Simultaneous polarimeter retrievals of microphysical aerosol and ocean color parameters from the "MAPP" algorithm with comparison to high-spectral-resolution lidar aerosol and ocean products.

We present an optimal-estimation-based retrieval framework, the microphysical aerosol properties from polarimetry (MAPP) algorithm, designed for simultaneous retrieval of aerosol microphysical properties and ocean color bio-optical parameters using multi-angular total and polarized radiances. Polarimetric measurements from the airborne NASA Research Scanning Polarimeter (RSP) were inverted by MAPP to produce atmosphere and ocean products. The RSP MAPP results are compared with co-incident lidar measurements made by the NASA High-Spectral-Resolution Lidar HSRL-1 and HSRL-2 instruments. Comparisons are made of the aerosol optical depth (AOD) at 355 and 532 nm, lidar column-averaged measurements of the aerosol lidar ratio and Ångstrøm exponent, and lidar ocean measurements of the particulate hemispherical backscatter coefficient and the diffuse attenuation coefficient. The measurements were collected during the 2012 Two-Column Aerosol Project (TCAP) campaign and the 2014 Ship-Aircraft Bio-Optical Research (SABOR) campaign. For the SABOR campaign, 73% RSP MAPP retrievals fall within ±0.04 AOD at 532 nm as measured by HSRL-1, with an R value of 0.933 and root-mean-square deviation of 0.0372. For the TCAP campaign, 53% of RSP MAPP retrievals are within 0.04 AOD as measured by HSRL-2, with an R value of 0.927 and root-mean-square deviation of 0.0673. Comparisons with HSRL-2 AOD at 355 nm during TCAP result in an R value of 0.959 and a root-mean-square deviation of 0.0694. The RSP retrievals using the MAPP optimal estimation framework represent a key milestone on the path to a combined lidar+polarimeter retrieval using both HSRL and RSP measurements.

Cancer risk among 21st century blood transfusion recipients.

Background: Some carcinogenic viruses are known to be transmissible by blood transfusion. Intensive viral screening of transfused blood now exists in most countries. In the UK, high-sensitivity nucleic acid amplification tests for hepatitis C virus were introduced in 1999 and it was thought that this would reduce, and possibly eliminate, transfusion-related liver cancer. We aimed to investigate cancer risk in recipients of blood transfusion in 2000 or after. Methods: A total of 1.3 million UK women recruited in 1998 on average were followed for hospital records of blood transfusion and for cancer registrations. After excluding women with cancer or precancerous conditions before or at the time of transfusion, Cox regression yielded adjusted relative risks of 11 site-specific cancers for women with compared to without prior blood transfusion. Results: During follow up, 11 274 (0.9%) women had a first recorded transfusion in 2000 or after, and 1648 (14.6%) of them were subsequently diagnosed with cancer, a mean 6.8 years after the transfusion. In the first 5 years after transfusion there were significant excesses for most site-specific cancers examined, presumably because some had preclinical cancer. However, 5 or more years (mean 8 years) after blood transfusion, there were significant excess risks only for liver cancer (adjusted relative risk = 2.63, 95%CI 1.45-4.78) and for non-Hodgkin lymphoma (adjusted relative risk = 1.74, 1.21-2.51). When analyses were restricted to those undergoing hip or knee replacement surgery, the commonest procedure associated with transfusion, these relative risks were not materially altered. Conclusions: In a large cohort of UK women, transfusions in the 21st century were associated with long-term increased risks of liver cancer and non-Hodgkin lymphoma. Some of these malignancies may have been caused by carcinogenic agents that are not currently screened for in transfused blood.

Perspectives on next steps in classification of oro-facial pain - Part 3: biomarkers of chronic oro-facial pain - from research to clinic.

The purpose of this study was to review the current status of biomarkers used in oro-facial pain conditions. Specifically, we critically appraise their relative strengths and weaknesses for assessing mechanisms associated with the oro-facial pain conditions and interpret that information in the light of their current value for use in diagnosis. In the third section, we explore biomarkers through the perspective of ontological realism. We discuss ontological problems of biomarkers as currently widely conceptualised and implemented. This leads to recommendations for research practice aimed to a better understanding of the potential contribution that biomarkers might make to oro-facial pain diagnosis and thereby fulfil our goal for an expanded multidimensional framework for oro-facial pain conditions that would include a third axis.

Birth weight and adult cancer incidence: large prospective study and meta-analysis.

BACKGROUND: Most evidence about associations between birth weight and adult cancer risk comes from studies linking birth records to cancer registration data, where information on known risk factors for cancer is generally lacking. Here, we report on associations between birth weight and cause-specific cancer risk in a large cohort of UK women, and investigate how observed associations are affected by other factors. METHODS: A total of 453 023 women, born in the 1930s and 1940s, reported their birth weight, maternal smoking, parental heights, age at menarche, adult height, adult smoking, and many other personal characteristics. They were followed for incident cancer. Using Cox regression, relative risks by birth weight were estimated for cancers with more than 1500 incident cases, adjusting for 17 potential confounding factors, individually and simultaneously. RESULTS: Birth weight reported in adulthood was strongly correlated with that recorded at birth (correlation coefficient = 0.78, P < 0.0001). Reported birth weight was associated with most of the potential confounding factors examined, the strongest association being with adult height. After 9.2 years follow-up per woman, 39 060 incident cancers were registered (4414 colorectal, 3175 lung, 1795 malignant melanoma, 14 542 breast, 2623 endometrial, 2009 ovarian, 1565 non-Hodgkin lymphoma, and 8937 other cancers). Associations with birth weight were null or weak and reduced after adjustment by adult height (P[trend] > 0.01 for every cancer, after adjustment). In contrast, adult height was strongly related to the risk of every cancer except lung cancer, after adjusting for birth weight and other factors (P[trend] < 0.0001 for most cancers). For lung cancer, adjusting for smoking reduced the association with birth weight. Meta-analyses were dominated by our findings. CONCLUSION: Birth weight and adult height are correlated and likely to be markers of some aspect of growth that affects cancer risk in adulthood. However, birth weight adds little, if any, additional information to adult height as a predictor of cancer incidence in women.

Cancer outcomes and all-cause mortality in adults allocated to metformin: systematic review and collaborative meta-analysis of randomised clinical trials.

AIMS/HYPOTHESIS: Observational studies suggest that metformin may reduce cancer risk by approximately one-third. We examined cancer outcomes and all-cause mortality in published randomised controlled trials (RCTs). METHODS: RCTs comparing metformin with active glucose-lowering therapy or placebo/usual care, with minimum 500 participants and 1-year follow-up, were identified by systematic review. Data on cancer incidence and all-cause mortality were obtained from publications or by contacting investigators. For two trials, cancer incidence data were not available; cancer mortality was used as a surrogate. Summary RRs, 95% CIs and I (2)statistics for heterogeneity were calculated by fixed effects meta-analysis. RESULTS: Of 4,039 abstracts identified, 94 publications described 14 eligible studies. RRs for cancer were available from 11 RCTs with 398 cancers during 51,681 person-years. RRs for all-cause mortality were available from 13 RCTs with 552 deaths during 66,447 person-years. Summary RRs for cancer outcomes in people randomised to metformin compared with any comparator were 1.02 (95% CI 0.82, 1.26) across all trials, 0.98 (95% CI 0.77, 1.23) in a subgroup analysis of active-comparator trials and 1.36 (95% CI 0.74, 2.49) in a subgroup analysis of placebo/usual care comparator trials. The summary RR for all-cause mortality was 0.94 (95% CI 0.79, 1.12) across all trials. CONCLUSIONS/INTERPRETATION: Meta-analysis of currently available RCT data does not support the hypothesis that metformin lowers cancer risk by one-third. Eligible trials also showed no significant effect of metformin on all-cause mortality. However, limitations include heterogeneous comparator types, absent cancer data from two trials, and short follow-up, especially for mortality.

Postmenopausal endometrial cancer risk and body size in early life and middle age: prospective cohort study.

BACKGROUND: Greater adiposity in early life has been linked to increased endometrial cancer risk in later life, but the extent to which this association is mediated through adiposity in later life is unclear. METHODS: Among postmenopausal women who had never used menopausal hormone therapies and reported not having had a hysterectomy, adjusted relative risks (RRs) of endometrial cancer were estimated using Cox regression. RESULTS: Among 249 791 postmenopausal women with 7.3 years of follow-up on average (1.8 million person-years), endometrial cancer risk (n=1410 cases) was strongly associated with current body mass index (BMI) at baseline (RR=1.87 per 5 kg m(-2) increase in BMI, 95% confidence interval (CI): 1.77-1.96). Compared with women thinner than average at age 10, the increased risk among women plumper at age 10 (RR=1.27, 95% CI: 1.09-1.49) disappeared after adjustment for current BMI (RR=0.90, 95% CI: 0.77-1.06). Similarly, compared with women with clothes size 12 or less at age 20, the increased risk among women with clothes size 16 or larger (RR=1.87, 95% CI: 1.61-2.18) was not significant after adjustment for current BMI (RR=1.03, 95% CI: 0.88-1.22). CONCLUSION: Among women who have never used hormone therapy for menopause, the association between body size in early life and endometrial cancer risk in postmenopausal women can be largely explained by women's current BMI.

A short-term increase in cancer risk associated with daytime napping is likely to reflect pre-clinical disease: prospective cohort study.

BACKGROUND: Sleep disturbance, a correlate of which is daytime napping, has been hypothesised to be associated with risk of breast and other cancers. METHODS: We estimated relative risks (RR) of breast and other invasive cancers by the reported frequency of daytime napping in a large prospective cohort of middle-aged women in the UK. RESULTS: During an average of 7.4 years of follow-up, 20 058 breast cancers and 31 856 other cancers were diagnosed. Over the first 4 years of follow-up, daytime napping (sometimes/usually vs rarely/never) was associated with slightly increased risks of breast cancer (RR=1.10, 95% CI 1.06-1.15) and of other cancers (RR=1.12, 1.08-1.15), but the RRs decreased significantly with increasing follow-up time (P=0.001 and P=0.01, respectively, for trend). Four or more years after baseline, there was no elevated risk of breast cancer (RR=1.00, 0.96-1.05), and only marginally greater risk of other cancers (RR=1.04, 1.01-1.07). CONCLUSION: The effect of pre-clinical disease is a likely explanation for the short-term increased risk of breast and other cancers associated with daytime napping.

Shift work and chronic disease: the epidemiological evidence.

BACKGROUND: Shift work, including night work, has been hypothesized to increase the risk of chronic diseases, including cancer, cardiovascular disease (CVD), metabolic syndrome and diabetes. Recent reviews of evidence relating to these hypotheses have focussed on specific diseases or potential mechanisms, but no general summary of the current data on shift work and chronic disease has been published. METHODS: Systematic and critical reviews and recent original studies indexed in PubMed prior to 31 December 2009 were retrieved, aided by manual searches of reference lists. The main conclusions from reviews and principle results from recent studies are presented in text and tables. RESULTS: Published evidence is suggestive but not conclusive for an adverse association between night work and breast cancer but limited and inconsistent for cancers at other sites and all cancers combined. Findings on shift work, in relation to risks of CVD, metabolic syndrome and diabetes are also suggestive but not conclusive for an adverse relationship. CONCLUSIONS: Heterogeneity of study exposures and outcomes and emphasis on positive but non-significant results make it difficult to draw general conclusions. Further data are needed for additional disease endpoints and study populations.

Characterisation, identification, clustering, and classification of disease.

The importance of quantifying the distribution and determinants of multimorbidity has prompted novel data-driven classifications of disease. Applications have included improved statistical power and refined prognoses for a range of respiratory, infectious, autoimmune, and neurological diseases, with studies using molecular information, age of disease incidence, and sequences of disease onset ("disease trajectories") to classify disease clusters. Here we consider whether easily measured risk factors such as height and BMI can effectively characterise diseases in UK Biobank data, combining established statistical methods in new but rigorous ways to provide clinically relevant comparisons and clusters of disease. Over 400 common diseases were selected for analysis using clinical and epidemiological criteria, and conventional proportional hazards models were used to estimate associations with 12 established risk factors. Several diseases had strongly sex-dependent associations of disease risk with BMI. Importantly, a large proportion of diseases affecting both sexes could be identified by their risk factors, and equivalent diseases tended to cluster adjacently. These included 10 diseases presently classified as "Symptoms, signs, and abnormal clinical and laboratory findings, not elsewhere classified". Many clusters are associated with a shared, known pathogenesis, others suggest likely but presently unconfirmed causes. The specificity of associations and shared pathogenesis of many clustered diseases provide a new perspective on the interactions between biological pathways, risk factors, and patterns of disease such as multimorbidity.

Alcohol intake and risk of colorectal cancer: results from the UK Dietary Cohort Consortium.

BACKGROUND: Epidemiological studies have suggested that excessive alcohol intake increases colorectal cancer (CRC) risk. However, findings regarding tumour subsites and sex differences have been inconsistent. METHODS: We investigated the prospective associations between alcohol intake on overall and site- and sex-specific CRC risk. Analyses were conducted on 579 CRC cases and 1996 matched controls nested within the UK Dietary Cohort Consortium using standardised data obtained from food diaries as a main nutritional method and repeated using data from food frequency questionnaire (FFQ). RESULTS: Compared with individuals in the lightest category of drinkers (>0-<5 g per day), the multivariable odds ratios of CRC were 1.16 (95% confidence interval (95% CI): 0.88, 1.53) for non-drinkers, 0.91 (95% CI: 0.67, 1.24) for drinkers with 5-<15 g per day, 0.90 (95% CI: 0.65, 1.25) for drinkers with 15-<30 g per day, 1.02 (95% CI: 0.66, 1.58) for drinkers with 30-<45 g per day and 1.19 (95% CI: 0.75, 1.91) for drinkers with >or=45 g per day. No clear associations were observed between site-specific CRC risk and alcohol intake in either sex. Analyses using FFQ showed similar results. CONCLUSION: We found no significantly increased risk of CRC up to 30 g per day of alcohol intake within the UK Dietary Cohort Consortium.

Pathophysiology of TMD pain--basic mechanisms and their implications for pharmacotherapy.

This article discusses the pathophysiology of temporomandibular disorders (TMD)-related pain and its treatment with analgesic drugs. Temporomandibular disorders are comprised of a group of conditions that result in temporomandibular joint pain (arthralgia, arthritis) and/or masticatory muscle pain (myofascial TMD). In at least some patients with TMD, a peripheral mechanism contributes to this pain. However, there is often a poor correlation between the severity of TMD-related pain complaints and evidence of definitive tissue pathology. This has led to the concept that pain in some patients with TMD may result from altered central nervous system pain processing and further that this altered pain processing may be attributable to specific genes that are heritable. Psychosocial stressors are also thought to contribute to the development of TMD-related pain, particularly masticatory muscle pain. Finally, substantially more women suffer from TMD than men. Although there are arguably multiple reasons for sex-related differences in the prevalence of TMD, one candidate for the increased occurrence of this disorder in women has been suggested to be the female sex hormone oestrogen. Analgesic drugs are an integral part of the primary treatment for TMD-related pain and dysfunction with more that 90% of treatment recommendations involving use of medications. The most commonly used agents include non-steroidal anti-inflammatory drugs, corticosteroids, muscle relaxants, anxiolytics, opiates and tricyclic antidepressants, however, evidence in support of the effectiveness of these drugs is lacking. Continued research into the pathophysiology of TMD-related pain and the effectiveness of analgesic treatments for this pain is required.

Emerging roles for chromatin remodeling in cancer biology.

Cell proliferation and differentiation are guided by changes in gene expression and require the coordinated efforts of the transcription machinery and chromatin-remodeling factors. However, aberrant regulation of chromatin structure can arise through mutations in chromatin-modifying and -remodeling proteins and can lead to improper gene expression and cancer. This review discusses how mutations in chromatin regulators might affect their targeting or activity, with an emphasis on the important insights revealed by leukemogenic fusion proteins. Understanding the normal and oncogenic role of these factors will be crucial for the design of therapeutic agents.

Chromatin remodeling machines: similar motors, ulterior motives.

Chromatin is a dynamic material; chromatin structures can repress transcription and their remodeling accompanies activation. Recent biochemical studies in Drosophila have revealed three multi-protein complexes with ATP-dependent chromatin restructuring activities. Although all contain the ATPase ISWI, their properties in vitro are markedly different, distinct from SWI-SNF and reveal intriguing connections to both transcription and chromatin assembly.

Demonstration of the safety and effectiveness of the RECELL® System combined with split-thickness meshed autografts for the reduction of donor skin to treat mixed-depth burn injuries.

INTRODUCTION: Split-thickness skin grafts (STSG) are the standard of care (SOC) for burns undergoing autografting but are associated with donor skin site morbidity and limited by the availability of uninjured skin. The RECELL® Autologous Cell Harvesting Device (RECELL® System, or RECELL) was developed for point-of-care preparation and application of a suspension of non-cultured, disaggregated, autologous skin cells, using 1cm2 of the patient's skin to treat up to 80cm2 of excised burn. METHODS: A multi-center, prospective, within-subject controlled, randomized, clinical trial was conducted with 30 subjects to evaluate RECELL in combination with a more widely meshed STSG than a pre-defined SOC meshed STSG (RECELL treatment) for the treatment of mixed-depth burns, including full-thickness. Treatment areas were randomized to receive standard meshed STSG (Control treatment) or RECELL treatment, such that each subject had 1 Control and 1 RECELL treatment area. Effectiveness measures were assessed and included complete wound closure, donor skin use, subject satisfaction, and scarring outcomes out to one year following treatment. RESULTS: At 8 weeks, 85% of the Control-treated wounds were healed compared with 92% of the RECELL-treated wounds, establishing the non-inferiority of RECELL treatment for wound healing. Control-treated and RECELL-treated wounds were similar in mean size; however, mean donor skin use was significantly reduced by 32% with the use of RECELL (p<0.001), establishing the superiority of RECELL treatment for reducing donor skin requirements. Secondary effectiveness and safety outcomes were similar between the treatments. CONCLUSIONS: In combination with widely meshed STSG, RECELL is a safe and effective point-of-care treatment for mixed-depth burns without confluent dermis, achieving short- and long-term healing comparable to standard STSG, while significantly decreasing donor skin use.

Apocynin improves outcome in experimental stroke with a narrow dose range.

Inflammation following ischemic stroke is known to contribute to injury. NADPH oxidase (NOX) is a major enzyme system originally studied in immune cells that leads to superoxide (O.*) generation. Apocynin is a NOX inhibitor that has been studied as a potential treatment in experimental stroke. Here we explored the effect of different doses of apocynin in a mouse model of 2 h transient middle cerebral artery occlusion (tMCAO) followed by 22 h reperfusion. Apocynin, given i.v. at a dose of 2.5 mg/kg 30 min before reperfusion, improved neurological function (P<0.01), reduced infarct volume (P<0.05), and reduced the incidence of cerebral hemorrhage (P<0.05), but not at higher doses of 3.75 and 5 mg/kg, where it actually increased brain hemorrhage. Apocynin also tended to reduce mortality at the lower dose, but not at higher doses. Using hydroethine fluorescence to delineate O.* in the brain, neurons and some microglia/macrophages, but not vascular endothelial cells were found to contain O.*. Apocynin at protective doses markedly prevented ischemia-induced increases in O.*. Our data suggested that apocynin can protect against experimental stroke, but with a narrow therapeutic window.

γ-Aminobutyric acid (GABA) oral rinse reduces capsaicin-induced burning mouth pain sensation: An experimental quantitative sensory testing study in healthy subjects.

BACKGROUND: In burning mouth patients, analgesia after oral administration of clonazepam may result from modulation of peripheral γ-aminobutyric acid (GABA) receptors. METHODS: The effect of oral administration of test solutions (water, 0.5 mol/L or 0.05 mol/L GABA, 1% lidocaine) was investigated for the amelioration of pain and sensitivity induced by application of capsaicin (1%, 2 min) to the tongue of thirty healthy male and female subjects in this four-session, randomized, placebo-controlled, double-blinded, cross-over study. Intra-oral quantitative sensory testing was used to assess cold (CDT), warm (WDT) and mechanical (MDT) detection thresholds as well as mechanical (MPT) and heat (HPT) pain thresholds. Capsaicin-induced pain intensity was continuously rated on a 0-10 electronic visual analogue scale (VAS). The area under the VAS curve (VASAUC) after rinsing was calculated for each solution. RESULTS: Capsaicin application on the tongue evoked burning pain with a peak of 4.8/10, and significantly increased CDT and MDT while significantly decreasing WDT, HPT, and MPT. The VASAUC was significantly smaller after oral rinse with 0.05 mol/L GABA, 0.5 mol/L GABA, and 1% lidocaine than after oral rinse with water. Rinse with 0.5 mol/L or 0.05 mol/L GABA were similarly effective in decreasing VASAUC. Rinsing with either 1% lidocaine, 0.5 mol/L or 0.05 mol/L GABA also significantly attenuated the effects of capsaicin on WDT and HPT in a treatment independent manner. There were no sex-related differences in these effects of GABA. CONCLUSIONS: Capsaicin-induced burning tongue pain and decreases in WDT and HPT can be ameliorated by rinsing the mouth with lidocaine and GABA solutions. SIGNIFICANCE: Rinsing the mouth with an oral GABA containing solution ameliorated burning pain and increased heat sensitivity produced by application of capsaicin to the tongue. This finding suggests that GABA can act as a local analgesic agent in the oral cavity.

VEGF antagonism reduces edema formation and tissue damage after ischemia/reperfusion injury in the mouse brain.

VEGF is mitogenic, angiogenic, and a potent mediator of vascular permeability. VEGF causes extravasation of plasma protein in skin bioassays and increases hydraulic conductivity in isolated perfused microvessels. Reduced tissue oxygen tension triggers VEGF expression, and increased protein and mRNA levels for VEGF and its receptors (Flt-1, Flk-1/KDR) occur in the ischemic rat brain. Brain edema, provoked in part by enhanced cerebrovascular permeability, is a major complication in central nervous system pathologies, including head trauma and stroke. The role of VEGF in this pathology has remained elusive because of the lack of a suitable experimental antagonist. We used a novel fusion protein, mFlt(1-3)-IgG, which sequesters murine VEGF, to treat mice exposed to transient cortical ischemia followed by reperfusion. Using high-resolution magnetic resonance imaging, we found a significant reduction in volume of the edematous tissue 1 day after onset of ischemia in mice that received mFlt(1-3)-IgG. 8-12 weeks after treatment, measurements of the resultant infarct size revealed a significant sparing of cortical tissue. Regional cerebral blood flow was unaffected by the administration of mFlt(1-3)-IgG. These results demonstrate that antagonism of VEGF reduces ischemia/reperfusion-related brain edema and injury, implicating VEGF in the pathogenesis of stroke and related disorders.

Sex-related differences in NMDA-evoked rat masseter muscle afferent discharge result from estrogen-mediated modulation of peripheral NMDA receptor activity.

In the present study, the hypothesis that sex-related differences in glutamate-evoked rat masseter muscle afferent discharge may result from estrogen-related modulation of peripheral N-methyl-d-aspartate (NMDA) receptor activity and/or expression was tested by examining afferent fiber discharge in response to masseter injection of NMDA and the expression of NR2A/B subunits by masseter ganglion neurons in male and female rats. The results showed that injection of NMDA into the masseter muscle evoked discharges in putative mechanonociceptive afferent fibers and increased blood pressure that was concentration-dependent, however, a systemic action of NMDA appeared responsible for increased blood pressure. NMDA-evoked afferent discharge was significantly greater in female than in male rats, was positively correlated with plasma estrogen levels in females and was significantly greater in ovariectomized female rats treated with a high dose (5 mug/day) compared with a low dose (0.5 mug/day) of estrogen. Pre-treatment of high dose estrogen-treated-ovariectomized female rats with the Src tyrosine kinase inhibitor PP2 did not affect NMDA-evoked afferent discharge. NMDA-evoked afferent discharge was attenuated by the antagonists ketamine and ifenprodil, which is selective for NR2B containing NMDA receptors. Fewer masseter ganglion neurons expressed the NR2A (16%) subunit as compared with the NR2B subunit (38%), which was expressed at higher frequencies in intact female (46%) and high dose estrogen-treated ovariectomized female (60%) rats than in male (31%) rats. Taken together, these results suggest that sex-related differences in NMDA-evoked masseter afferent discharge are due, at least in part, to an estrogen-mediated increase in expression of peripheral NMDA receptors by masseter ganglion neurons in female rats.

TFG/TAF30/ANC1, a component of the yeast SWI/SNF complex that is similar to the leukemogenic proteins ENL and AF-9.

The SWI1/ADR6, SWI2/SNF2, SWI3, SNF5, and SNF6 gene products are all required for proper transcriptional control of many genes in the yeast Saccharomyces cerevisiae. Genetic studies indicated that these gene products might form a multiprotein SWI/SNF complex important for chromatin transitions preceding transcription from RNA polymerase II promoters. Biochemical studies identified a SWI/SNF complex containing these and at least six additional polypeptides. Here we show that the 29-kDa component of the SWI/SNF complex is identical to TFG3/TAF30/ANC1. Thus, a component of the SWI/SNF complex is also a member of the TFIIF and TFIID transcription complexes. TFG3 interacted with the SNF5 component of the SWI/SNF complex in protein interaction blots. TFG3 is significantly similar to ENL and AF-9, two proteins implicated in human acute leukemia. These results suggest that ENL and AF-9 proteins interact with the SNF5 component of the human SWI/SNF complex and raise the possibility that the SWI/SNF complex is involved in acute leukemia.