tbuckley/cabot-search huggingface dataset:
Phase I study of icotinib combined with whole brain radiotherapy for EGFR-mutated non-small cell lung cancer patients with brain metastases: neurocognitive and quality-of-life analysis.
Authors: You Lu, Baoqing Chen, Lin Zhou, Jiazhuo He, Weijie Xiong, Yongmei Liu, Lei Deng, Jing Xiang, Qin Yu, Maozhi Liang, Xiaojuan Zhou, Zhenyu Ding, Meijuan Huang, Li Ren, Jiang Zhu, Lu Li, Mei Hou
Journal: Journal of Clinical Oncology (2016)

e20009 Background: We previously reported that WBRT with concurrent and maintenance icotinib were well tolerated in EGFR-mutated NSCLC patients with brain metastases. This study reports the impact of the combination WBRT with icotinib on neurocognitive function and quality of life (QoL) in these patients. Methods: Patients were treated with icotinib and WBRT in a ‘3+3’ design, the icotinib was started 7 days before and continued during WBRT (37.5Gy/15f/21d), and maintained until disease progression or intolerable toxicities occurred. The mini-mental status examination (MMSE) and functional assessment of cancer therapy-lung (FACT-L) questionnaire were administered into all patients before treatment and every 8 weeks during treatment or follow-up to assess the neurocognitive function and quality of life. Results: Between 2012 and 2013, 15 NSCLC patients with brain metastasis were enrolled. Seven of 15 patients (46%)suffered neurocognitive decline, which mostly occurred (6 of 7, 86%) after intracranial disease progression. Median time from intracranial disease progression to neurocognitive decline was 9.3 months (95%CI: 0.4-18.3 months). The average decline in overall FACT-Lung score at 4, 8, 12, 36 and 76 weeks during treatment or follow up was 5.7±3.04 with a increase trend (P = 0.007). Ten of 15 patients(66%)suffered QoL deterioration before disease progression. Median time to QoL deterioration was 2.8 months (95%CI: 1.5-4.2 months). There were no significant differences between decline scores of five subscales to baseline at 4, 8, 12, 36 and 76 weeks (P = 0.096, 0.513, 0.757, 0.119 and 0.131 respectively). A statistical difference between high and low dose (>375mg and ≤ 375mg) icotinib groups was observed in Total Outcome Index score at 36 weeks of follow-up when compared to baseline (-4.7 vs -14.7,P = 0.009;) Conclusions: Neurocognitive function decline mostly happened after intracranial disease progression suggests the combination of WBRT with icotinib has the effect on neurocognitive preservation in EGFR-mutated NSCLC patients with brain metastases. However, it showed no impact on QoL improvement. Clinical trial information: 2011S00487.
Pathologic findings at risk-reducing salpingo-oophorectomy in germline <i>BRCA</i> mutation carriers: Optimal age of bilateral RRSO.
Authors: Yong-Man Kim, Shin-Wha Lee, Young-jae Lee
Journal: Journal of Clinical Oncology (2017)

e13046 Background: Most BRCA1/2 carriers do not undergo risk-reducing salpingo-oophorectomy (RRSO) by the recommended age of 40. Methods: We retrospectively reviewed breast cancer patients identified as BRCA mutation carriers who underwent RRSO at Asan Medical Center, Seoul, Korea, from 2013 to 2015. Both fallopian tubes of all cases were examined according to the SEE/FIM protocol and immunohistochemically (IHC) staining was performed when a precursor lesion was suspected. Results: RRSO was performed in 55 patients. The median age at RRSO was 44 years (32–73 years). Of the 36 patients with IHC staining, 7 showed p53 overexpression, 1 showed Ki-67 overexpression, 2 showed serous tubal intraepithelial carcinoma, 2 showed occult cancer, and 1 showed metastatic cancer of breast origin. All occult invasive cancer cases were tubal origin and detected in patients older than 40 years. The detection rate of premalignant lesions or cancer was 21.8% (12/55). Among patients who underwent RRSO under the age of 40, premalignant lesions were found only in BRCA 1 mutation carriers (40.0% vs 0%). In BRCA 2 mutation carriers, premalignant lesions were only detected in those older than 40 years of age, indicating the possible faster occurrence of premalignant lesions in BRCA1 mutation carriers. Conclusions: Many patients still tend to delay RRSO until after they are 40 years old. Our findings support the significance of RRSO before the age of 40 in germline BRCA mutation carriers, especially in BRCA 1 mutation carriers.
Association of SDF1 inhibition with local control and relative cerebral blood volume of glioblastoma.
Authors: Reena Parada Thomas, Seema Nagpal, Michael Iv, Scott G. Soltys, Cathy Kahn Recht, Sophie Bertrand, Sherif Mark Makar, Zachary Corbin, Kseniya Mandic, Gwen Coffey, Shanika Pelpola, Isabel P Prado, Martin Brown, Lawrence David Recht
Journal: Journal of Clinical Oncology (2017)

2058 Background: Glioblastoma is the most common and aggressive primary brain tumor, with 75-85% of patients historically having recurrence within the original tumor site. We have shown in preclinical studies that inhibition of the SDF1/CXCR4 pathway by the CXCR4 inhibitor Plerixafor increases tumor response to irradiation by inhibition of the recovery of tumor blood vessels. Methods: Newly diagnosed glioblastoma patients were enrolled to the clinical trial using the investigational agent Plerixafor after standard radiation therapy and temozolomide (NCT01977677). To date, 28 patients out of the planned accrual of 29 have been enrolled to this study. Normalized relative cerebral blood volume (rCBV) ratios were calculated by the mean rCBV within the 95% isodose radiation field one month post-radiation as compared to contralateral white matter outside of the radiation field. Our imaging analysis compares patients treated with Plerixafor compared to a control group receiving standard therapy (chemo-RT). Results: There was a significant reduction in rCBV measured by DSC-MRI within the 95% isodose field one month after radiation therapy in patients receiving Plerixafor compared to control (p &lt; 0.02). The rCBV out of the radiation field was similar between patients receiving Plerixafor compared to control patients one-month post radiation therapy. As of February 7, 2017, only 2 of the total of 9 recurrences occurred within the irradiated field. The rate of out of field recurrence (77%) was therefore much higher than expected (20%), with statistical significance (p &lt; 0.03, Fisher’s exact test). Conclusions: We show that Plerixafor has a meaningful impact on local control of glioblastoma. Furthermore, DSC-MRI could be a useful biomarker of its efficacy.
Incidence of bone metastases in U.S. patients with solid tumors.
Authors: Rohini K Hernandez, Sally W Wade, Adam Reich, Melissa A. Pirolli, Alexander Liede, Gary H. Lyman
Journal: Journal of Clinical Oncology (2016)

e13099 Background: Solid tumors frequently metastasize to bone, which can lead to serious bone complications. Population-based estimates of bone metastasis incidence are limited, often based on autopsy data, and may not reflect recent treatment advances. Methods: Electronic medical records (OSCER, Oncology Services Comprehensive Electronic Records, 569,000 patients, 52 US cancer centers) were used to identify patients ≥18 years newly diagnosed with a solid tumor between 1/1/2004 and 12/31/2013, excluding patients with hematologic tumors or multiple primaries. Kaplan-Meier analyses quantified bone metastasis incidence with follow-up censored at last clinic visit, new primary tumor, bone metastasis, or 12/31/2014. Estimates were stratified by tumor type, stage at diagnosis, and calendar year. Results: Among 382,733 patients (mean age 64 years; mean follow-up 940 days), breast (36%), lung (15%), and colorectal (12%) tumors were most common. Mean time to bone metastasis was 410 days, with 1-year incidence 4.6% (95% CI 4.5–4.7), 5-year 6.7% (95% CI 6.7–6.8), and 10-year 8.2% (95% CI 8.1–8.3). Incidence varied substantially by tumor type and stage at diagnosis (stage IV 5-year 23.1% [95% CI 22.7–23.6]). Prostate cancer incidence was highest (stage IV 10-year 71.1% [68.2 – 73.9]) (Table). Conclusions: This study estimated bone metastasis incidence using real world electronic medical record data from oncology practices in the US. Underestimation is possible given reliance on coded diagnoses. National prevalence may be estimated using these more recent incidence data otherwise not available in cancer registries. Tumor type and stage at diagnosis Incidence of bone metastases (%) 1-year (95% CI) 5-year (95% CI) 10-year (95% CI) Breast (N=137,720) 3.3 (3.2–3.4) 5.8 (5.7–6.0) 7.9 (7.7–8.1) Stage IV (N = 5,985) 35.7 (34.5 – 36.9) 49.9 (48.6 – 51.3) 60.8 (58.9 – 62.6) Prostate (N=22,801) 17.5 (17.0–18.0) 24.0 (23.4–24.6) 28.3 (27.5–29.2) Stage IV (N = 3,908) 44.5 (43.0 – 46.1) 60.4 (58.7 – 62.1) 71.1 (68.2 – 73.9) Lung (N=59,344) 10.0 (9.8–10.3) 12.0 (11.7–12.3) 12.7 (12.3–13.2) Stage IV (N = 13,487) 22.1 (21.4 – 22.8) 25.0 (24.3 – 25.8) N/A Other Tumors (N=162,868) 1.9 (1.9–2.0) 3.1 (3.1–3.2) 3.8 (3.6–3.9) Stage IV (N = 22,147) 5.1 (4.8 – 5.4) 7.8 (7.4 – 8.2) N/A
Abstract P171: Low Concentrations of Aspirin Activate Cytoprotective Signaling Pathway Genes in Human Endothelial Cells: A Gene Expression Profiling Study
Authors: Reena V Kartha, Belinda W Cheung, Subbaya Subramanian, Henning Schröder
Journal: Circulation Research (2011)

Low-dose aspirin is recommended for individuals with risk for heart disease and stroke in order to prevent thrombotic occlusive events. In addition to its well-established platelet inhibitory effects, increased expression of the antioxidant heme oxygenase-1 is considered to contribute to cardiovascular protection by aspirin. However little is known about the genome-wide changes in gene expression mediated by aspirin. In order to identify other molecular pathways and targets affected by aspirin, we investigated the global effects of aspirin treatment (3 μM and 100 μM) in vitro in human endothelial cells (Ea.hy 926) using HT-12 bead arrays (Illumina). The filtered genes were further analyzed using Ingenuity Pathway Analysis (IPA) software. We determined the gene expression profiles of endothelial cells treated with aspirin (3 μM and 100 μM) along with vehicle controls. Gene microarray analysis revealed significant upregulation of 134 genes (p &lt;0.005 and &gt;2 fold change) and downregulation of over 100 genes (p &lt;0.005 and ≤0.5 fold change). Interestingly, the pattern of gene expression was similar between the two analyzed concentrations of 3 μM and 100 μM. The majority of upregulated genes were involved in gene expression, transcriptional regulation, cell-to-cell signalling and interaction and encoded transcription factors such as MAP kinases, phosphoinositide-3-kinases and cell cycle regulators (p&lt;0.005). Several components of heterotrimeric G-proteins and G-protein-coupled receptors were also found to be upregulated which can potentially trigger phospholipase C signaling, suggesting an increase in overall intracellular second messenger signaling. In summary, our gene expression analysis suggests that aspirin at low and therapeutically relevant concentrations (3 μM) is effective in triggering cytoprotective signaling pathways some of which play a role in the regulation of heme oxygenase-1. Moreover, our study shows that low-dose aspirin results in altered expression profiles of a variety of genes. Future studies will have to address the biological and clinical relevance of these novel aspirin targets.
Abstract 18846: The Dual Effects of Shear Stress on Vascular Endothelial Autophagy and Mitochondrial DNA Damage
Authors: Nelson Jen, Rongsong Li, Karen Fang, Katherine Quigley, Tyler Beebe, Juhyun Lee, Hung Cao, David Ann, Tzung Hsiai
Journal: Circulation (2013)

Vascular oxidative stress preferentially develops at arterial curvatures and branching points where oscillatory shear stress (OSS) occurs. Autophagy, a tightly regulated intracellular bulk degradation/recycling system, is implicated in endothelial homeostasis. In this study, we assessed the effects of OSS on autophagy and mitochondrial DNA (mtDNA) damage. Human aortic endothelial cells (HAEC) exposed to OSS (τ av g = 0±3 dyne/cm 2 for 4 hours) increased relative LC3-II/LC3-I ratios (control: 1.0±0.02, OSS: 2.4±0.51, p &lt;0.01, n=4), as supported by an increase in autophagosome punctures by LC3-green fluorescence protein (LC3-GFP). OSS-induced increase in LC3-II/LC3-I ratios were significantly attenuated in response to N-acetyl cysteine (NAC), MnSOD over-expression, and JNK siRNA (siJNK) knockdown ( p &lt;0.05, n=4). Inhibition of autophagy by ATG5 siRNA increased OSS-induced MitoSox intensity for mitochondrial superoxide (mtO 2 •- ) by 2.03±0.25-fold ( p &lt; 0.05, n=4), whereas Rapamycin-induced autophagy reduced OSS induced MitoSox intensity by 78.4% ( p &lt;0.05, n=4). OSS-induced reduction of mitochondrial complex II activity was also attenuated in response to Rapamycin (OSS: 62.1±11.2%; Rapamycin+OSS: 130.1±40.4% (relative to static control), p &lt;0.05, n=4). In comparison with static and pulsatile flow (PSS=23 dyne/cm 2 ) conditions, OSS also significantly increased mtDNA damage by 4.5±1.3-fold ( p &lt;0.01, n=4), which was significantly reversed in response to NAC, MnSOD over-expression, and siJNK knockdown ( p &lt;0.05, n=4). In the fat-fed New Zealand White rabbits, quantification for immuno-staining revealed prominent endothelial JNK phosphorylation and DNA damage in the OSS-exposed aortic arch in contrast with nearly absent staining in the PSS-exposed descending aorta ( p &lt; 0.05, n=4). Furthermore, analysis of caspase-3 activity was negative for OSS-exposed HAEC and OSS-exposed aorta area from normal diet-fed animals. Despite atherogenic nature of OSS, our findings suggest that OSS imparts dual effects in endothelial autophagy and mtDNA damage with an implication in maintaining homeostasis.
Phase 1/2a trial of daily oral BAL101553, a novel tumor checkpoint controller (TCC), in advanced solid tumors.
Authors: Rebecca Sophie Kristeleit, T.R. Jeffry Evans, Alvaro Henrique Ingles Garces, Sarah Slater, Yvette Drew, Michael-John Devlin, Noor R Md Haris, Nikolaos Diamantis, Julie MacDonald, Felix Bachmann, Alison L. Hannah, Stephanie Anderson, Heidi A Lane, Anne Schmitt-Hoffmann, Phil McKernan, Marc Frederick Engelhardt, Alastair Greystoke, Rowan Miller, Elizabeth R. Plummer, Juanita Suzanne Lopez
Journal: Journal of Clinical Oncology (2017)

2532 Background: BAL101553 (prodrug of BAL27862) is a small molecule TCC that binds microtubules and promotes tumor cell death by activation of the spindle assembly checkpoint. In a previous study (NCT01397929, Lopez et al. JCO 34, 2016; abstr 2525), 2-h IV infusion on Days 1, 8, 15 (q28d) of BAL101553 up to 80 mg/m 2 (maximum administered dose, MAD) showed vascular toxicities, including transient hypertension, which appeared to be C max related. The recommended Phase 2 dose (RP2D) was 30 mg/m 2 weekly IV. Based on nonclinical models, antiproliferative effects of BAL27862 are driven by AUC. This trial explores whether once daily oral administration of BAL101553 reduces C max -related toxicity and improves the therapeutic window (NCT02490800). Methods: Patients (pts) with advanced solid tumors who failed standard therapy, received QD oral BAL101553 (28-d cycles) in a 3+3 dose-escalation design to determine the MTD. Adverse events were assessed by CTCAEv4 grade (G); tumor response by RECIST 1.1; serial PK on Day 1 of Cycles 1 and 2. Results: In the ongoing study, 19 pts (9M/10F; median age 67 y) received doses of 2, 4, 8, 16 or 30 mg oral BAL101553 QD. The MAD was 30 mg with DLTs of reversible G2 hallucination and asymptomatic, reversible G3 electrolyte imbalances. No DLTs were observed at ≤ 16 mg. Dosing is ongoing between 16 and 30 mg QD to determine the MTD. BAL27862 exposures after oral QD dosing of BAL101553 compared to weekly 2-h infusions suggested high relative oral bioavailability. The BAL27862 weekly AUC at the oral MAD (30 mg QD) compared to the RP2D of 30 mg/m 2 for 2-h IV was more than 5-fold higher (19,656 vs 3,584 ng*h/mL) and C max was 1.5-fold lower (171 vs 266 ng/mL). Both C max and AUC were dose-proportional, with low/moderate variability. Oral BAL101553 had no effects on blood pressure and showed no vascular toxicity. 5 pts had stable disease (2 pts [cholangiocarcinoma, neuroendocrine pancreatic cancer] &gt; 4 cycles). Conclusions: Daily oral BAL101553 enables higher weekly exposures of BAL27862 with lower C max levels compared with a 2-h weekly infusion, due to the absence of C max related vascular toxicity. Doses up to 16 mg QD are well tolerated. The MAD has been identified as 30 mg QD; definition of the MTD is ongoing. Clinical trial information: NCT02490800.
Prevalence of germline cancer susceptibility gene mutations in a consecutive series of 799 colorectal cancer (CRC) patients (pts).
Authors: Matthew B. Yurgelun, Brian Allen, Lauren K. Brais, Philip G. McNamara, Chinedu I. Ukaegbu, Hajime Uno, John Kidd, Nanda Singh, Jason L. Hornick, Richard J. Wenstrup, Charles S. Fuchs, Matthew H. Kulke, Anne-Renee Hartman, Sapna Syngal
Journal: Journal of Clinical Oncology (2016)

1501 Background: Microsatellite instability (MSI) and mismatch repair protein immunohistochemistry (MMR IHC) are standard of care to screen for the 3% of CRCs that arise due to Lynch syndrome (LS). The prevalence of other inherited factors in CRC pts is poorly understood. Methods: 799 consecutive CRC pts who consented to research from 2008-12 while receiving care at the Dana-Farber Cancer Institute underwent germline testing with a 25-gene hereditary cancer panel. The primary outcome was prevalence of pathogenic germline mutations in cancer risk genes. Results: 782 pts had available germline data (mean age at CRC diagnosis 55.6 years), of whom 437 (56%) were male, 19 (2%) had > 1 CRC diagnoses, and 105 (13%) had a history of non-CRC cancer. 78/782 (10.0%; 95% CI 8.0-12.3%) CRC pts had pathogenic germline mutations: 24 (3.1%) with LS; 16 (2.0%) with high penetrance non-LS mutations [5 (0.6%) APC, 3 (0.4%) biallelic MUTYH, 8 (1.0%) other (4 BRCA2, 2 PALB2, 1 CDKN2A, 1 TP53)]; 30 (3.8%) with moderate penetrance CRC gene mutations (15 monoallelic MUTYH, 13 APC I1307K, 2 CHEK2); 10 (1.3%) with other moderate penetrance mutations (5 ATM, 2 BRIP1, 2 NBN, 1 BARD1). 1 pt had both MLH1 and BRCA2 mutations, and 1 had MSH2 and APC I1307K mutations. 278/782 (36%) pts had ≥ 1 germline variant of uncertain significance. Of the 24 pts with LS mutations (9 MLH1, 6 MSH2, 4 MSH6, 5 PMS2), 23 (96%) had PREMM1,2,6 scores ≥ 5% and 19/20 (95%) had abnormal MSI/MMR IHC (4 had missing MSI/MMR IHC data). Compared to pts with no germline mutations, pts with any non-LS mutation were more likely to have > 1 CRC (OR 8.0; 95% CI 2.4-26.3) and somatic KRAS G12C mutations (OR 7.3; 95% CI 2.5-21.8) whereas pts with high penetrance non-LS mutations were more likely to have KRAS G12C mutations (OR 9.4; 95% CI 2.1-42.8). Neither sex, age, race, CRC site, stage, history of non-CRC cancer, nor PREMM1,2,6 score ≥ 5% were associated with presence of any non-LS mutations or high penetrance non-LS mutations. Conclusions: Mutations in non-LS cancer susceptibility genes are found in a substantial number of CRC pts. Although MSI/MMR IHC and PREMM1,2,6 reliably identify CRC pts with LS, the optimal strategy for identifying CRC pts with mutations in non-LS genes is unclear.
GMI-1271, a novel E-selectin antagonist, in combination with chemotherapy in relapsed/refractory AML.
Authors: Daniel J. DeAngelo, Brian Andrew Jonas, Jane Liesveld, Michael O'Dwyer, Dale Bixby, Anjali S. Advani, Paula Marlton, John Magnani, Helen M. Thackray, Pamela S. Becker
Journal: Journal of Clinical Oncology (2017)

2520 Background: GMI-1271 is a novel antagonist of E-selectin (E-sel) that down-regulates cell survival pathways and enhances chemotherapy response. We assessed GMI-1271 plus salvage chemotherapy with mitoxantrone, etoposide, and cytarabine (MEC) for the treatment of patients (pts) with relapsed/refractory (R/R) AML. Methods: A phase (Ph) 1trial in pts with R/R AML escalated GMI-1271 across pharmacologically active doses from 5-20 mg/kg combined with MEC. Safety, tolerability and anti-leukemia activity were assessed. GMI-1271 was given 24 hrs prior, then every 12 hrs during and for 48 hrs post induction/consolidation. Eligible pts had an ECOG score 0-2, received ≤2 prior inductions, WBC &lt; 20K ( &lt; 40K after 2 dose levels), no active CNS disease, and adequate renal/hepatic function. E-sel expression was assessed. After confirming safety and tolerability, a Ph 2 study of GMI-1271 at 10 mg/kg plus MEC was initiated. Results: To date, 47 pts have enrolled (Ph 1 = 19; Ph 2 = 28 of planned 47). The recommended Ph 2 dose is 10 mg/kg based on drug exposure, time over IC50 for E-sel binding, lack of DLT, and clinical outcomes. Ph1/Ph2 combined median age was 55yrs (range 26-84) with 70% male pts. Prior AML history included 26% primary refractory, 36% CR1 &lt; 6 mos; 17% prior SCT; 55% unfavorable cytogenetics (by SWOG). Common Gr 3/4 AEs were febrile neutropenia (36%), sepsis (26%), bacteremia (13%), hypoxia (13%). 30 and 60 d mortality were 0 and 7%, respectively. ORR (CR/CRi/MLFS/PR) was 21/42 evaluable (50%). Remission rate (CR/CRi) was 45%. Observed/expected remission (CR/CRi) ratio was &gt; 2.75 (Estey, Blood 1996). With a median follow-up of 11 mos, the Ph 1 median Leukemia Free Survival was not reached and Overall Survival was 7.6 mos. The median E-sel ligand binding at baseline was 35% of blasts (range, 1-75%) and was higher in those achieving remission. Conclusions: The addition of GMI-1271, a novel E-sel antagonist, to MEC chemotherapy is well tolerated with a high ORR, low induction mortality, and promising initial survival outcomes in pts with R/R AML. Furthermore, the baseline expression of E-sel ligand is predictive of response. Clinical trial information: NCT02306291.
Treatment related issues in breast cancer survivors among Nepalese.
Authors: Sachin Shakya
Journal: Journal of Clinical Oncology (2016)

e12523 Background: The increasing number of breast cancer survivors makes the issues arising after treatment more relevant for the quality of life of these patients. Methods: Breast cancer patients who had completed treatment for more than 1 year were included. A survey was developed to assess socio-demographic and medical characteristics, menstrual status, hair loss and lymphedema. Breast cancer patients who had registered in Nepal Cancer Support Group,an NGO working to provide supportive services to cancer patients, were invited to take part in the study. Data has been presented using descriptive statistics. Results: Fifty eligible respondents completed the survey. Mean age at breast cancer diagnosis was 44.84± 8.03. Eighty-eight percent of the patients were married. Patients were in stage I: 44%, stage II: 44% and stage III: 12% during diagnosis. Majority had undergone surgery + chemotherapy + radiotherapy (78%) and33 out of 50 had undergone mastectomy. Thirty-nine were menstruating before starting chemotherapy. During chemotherapy, 32 out of 39 reported absence of menstruation. Out of those 32, 18 of them reported absence of menstruation after the first cycle of chemotherapy and 8 of them reported absence of menstruation after the second cycle of chemotherapy. Among 32 normally menstruating earlier, 26 didn’t menstruate after chemotherapy. Upon asking about their body image, 40% of them said they don’t feel any difference, 26% of them said, they feel uneasy, while one said, she feels it’s all because of her KARMA. Most of them stated, hair that grew back was same as before (42%), 24% of them reported having curly hair.Thirty out of 50 reported lymphedema. Forty-eight out of 50 informed following all the precautions that their doctors instructed and 30 exercised their arm regularly. Fear of relapse was perceived by 56%. Conclusions: The issues highlighted by this study may be helpful to clinicians in their interactions with patients.
High Frequency of Somatic Mutations of KMT2D and CARD11 Genes in Cold Agglutinin Disease
Authors: Agnieszka Malecka, Gunhild Trøen, Anne Tierens, Ingunn Østlie, Jedrzej Malecki, Ulla Randen, Sigbjørn Berentsen, Geir E. Tjønnfjord, Jan M.A. Delabie
Journal: Blood (2016)