately few effective therapeutic options are available in hormone refractory prostate cancer. However, the recent development of new active agents might reverse this situation. Recently a case of acute disseminated intravascular coagulation associated with hormone refractory prostate cancer was successfully treated with samarium 153.1 However, radiopharmaceutical treatment should be used with caution since a death related to the development of acute disseminated intravascular coagulation following administration of strontium 89 has been reported.2 Mitoxantrone chemotherapy has also been reported to be effective but normalization of blood tests requires at least 1 week.3 Since docetaxel is a promising drug in hormone refractory prostate cancer, we used a combination of docetaxel and cisplatin, which resulted in prompt resolution of the hematological disorders. The success of treatment was probably related to cytotoxic activity since reversal of hemostatic diathesis was associated with a decrease in serum PSA. Chemosensitivity might be related to a neuroendocrine component as suggested by increased serum NSE levels but in this case only classic adenocarcinoma cells were observed on liver biopsy. REFERENCES