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  • American Association for Cancer Research (AACR)  (25)
  • English  (25)
  • 1
    In: Cancer Prevention Research, American Association for Cancer Research (AACR), Vol. 14, No. 2 ( 2021-02-01), p. 215-222
    Abstract: Juvenile polyposis syndrome (JPS) is a clinically diagnosed hamartomatous polyposis syndrome that increases the risk of gastrointestinal cancer. Approximately 40%–50% of JPS is caused by a germline disease-causing variant (DCV) in the SMAD4 or BMPR1A genes. The aim of this study was to characterize the phenotype of DCV-negative JPS and compare it with DCV-positive JPS. Herein, we analyzed a cohort of 145 individuals with JPS from nine institutions, including both pediatric and adult centers. Data analyzed included age at diagnosis, family history, cancer history, need for colectomy/gastrectomy, and polyp number and location. Compared with DCV-positive JPS, DCV-negative JPS was associated with younger age at diagnosis (P & lt; 0.001), lower likelihood of having a family history of JPS (P & lt; 0.001), and a lower risk of colectomy (P = 0.032). None of the DCV-negative individuals had gastric or duodenal polyps, and polyp burden decreased after the first decade compared with DCV-positive JPS. Subgroup analysis between SMAD4 and BMPR1A carriers showed that SMAD4 carriers were more likely to have a family history of JPS and required gastrectomy. Taken together, these data provide the largest phenotypic characterization of individuals with DCV-negative JPS to date, showing that this group has distinct differences compared with JPS due to a SMAD4 or BMPR1A variant. Better understanding of phenotype and cancer risk associated with JPS both with and without a DCV may ultimately allow for individualized management of polyposis and cancer risk. Prevention Relevance: Juvenile Polyposis Syndrome (JPS) is a gastrointestinal cancer predisposition syndrome requiring lifelong surveillance, however there is limited data comparing individuals with and without a germline disease-causing variant in SMAD4 or BMPR1A. Herein we show that individuals with JPS without an underlying disease-causing variant have distinct phenotypic differences including lack of upper gastrointestinal polyps and lower rates of a family history of JPS, suggesting that a different approach to management may be appropriate in this population.
    Type of Medium: Online Resource
    ISSN: 1940-6207 , 1940-6215
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2021
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  • 2
    In: Cancer Prevention Research, American Association for Cancer Research (AACR), Vol. 13, No. 3 ( 2020-03-01), p. 291-298
    Abstract: Prior small reports have postulated a link between gastrointestinal polyposis and childhood and young adulthood cancer (CYAC) treatment (therapy-associated polyposis; TAP), but this remains a poorly understood phenomenon. The aim of this study was to describe the phenotypic spectrum of TAP in a multi-institutional cohort. TAP cases were identified from eight high-risk cancer centers. Cases were defined as patients with ≥10 gastrointestinal polyps without known causative germline alteration or hereditary colorectal cancer predisposition syndrome who had a history of prior treatment with chemotherapy and/or radiotherapy for CYAC. A total of 34 TAP cases were included (original CYAC: 27 Hodgkin lymphoma, three neuroblastoma, one acute myeloid leukemia, one medulloblastoma, one nephroblastoma, and one non-Hodgkin lymphoma). Gastrointestinal polyposis was first detected at a median of 27 years (interquartile range, 20–33) after CYAC treatment. A total of 12 of 34 (35%) TAP cases had ≥50 colorectal polyps. A total of 32 of 34 (94%) had & gt;1 histologic polyp type. A total of 25 of 34 (74%) had clinical features suggestive of ≥1 colorectal cancer predisposition syndrome [e.g., attenuated familial adenomatous polyposis (FAP), serrated polyposis syndrome, extracolonic manifestations of FAP, mismatch repair–deficient colorectal cancer, or hamartomatous polyposis] including 8 of 34 (24%) with features of multiple such syndromes. TAP is an apparently acquired phenomenon that should be considered in patients who develop significant polyposis without known causative germline alteration but who have had prior treatment for a CYAC. Patients with TAP have features that may mimic various hereditary colorectal cancer syndromes, suggesting multiple concurrent biologic mechanisms, and recognition of this diagnosis may have implications for cancer risk and screening.
    Type of Medium: Online Resource
    ISSN: 1940-6207 , 1940-6215
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2020
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  • 3
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 81, No. 4_Supplement ( 2021-02-15), p. PS17-23-PS17-23
    Abstract: Organoid cultures are being explored as intermediate preclinical models in numerous cancer types including colon, liver and brain. Recently it has been demonstrated that organoids can be robustly isolated and cultured from breast cancer subtypes, that they maintain the histological, genomic and transcriptomic signatures of the primary tumor tissue, and that ER expression can be preserved (Sachs et al, 2018). The Institute for Precision Medicine (IPM), a collaboration between UPMC and the University of Pittsburgh initiated a program to develop breast cancer organoids in 2018. The IPM works closely with surgeons to consent patients with primary or metastatic breast cancer for tissue collection, and with an institutional biospecimen core for tissue procurement and deidentification. The IPM receives fresh, deidentified tissue typically within 60 minutes of the patient’s operation. Based on the protocol by Sachs et al, to date we have established 49 organoids from a total of 60 tumor samples received from patients undergoing resection of their primary or metastatic breast tumor, resulting in a success rate of 82%. Our current collection includes organoids from 17 treatment-naïve invasive ductal carcinomas, 12 treatment-naïve invasive lobular carcinomas, 10 primary tumors excised after neoadjuvant therapy and 5 from breast cancer metastasized to bone or ovary. Our organoids demonstrate a range of growth morphologies, consistent with those previously described. ER expression can be detected in a subset of our cultures as well as robust response to estradiol as indicated by the induction of GREB1 gene expression. We have further demonstrated that organoids are amenable to transient transfection of siRNA and lentiviral infection of reporter constructs which allows for RFP and luciferase-based detection of cells both in vitro and in vivo as well as expression of genes of interest. We additionally recognized that some of our organoid cultures can give rise to suspension cultures when maintained in organoid culture medium but without 3D matrix. This observation allows the opportunity for further phenotypic evaluation by increasing the number of assays amenable to these unique patient derived cultures. Single cell RNA sequencing (10X Genomics) of organoid cultures and paired tumor tissue confirms that organoid cultures faithfully maintain the heterogeneity of epithelial subpopulations found in the surgically resected tumors. Further, organoids show greater epithelial diversity and heterogeneity compared to single cell sequencing of breast cancer cell lines. We have further used sequencing data to identify targetable pathways in individual organoid cultures and demonstrate that drug sensitivity can be correlated with gene expression in these models. Collectively, these data indicate that breast cancer organoids represent a valuable model for preclinical breast cancer research. Citation Format: Daniel D Brown, Kai Ding, Fangyuan Chen, Jian Chen, Brian Orr, Sarah Taylor, Kurt Weiss, Steffi Oesterreich, Peter C Lucas, Priscilla F McAuliffe, Jennifer M Atkinson, Adrian V Lee. Development of a breast cancer organoid resource faithfully representing epithelial heterogeneity and drug response [abstract]. In: Proceedings of the 2020 San Antonio Breast Cancer Virtual Symposium; 2020 Dec 8-11; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2021;81(4 Suppl):Abstract nr PS17-23.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
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    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2021
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  • 4
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 82, No. 12_Supplement ( 2022-06-15), p. 81-81
    Abstract: Occurring in 65-80% of metastatic breast cancer (BC), bone metastasis (BoM) is the major cause of BC related mortality. Lack of understanding of BoM evolution and heterogeneity at patient specific levels and precise application of targeted therapies are major challenges of managing BoM. In this study, we described in depth histologic and molecular characterization of a case of invasive lobular breast cancer (ILC) bilateral metastasis to bone, and identified and tested potential targets for treating BoM. H & E/IHC staining, whole exome sequencing (WES), and RNAseq were performed on FFPE primary tumor and pelvis and tibia BoMs collected from our study case. Organoids were derived from the two BoMs and single cell RNA sequencing (scRNAseq) undertaken on the organoids and their originating tumors. H & E/IHC demonstrated evolution of the disease from an ER+ primary ILC to ER- BoM with mixed lobular and ductal carcinoma features. WES revealed two druggable mutations including PIK3CA (E545K) and BRCA1 (D1813H/H399P). RNAseq revealed upregulation of TGF-β, Wnt/beta-catenin and PI3K pathways, epithelial to mesenchymal transition (EMT) and angiogenesis in BoM compared to primary tumor, representing promising targets for BoM. scRNAseq revealed 5 major cell types including epithelial, fibroblasts, immune, osteoclasts and endothelial cells, and pronounced intracellular heterogeneity. Six epithelial clusters were identified, featuring high TNF-α signaling, high partial EMT signatures regulated by PRRX1/2, TWIST1/2, and FOXS1, high proliferation, and endocrine resistance signatures. In fibroblasts, 9 clusters were identified representing ECM remodeling, angiogenesis, osteoclast-like, MSC, IFN response and myofibroblasts. Immune cells majorly composed of monocytes/macrophages, CD4+, CD8+ and Treg T cells, and NK cell. WES and scRNAseq analysis demonstrated that organoids preserved mutational landscape and cellular heterogeneity of matched BoMs. Consistent with the BRCA1 and PIK3CA mutations, organoids were responsive to a PARP (Talazoparib: IC50 1.3uM) and PI3K (Alpelisib: IC50 4-9uM) inhibitors. In summary, we have identified potential therapeutic targets from understanding evolution and heterogeneity of BC BoM, and evaluated these in patient-specific organoids, thereby providing insights for the design of a precision medicine based clinical treatment strategy. Citation Format: Kai Ding, Fangyuan Chen, Nolan Priedigkeit, Daniel D. Brown, Tanya Heim, Rebecca Watters, Kurt Weiss, Peter C. Lucas, Jennifer M. Atkinson, Steffi Oesterreich, Adrian V. Lee. In depth single cell profiling of a case of breast cancer bone metastases with associated organoid models reveal a precision medicine approach to treatment [abstract] . In: Proceedings of the American Association for Cancer Research Annual Meeting 2022; 2022 Apr 8-13. Philadelphia (PA): AACR; Cancer Res 2022;82(12_Suppl):Abstract nr 81.
    Type of Medium: Online Resource
    ISSN: 1538-7445
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2022
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  • 5
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 72, No. 8_Supplement ( 2012-04-15), p. 1029-1029
    Abstract: Excess body weight is a known risk factor for endometrial cancer but whether it differentially affects histological subtypes of endometrial cancer is unclear. The two proposed main subtypes are the “estrogen-dependent Type I” and “non estrogen-dependent and clinically aggressive Type II”. Little is known about risk factors for Type II tumors mainly because most epidemiologic studies lack sufficient cases to study these rare tumors separately. Here we examined the association between recent adult body mass index (BMI) and endometrial tumor subtypes in a pooled analysis of 25 studies in the Epidemiology of Endometrial Cancer Consortium (E2C2). Individual-level data from 10 cohort studies and 15 case-control studies provided a total of 14,409 endometrial cancer cases and 35,950 controls for this analysis. Cohort studies were analyzed using a nested case-control design. The majority of women were white (86%) and postmenopausal (83%). Endometrial cancer cases were classified into two subtypes: Type I (endometrioid adenocarcinomas, adenocarcinoma tubular, papillary adenocarcinomas, mucinous adenocarcinomas, adenocarcinomas with squamous metaplasia, n=13,286) and Type II (serous, squamous cell, small cell, mixed cell, n=1,123). The associations of BMI with the risk of tumor subtypes were evaluated by calculating odds ratios (OR) and 95% confidence intervals (95% CI) using polytomous logistic regression models. Potential confounders included in the analysis were age, race, parity, age at menarche, oral contraceptive (OC) use, menopausal hormone (PMH) use, and smoking status. BMI was positively associated with both Type I and Type II tumors, but the association was stronger for Type I than for Type II tumors (P value for the difference in OR between Type I and Type II was & lt;0.0001). The OR associated with each five kg/m2 increase in BMI (OR5) was 1.58 (95% CI: 1.55, 1.62) for Type I and 1.35 (95% CI: 1.28, 1.42) for Type II. In the analysis of individual histologic types, the OR5 was lowest for serous tumors (1.28), moderate for mixed cell and clear cell (1.33-1.37), and highest for endometrioid tumors (1.60) and various adenocarcinoma groups (1.54-1.58). The associations of BMI with both Type I and II tumors were greater among postmenopausal women who never used PMH [OR5 = 1.84 (95% CI: 1.78, 1.89) for Type I and 1.48 (95% CI: 1.38, 1.58) for Type II] than among estrogen-only users [OR5 = 1.20 (95% CI: 1.13, 1.28) for Type I and 1.05 (95% CI: 0.87, 1.26) for Type II] or among estrogen-progestin users [OR5 = 1.33 (95% CI: 1.25, 1.41) for Type I and 1.12 (95% CI: 0.95, 1.33) for Type II]. Other known endometrial cancer risk factors such as OC use, parity, and smoking did not appear to modify the association between BMI and tumor subtype. In this large pooled analysis, we observed that BMI is a risk factor for all types of endometrial cancer, although, the association is consistently stronger for Type I than for Type II tumors. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 1029. doi:1538-7445.AM2012-1029
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
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    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2012
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  • 6
    Online Resource
    Online Resource
    American Association for Cancer Research (AACR) ; 2005
    In:  Cancer Epidemiology, Biomarkers & Prevention Vol. 14, No. 11 ( 2005-11-01), p. 2524-2530
    In: Cancer Epidemiology, Biomarkers & Prevention, American Association for Cancer Research (AACR), Vol. 14, No. 11 ( 2005-11-01), p. 2524-2530
    Abstract: Exposure to estrogens is a likely cause of endometrial cancer, but the means by which estrogens exert this effect are not entirely clear. One hypothesis is that certain estrogen metabolites bind to the DNA, forming bulky adducts that damage the DNA and initiate carcinogenesis. A woman's reduced capacity to repair such damage may increase her risk of endometrial cancer. We conducted a population-based case-control study in western Washington State to address the role of variation in nucleotide excision repair genes on the risk of endometrial cancer. Case women (n = 371), ages 50 to 69 years, were diagnosed with invasive endometrial cancer between 1994 and 1999. Control women (n = 420) were selected using random-digit dialing (ages 50-65 years) and by random selection from Health Care Financing Administration data files (ages 66-69 years). Genotyping assays were done for ERCC1, ERCC2 (XPD), ERCC4 (XPF), ERCC5 (XPG), XPA, and XPC. No appreciable differences between cases and controls were observed in the genotype distributions of ERCC1 (c8092a and c19007t), ERCC2 (D312N, K751Q, and c22541a), ERCC4 (R415Q and t30028c), or ERCC5 (D1104H). Carriage of at least one variant allele for XPA G23A was associated with decreased risk of endometrial cancer [odds ratio (OR), 0.70; 95% confidence interval (95% CI), 0.53-0.93]. Carriage of at least one XPC A499V variant allele was associated with a modest decrease in risk (OR, 0.79; 95% CI, 0.59-1.05). Women with variant alleles at both XPC A499V and K939Q had 58% of the risk of women with no XPC variant alleles (OR, 0.58; 95% CI, 0.35-0.96). Our data suggest that interindividual variation in XPA and XPC influences a woman's risk of endometrial cancer.
    Type of Medium: Online Resource
    ISSN: 1055-9965 , 1538-7755
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2005
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  • 7
    In: Cancer Epidemiology, Biomarkers & Prevention, American Association for Cancer Research (AACR), Vol. 29, No. 5 ( 2020-05-01), p. 910-917
    Abstract: The Center to Reduce Cancer Health Disparities (CRCHD), National Cancer Institute (NCI), launched Screen to Save, NCI's Colorectal Cancer Outreach and Screening Initiative to promote awareness and knowledge of colorectal cancer in racial/ethnic and rural populations. Methods: The initiative was implemented through CRCHD's National Outreach Network (NON) and Comprehensive Partnerships to Advance Cancer Health Equity (CPACHE) programs. NON is a national network of Community Health Educators (CHEs), aligned with NCI-designated Cancer Centers (CCs). CPACHE are partnerships between a CC and a minority-serving institution with, among other components, an Outreach Core and a CHE. In phases I and II, the CHEs disseminated cancer-related information and implemented evidence-based educational outreach. Results: In total, 3,183 pre/post surveys were obtained from participants, ages 50 to 74 years, during 347 educational events held in phase I. Results demonstrated all racial/ethnic groups had an increase in colorectal cancer-related knowledge, and each group agreed that the educational event increased the likelihood they would engage in colorectal cancer-related healthful behaviors. For phase II, Connections to Care, participants were linked to screening. Eighty-two percent of participants who were screened during the follow-up period obtained their results. Conclusions: These results suggest that culturally tailored, standardized educational messaging and data collection tools are key elements that can serve to inform the effectiveness of educational outreach to advance awareness and knowledge of colorectal cancer. Impact: Future initiatives should focus on large-scale national efforts to elucidate effective models of connections to care related to colorectal cancer screening, follow-up, and treatments that are modifiable to meet community needs.
    Type of Medium: Online Resource
    ISSN: 1055-9965 , 1538-7755
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2020
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  • 8
    In: Clinical Cancer Research, American Association for Cancer Research (AACR), Vol. 27, No. 5 ( 2021-03-01), p. 1278-1286
    Abstract: Immunotherapy is currently ineffective for nearly all pancreatic ductal adenocarcinomas (PDAC), largely due to its tumor microenvironment (TME) that lacks antigen-experienced T effector cells (Teff). Vaccine-based immunotherapies are known to activate antigen-specific Teffs in the peripheral blood. To evaluate the effect of vaccine therapy on the PDAC TME, we designed a neoadjuvant and adjuvant clinical trial of an irradiated, GM-CSF-secreting, allogeneic PDAC vaccine (GVAX). Patients and Methods: Eighty-seven eligible patients with resectable PDAC were randomly assigned (1:1:1) to receive GVAX alone or in combination with two forms of low-dose cyclophosphamide. Resected tumors following neoadjuvant immunotherapy were assessed for the formation of tertiary lymphoid aggregates (TLA) in response to treatment. The clinical endpoints are disease-free survival (DFS) and overall survival (OS). Results: The neoadjuvant treatment with GVAX either alone or with two forms of low-dose cyclophosphamide is safe and feasible without adversely increasing the surgical complication rate. Patients in Arm A who received neoadjuvant and adjuvant GVAX alone had a trend toward longer median OS (35.0 months) than that (24.8 months) in the historical controls who received adjuvant GVAX alone. However, Arm C, who received low-dose oral cyclophosphamide in addition to GVAX, had a significantly shorter DFS than Arm A. When comparing patients with OS & gt; 24 months to those with OS & lt; 15 months, longer OS was found to be associated with higher density of intratumoral TLA. Conclusions: It is safe and feasible to use a neoadjuvant immunotherapy approach for PDACs to evaluate early biologic responses. In-depth analysis of TLAs is warranted in future neoadjuvant immunotherapy clinical trials.
    Type of Medium: Online Resource
    ISSN: 1078-0432 , 1557-3265
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    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2021
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  • 9
    In: Clinical Cancer Research, American Association for Cancer Research (AACR), Vol. 24, No. 21 ( 2018-11-01), p. 5347-5356
    Abstract: Purpose: We have shown that the aged microenvironment increases melanoma metastasis, and decreases response to targeted therapy, and here we queried response to anti-PD1. Experimental Design: We analyzed the relationship between age, response to anti-PD1, and prior therapy in 538 patients. We used mouse models of melanoma, to analyze the intratumoral immune microenvironment in young versus aged mice and confirmed our findings in human melanoma biopsies. Results: Patients over the age of 60 responded more efficiently to anti-PD-1, and likelihood of response to anti-PD-1 increased with age, even when we controlled for prior MAPKi therapy. Placing genetically identical tumors in aged mice (52 weeks) significantly increased their response to anti-PD1 as compared with the same tumors in young mice (8 weeks). These data suggest that this increased response in aged patients occurs even in the absence of a more complex mutational landscape. Next, we found that young mice had a significantly higher population of regulatory T cells (Tregs), skewing the CD8+:Treg ratio. FOXP3 staining of human melanoma biopsies revealed similar increases in Tregs in young patients. Depletion of Tregs using anti-CD25 increased the response to anti-PD1 in young mice. Conclusions: While there are obvious limitations to our study, including our inability to conduct a meta-analysis due to a lack of available data, and our inability to control for mutational burden, there is a remarkable consistency in these data from over 500 patients across 8 different institutes worldwide. These results stress the importance of considering age as a factor for immunotherapy response. Clin Cancer Res; 24(21); 5347–56. ©2018 AACR. See related commentary by Pawelec, p. 5193
    Type of Medium: Online Resource
    ISSN: 1078-0432 , 1557-3265
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    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2018
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  • 10
    In: Cancer Discovery, American Association for Cancer Research (AACR), Vol. 10, No. 3 ( 2020-03-01), p. 394-405
    Abstract: Acalabrutinib is a selective irreversible Bruton tyrosine kinase (BTK) inhibitor that does not affect IL2-associated tyrosine kinase or antibody-dependent cellular cytotoxicity, making it an attractive candidate for combination therapy with anti-CD20 antibodies. We investigated acalabrutinib plus obinutuzumab in a phase Ib/II study (NCT02296918) of patients with treatment-naïve or relapsed/refractory chronic lymphocytic leukemia (CLL). Nineteen treatment-naïve and 26 relapsed/refractory patients were treated with acalabrutinib (100 mg twice daily) until progression and obinutuzumab (cycle 1: 100 mg day 1, 900 mg day 2, 1000 mg days 8 and 15; cycles 2–6: 1,000 mg day 1). Grade 3/4 adverse events occurred in 71% of patients. Overall response rates were 95% (treatment-naïve) and 92% (relapsed/refractory). Thirty-two percent of treatment-naïve and 8% of relapsed/refractory patients achieved complete remission. At 36 months, 94% (treatment-naïve) and 88% (relapsed/refractory) were progression free. Acalabrutinib plus obinutuzumab was well tolerated, producing high and durable responses in treatment-naïve and relapsed/refractory CLL. Significance: Rituximab plus the less selective BTK inhibitor ibrutinib has not shown benefit in CLL; however, the selective BTK inhibitor acalabrutinib plus the antibody-dependent cellular cytotoxicity–enhanced antibody obinutuzumab yielded durable responses that deepened over time in treatment-naïve and relapsed/refractory CLL, supporting the evaluation of this approach in larger, comparative studies in CLL. This article is highlighted in the In This Issue feature, p. 327
    Type of Medium: Online Resource
    ISSN: 2159-8274 , 2159-8290
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2020
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