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  • 1
    In: Journal of Clinical Oncology, American Society of Clinical Oncology (ASCO), Vol. 41, No. 16_suppl ( 2023-06-01), p. e16299-e16299
    Abstract: e16299 Background: Pancreatic adenocarcinoma (PDAC) is associated with poor survival and low response rates to available therapies, warranting a critical need for new treatment paradigms. Enrichment of tumor epithelium via laser microdissection (LMD) prior to reverse phase protein array (RPPA) analysis allows for the quantitative measurement and functional assessment of the activation state of protein drug targets. As part of an IRB-approved Molecular Tumor Board study at Inova Schar Cancer Institute, we harvested enriched tumor epithelium using LMD to support CLIA-based RPPA analysis of patients with pancreatic, breast, and other solid tumor malignancies to examine quantitative expression and activation (phosphorylation) of HER-2/3 and other known cancer-related pathways. Methods: Formalin fixed paraffin embedded (FFPE) primary and/or metastatic tumor biopsy specimens were obtained from 14 patients with PDAC, 14 patients with breast cancer, and 40 patients with other solid tumor malignancies. Tumor epithelium (5-10 µm 2 ) was enriched via LMD prior to RPPA analysis for quantification of HER-2 Total and phosphorylated (p)HER-2 Y1248 and (p)HER-3 Y1289 abundances as part of a 32-marker, CLIA-based RPPA panel examining the total and phosphoprotein abundances of targets with known relevance in solid tumors. Next generation sequencing (NGS; DNA-seq and RNA-seq) was performed on remaining tissue from each specimen. Fisher’s Exact test was used to compare activated HER2 Total , pHER2 Y1248 and pHER3 Y1289 . Results: RPPA analysis of LMD enriched tumor samples revealed significant HER-2 Total expression in patients with PDAC vs other solid tumors (p=0.0112), with HER-2 Total levels comparable to those measured in patients with breast cancer (p=0.0962). The mean HER-2 Total abundances in PDAC, breast, and all other solid tumor malignancies were 1.6, 1.3, and 0.9, respectively. Activated pHER-2 Y1248 and pHER-3 Y1289 abundances did not differ between patients with PDAC vs all other solid tumors or between patients with PDAC vs breast cancer (p 〉 0.05). RNA-seq analysis revealed ERBB2 overexpression in four of the 14 PDAC patients, while ERBB2 amplification by DNA-seq was not observed in any of the PDAC cases. Conclusions: HER-2 expression is not routinely evaluated in clinical practice in PDAC, but our results show higher median expression in PDAC than our solid tumor cohort, with nearly 50% of PDAC cases having total HER2 expression of 2+ or above. Our results may have clinical implications, especially as new classes of HER2 antibody drug conjugates are considered for patients with HER2 non amplified tumors across organ sites, and justify further investigation in a larger cohort. Clinical trial information: U20-11-4308 . [Table: see text]
    Type of Medium: Online Resource
    ISSN: 0732-183X , 1527-7755
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    Language: English
    Publisher: American Society of Clinical Oncology (ASCO)
    Publication Date: 2023
    detail.hit.zdb_id: 2005181-5
    detail.hit.zdb_id: 604914-X
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  • 2
    In: Journal of Clinical Oncology, American Society of Clinical Oncology (ASCO), Vol. 41, No. 16_suppl ( 2023-06-01), p. 10518-10518
    Abstract: 10518 Background: Mismatch repair deficiency (MMRd) occurs in ~15% of colorectal (CRC) and ~30% of endometrial (EC) cancers, of which ~20% are caused by Lynch syndrome (LS). Universal screening of all incident CRC and EC for MMRd uses MLH1 methylation (in tumors with MLH1-loss by immunohistochemistry) to omit common sporadic cases from follow-up germline testing for LS. However, this overlooks unusual cases with constitutional MLH1 methylation (epimutation), a poorly-recognized high-risk mechanism for LS-type cancers that are MLH1 methylated. We aimed to determine the role and prevalence of constitutional MLH1 methylation among CRC and EC cases with tumor MLH1 methylation from clinical and population-based series and if age limits could be used to triage cases warranting additional germline methylation testing. Methods: We screened blood DNA for constitutional MLH1 methylation by pyrosequencing and methylation-specific qPCR in patients with MLH1-loss, MLH1 methylated CRC and EC ascertained from: i) cancer clinics, referred by oncologists and genetic counsellors; ii) Ohio population-based “Columbus” and “OCCPI” cohorts. Bisulfite sequencing confirmed constitutional MLH1 methylation. Results: In clinical cases, constitutional MLH1 methylation was identified in 3/7 EC and 3/8 CRC cases 〈 60 years. In population-based cohorts, constitutional MLH1 methylation was identified in 4/95 (4.2%) and 4/281 (1.4%) CRC cases of all ages from Columbus and OCCPI, respectively. Highest rates of detection with the majority of cases detected were at age ≤55 years, with 3/4 (75%) in Columbus and 4/17 (23.5%) in OCCPI ≤55 years. For EC, constitutional MLH1 methylation was identified in 0/68 Columbus cases of all ages and 1/24 OCCPI cases 〈 60 years (age-limited testing). She was one of six (~17%) cases 〈 50 years in the combined cohorts. EC was the first/dual-first presenting “sentinel” cancer in three female patients with constitutional MLH1 methylation. Of the 14 cases with constitutional MLH1 methylation, nine had hemiallelic methylation (~50% alleles methylated, affecting a single parental allele) and five had mosaicism across various normal tissues. Somatic “second-hits” affecting the unmethylated allele were found in the tumors of mosaic cases, demonstrating causation. Conclusions: A correct diagnosis of constitutional MLH1 methylation at first cancer presentation is important as it will significantly alter clinical management of these high-risk patients. Although rare overall, high rates of detection were found ≤55 years for CRC and ≤50 years for EC cases with a MMRd, MLH1 methylated tumor, entailing minimal extra screening. Testing for constitutional MLH1 methylation is warranted in patients with young-onset CRC or EC, or syn/metachronous cancers at any age, with MMRd and MLH1 methylated tumor(s).
    Type of Medium: Online Resource
    ISSN: 0732-183X , 1527-7755
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    Language: English
    Publisher: American Society of Clinical Oncology (ASCO)
    Publication Date: 2023
    detail.hit.zdb_id: 2005181-5
    detail.hit.zdb_id: 604914-X
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  • 3
    In: Journal of Clinical Oncology, American Society of Clinical Oncology (ASCO), Vol. 42, No. 3_suppl ( 2024-01-20), p. 698-698
    Abstract: 698 Background: Several Wnt pathway genes (RNF43, GNAS, CTNNB1, APC) are mutated in PDAC but their clinical implications remain unclear. Both RNF43, a membrane E3 ubiquitin ligase that negatively regulates Wnt via FZD, and GNAS, a mediator of GPCR signaling, are enriched in IPMN-associated PDAC whereas CTNNB1 is a hallmark of solid pseudopapillary neoplasms. Here, we retrospectively analyzed progression-free survival (PFS) and overall survival (OS) in a PDAC cohort to understand potential therapeutic and prognostic differences between tumors with (MUT) or without (WT) Wnt pathway mutations. Methods: We analyzed longitudinal outcomes across 774 patients (pts) with NGS results from Perthera’s Real-World Evidence database who received at least 1 line of therapy in the advanced setting for PDAC. PFS was evaluated from initiation of 1st line for advanced disease until discontinuation due to disease progression. Hazard ratios and p-values were computed via Cox regression when comparing PFS within subsets that received either 1st line FOLFIRINOX (FFX) or 1st line gemcitabine/nab-paclitaxel (GA). Differences in frequencies of genomic alterations outside the Wnt pathway were analyzed by Fisher’s exact test. Results: Within the analysis cohort (N = 774), Wnt pathway alterations were present in 72 (9.3%) of PDAC tumors based on mutations in either RNF43 (4%), GNAS (3%), CTNNB1 ( 〈 1%), or APC (2%). Median OS (relative to advanced diagnosis) was significantly longer in the MUT subgroup compared to WT (Table). Median PFS on 1st line GA was significantly longer in MUT pts, and a similar insignificant trend was noted for PFS on 1st line FFX (Table). MSI-high and PIK3CA mutations were enriched for co-occurrence with Wnt pathway alterations whereas common PDAC mutations in KRAS and TP53 were less frequent in MUT pts (Table). Gene-specific trends and potential confounders will be discussed in the context of multivariate OS/PFS analyses. Conclusions: The presence of Wnt pathway alterations identifies a subgroup of advanced PDAC with improved PFS and OS.[Table: see text]
    Type of Medium: Online Resource
    ISSN: 0732-183X , 1527-7755
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    Language: English
    Publisher: American Society of Clinical Oncology (ASCO)
    Publication Date: 2024
    detail.hit.zdb_id: 2005181-5
    detail.hit.zdb_id: 604914-X
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  • 4
    Online Resource
    Online Resource
    American Society of Clinical Oncology (ASCO) ; 2023
    In:  Journal of Clinical Oncology Vol. 41, No. 16_suppl ( 2023-06-01), p. e18582-e18582
    In: Journal of Clinical Oncology, American Society of Clinical Oncology (ASCO), Vol. 41, No. 16_suppl ( 2023-06-01), p. e18582-e18582
    Abstract: e18582 Background: The Inova Schar Cancer Institute Molecular Tumor Board (ISCI MTB) is a multi-disciplinary group that meets biweekly to discuss molecular test results for patients with advanced cancer to inform potential targeted therapy and clinical trial options. Previous work analyzing the racial distribution of patients in the ISCI MTB compared to the institutional cancer registry (CR) demonstrated that self-identified Black/African American patients were under-represented in the MTB. We next sought to evaluate the association between race and the implementation of MTB-recommended therapy. Methods: We evaluated ISCI MTB records from 1/1/16 to 12/31/21 and identified patients with at least one treatment recommendation informed by molecular biomarker results, including clinical trials, targeted medications, immunotherapy, and chemotherapy. Patient data were extracted from the EMR using the Epic Slicer/Dicer Tool and integrated with the MTB REDCap database. Manual chart review was used to fill missing data and identify patients for whom at least one MTB recommendation was implemented. Recommendation implementation was defined as treatment with or prescription of a recommended therapy or evaluation for a clinical trial. Results: 244 of 530 patients (46%) had one or more MTB recommendations implemented. There was no clear distinction in age at MTB presentation (64 vs 65) or sex (45% of males and 47% of females vs 55% of males and 53% of females) between patients who had recommendations implemented and those who did not. 45% of White/Caucasian, 41% of Asian, 56% of Black/African American, and 58% of Hispanic/Latino patients had MTB recommendations implemented. No statistically significant differences in implementation of recommendations were observed for age, sex, or race. Conclusions: Fewer than half of patients with advanced cancer receive biomarker-directed or investigational therapies recommended by an institutional MTB. White and Asian patients are less likely than Black/African American and Hispanic/Latino patients to be treated with MTB-recommended therapy, although these differences did not reach statistical significance. Further investigation of confounding variables including payor status and care fragmentation is necessary to clarify potential disparities and barriers to accessing innovative cancer care.
    Type of Medium: Online Resource
    ISSN: 0732-183X , 1527-7755
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    Language: English
    Publisher: American Society of Clinical Oncology (ASCO)
    Publication Date: 2023
    detail.hit.zdb_id: 2005181-5
    detail.hit.zdb_id: 604914-X
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  • 5
    In: Journal of Clinical Oncology, American Society of Clinical Oncology (ASCO), Vol. 40, No. 16_suppl ( 2022-06-01), p. 10581-10581
    Abstract: 10581 Background: MSI-H colorectal cancer is most often a result of deleterious mutations in mismatch repair genes, but can also occur through repressed gene transcription due to hypermethylation of the MLH1 promoter, often associated with BRAF V600E mutations. However, there is a subset of patients who have a “constitutional epimutation”, resulting in hypermethylation of MLH1 throughout normal tissue. We observed a young patient develop a second primary Lynch associated malignancy (see Table 1) who was found to have a constitutional epimutation in MLH1 that prompted us to review the frequency with which the test was ordered and the positivity rate, as well as outline the clinical history in the positive cases. Methods: We reviewed all of the testing ordered for MLH1 hypermethylation of peripheral blood (MLHPB) at the Mayo Clinic Laboratory between 09/01/2020 and 09/01/2021. To the best of our knowledge, this is the only clinically available testing lab in the United States. We reviewed positive casesfor characteristics including the number of malignancies, age of diagnosis, and family history. Results: 33 MLHPB total tests were ordered in the United States at the Mayo Clinic laboratories between 09/01/2020 and 09/01/2021. Three of the tests were positive, including the single test ordered by our institution, and one of the two additional positive tests was available for detailed review. Our institution’s positive test case was a 41 year old women who developed T4N2M0 colorectal cancer 5 years after being treated for endometrial cancer. She had endometrial cancer with absence of MLH1 and PMS2 staining and had a negative germline cancer risk panel at age 36. Five years later, she developed a T4N2 colorectal cancer after which repeat germline testing with RNA sequencing was negative and she was found to have constitutional MLH1 promoter hypermethylation. We were able to obtain clinical information about two of the three individuals with positive tests (See Table). Conclusions: Recognition of constitutional MLH1 hypermethylation may allow for earlier recognition of Lynch related malignancies in affected patients and families. Testing appears infrequent and this condition often goes unrecognized. Specific consensus guidelines may improve recognition and cancer screening in this population. [Table: see text]
    Type of Medium: Online Resource
    ISSN: 0732-183X , 1527-7755
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    Language: English
    Publisher: American Society of Clinical Oncology (ASCO)
    Publication Date: 2022
    detail.hit.zdb_id: 2005181-5
    detail.hit.zdb_id: 604914-X
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  • 6
    Online Resource
    Online Resource
    American Society of Clinical Oncology (ASCO) ; 2022
    In:  Journal of Clinical Oncology Vol. 40, No. 16_suppl ( 2022-06-01), p. e16259-e16259
    In: Journal of Clinical Oncology, American Society of Clinical Oncology (ASCO), Vol. 40, No. 16_suppl ( 2022-06-01), p. e16259-e16259
    Abstract: e16259 Background: Advanced PDAC is associated with a poor prognosis and median survivals of less than one year. FOLFIRINOX and Gemcitabine/Nab-Paclitaxel are both considered standard of care in the first line setting, though there is considerable variability among oncologists regarding sequencing of these regimens. Pre-clinical and clinical data support the use of platinum therapy in HRD+ PDAC, but little is known about how this translates into best practices regarding sequencing of treatment or clinical benefit relevant to Gemcitabine based therapies in this population. Methods: Using the cancer registry and Inova molecular tumor board database, we retrospectively reviewed all patients from January 2015 until November 2021 with unresectable PDAC who had NGS performed and stratified by the presence or absence of HRD mutation. HRD mutations included by BRCA1, BRCA2, PALB2, ATM, ATR, CHEK2, ARID1A, FANCA, FANCL. We analyzed for RR to Folfirinox/Folfox and Gemcitabine based therapies, adjusted time to progression on Folfirinox/Folfox (time from first dose of oxaliplatin based combination to first dose of gemcitabine to account for those who stopped oxaliplatin early for neuropathy or received maintenance therapy), and time on gemcitabine based therapy. Results: 142 consecutive patients with advanced PDAC were examined, including 20 with HRD variants. When excluding those who eventually received surgery and those who never received platinum therapy, we were left with 87 (74 in Control and 13 in HRD) for analysis. RR to Folfirinox/Folfox was 60% in HRD+ and 31.25% in control (p = 0.71) (Table). Mean adjusted time to progression on Folfirinox/Folfox was 320.0 days in HRD+ group and 252.9 in the control group (p = 0.57) (Table 2). The time on treatment for gemcitabine based combination therapy was 260.7 in HRD+ and 165.1 in control group. Conclusions: HRD+ patients had longer durations of treatment on both 5-FU based therapy and Gemcitabine based combinations. These data challenges the importance of first line platinum therapy in HRD+ patients, and further exploration should be considered.[Table: see text]
    Type of Medium: Online Resource
    ISSN: 0732-183X , 1527-7755
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    Language: English
    Publisher: American Society of Clinical Oncology (ASCO)
    Publication Date: 2022
    detail.hit.zdb_id: 2005181-5
    detail.hit.zdb_id: 604914-X
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  • 7
    In: Journal of Clinical Oncology, American Society of Clinical Oncology (ASCO), Vol. 37, No. 15_suppl ( 2019-05-20), p. 9041-9041
    Abstract: 9041 Background: TAPUR is a phase II basket study evaluating anti-tumor activity of commercially available targeted agents in pts with advanced cancers with genomic alterations. Results in a cohort of NSCLC pts with CDKN2A loss or mutation treated with P are reported. Methods: Eligible pts had advanced NSCLC, no standard treatment options, measurable disease, ECOG PS 0-2 and adequate organ function. Genomic testing was performed using commercially available tests. Pts matched to P had NSCLC with CDKN2A loss or mutation and no RB mutations. A Simon two-stage design was used to test a null rate of 15% vs. 35% (power = 0.85; α = 0.10). If ≥2 of 10 pts in stage 1 have disease control (DC) (objective response (OR) or stable disease at 16 weeks (wks) (SD16+)), an additional 18 pts are enrolled. If ≥7 of 28 pts have DC, the drug is considered worthy of further study. Secondary endpoints are progression-free survival (PFS), overall survival (OS) and safety. Results: Twenty-nine pts were enrolled from January 2017 to June 2018; 1 pt was unevaluable for response but is included in safety analyses. Pts received P at 125 mg orally once daily for 21 days, followed by 7 days off. Demographics and outcomes are summarized in Table (N = 28). One PR and 6 SD16+ were observed for a DC rate of 29% (90% CI, 15% to 37%). 10 pts had at least one grade 3 or 4 AE or SAE at least possibly related to P with the most common being cytopenias. Other grade 3-4 AEs or SAEs at least possibly related to P included fatigue, anorexia, febrile neutropenia, myocardial infarction, sepsis, vomiting, and hypophosphatemia. Conclusions: Monotherapy with P demonstrated evidence of anti-tumor activity in heavily pre-treated NSCLC pts with CDKN2A loss or mutation . Additional study is warranted to confirm the efficacy of P in pts with NSCLC with CDKN2A loss or mutation. Clinical trial information: NCT02693535. [Table: see text]
    Type of Medium: Online Resource
    ISSN: 0732-183X , 1527-7755
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    Language: English
    Publisher: American Society of Clinical Oncology (ASCO)
    Publication Date: 2019
    detail.hit.zdb_id: 2005181-5
    detail.hit.zdb_id: 604914-X
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  • 8
    Online Resource
    Online Resource
    American Society of Clinical Oncology (ASCO) ; 2018
    In:  Journal of Clinical Oncology Vol. 36, No. 4_suppl ( 2018-02-01), p. 483-483
    In: Journal of Clinical Oncology, American Society of Clinical Oncology (ASCO), Vol. 36, No. 4_suppl ( 2018-02-01), p. 483-483
    Abstract: 483 Background: Inova Schar Cancer Institute formed a molecular tumor board in early 2016 to identify treatment options for patients with gastrointestinal malignances based on molecular testing and to track outcomes. Methods: From March 2016 to June 2017, 78 patients with advanced gastrointestinal malignancies were presented at our molecular tumor board. The most common mutations, the percentage of patients who received targeted therapies, responded to targeted therapies, died or went on hospice prior to receiving a recommended therapy, and had an available Association of Molecular Pathology Tier 1 or Tier 2 recommendation available were reviewed retrospectively. We also compared the overall survival of patients who received a new treatment after MTB compared to those who did not. N-of-One, Inc. provided curation of molecular testing and participated in the MTB. Results: 78 patients with gastrointestinal cancers were presented between March 2016 and June 2017. Thirteen (19%) patients received targeted therapy and 31% had partial response, 15% had Stable Disease, and 54% had progression of disease. 12 patients (15%) died or went on hospice before recommendations could start and 11 patients (14%) are waiting to start recommended therapy. 38 (49%) patients did not have a mutation that prompted a MTB recommendation. Median OS of the 33 patients who started a new therapy (including chemotherapy or unrelated clinical trials) after MTB was 15.3 months vs. 11.5 months in 40 patients who continued current therapy (P = 0.016 Wilcoxon). The three most common mutations detected were TP53, KRAS, and APC. The majority of cases had more than one variant. 18% of cases had a variant classified as Tier 1; 74% of cases had a variant with the highest AMP classification of Tier 2. Conclusions: The majority of patients with Gastrointestinal malignancies presented to the Inova MTB had a finding that supported a molecularly-guided therapy, with a small but meaningful number of partial responses. Barriers to the use of molecular guided therapy included molecular testing and presentation at a late disease stage, and alternative chemotherapeutic options.
    Type of Medium: Online Resource
    ISSN: 0732-183X , 1527-7755
    RVK:
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    Language: English
    Publisher: American Society of Clinical Oncology (ASCO)
    Publication Date: 2018
    detail.hit.zdb_id: 2005181-5
    detail.hit.zdb_id: 604914-X
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  • 9
    In: Journal of Clinical Oncology, American Society of Clinical Oncology (ASCO), Vol. 40, No. 16_suppl ( 2022-06-01), p. 3008-3008
    Abstract: 3008 Background: TAPUR is a phase II basket study evaluating anti-tumor activity of commercially available targeted agents in pts with advanced cancers with genomic alterations. Results in a cohort of pts with solid tumors with BRAF V600E/D/K/R mutation (mut) treated with C+V are reported. Methods: Eligible pts had advanced solid tumors, no standard treatment (tx) options, measurable disease, ECOG performance status (PS) 0-2, and adequate organ function. Genomic testing was performed in CLIA-certified, CAP-accredited site selected labs. Pts matched to C+V had various solid tumors with BRAF V600E/D/K/R mut, or other BRAF mut if approved by the Molecular Tumor Board, and no MAP2K1/2, MEK1/2, NRAS mut. Recommended dosing was C, 60 mg orally daily for 21 days, 7 days off and V, 960 mg orally every 12 hours. Primary endpoint was disease control (DC), defined as complete (CR) or partial (PR) response or stable disease at 16+ wks (SD 16+) (RECIST v1.1). Low accruing histology-specific cohorts with the same genomic target and tx were collapsed into a single histology-pooled cohort for this analysis. For histology-pooled cohorts with sample size of 28, the results are evaluated based on a one-sided exact binomial test with a null DC rate of 15% vs. 35% (power = 0.84; α = 0.10) and one-sided 90% confidence interval (CI). Other efficacy endpoint estimates are presented with two-sided 95% CIs. Secondary endpoints were progression-free survival (PFS), overall survival (OS) and safety. Results: 31 pts with solid tumors (13 histologies; 6/31 ovarian cancer) with BRAF muts were enrolled from Dec 2016 to Jan 2021 and collapsed into one histology pooled cohort for analysis. 3 pts were not evaluable due to lack of post-baseline tumor evaluation and excluded from efficacy analyses. Demographics and outcomes are summarized in the Table. Pts had tumors with BRAF V600E mut (N = 26), G469V mut (N = 1), K601E mut (N = 2), N581I (N = 1) and T599_V600insT (N = 1). 2 CR (breast and ovarian cancer; V600E), 14 PR (13 V600E, 1 N581I), and 3 SD16+ (2 V600E, 1 T599_V600insT) were observed for a DC rate of 68% (90% CI: 54%, 100%) and an objective response (OR) rate of 57% (95% CI: 37%, 76%). CR durations were 5.1 (ovarian cancer) and 108.9 wks (breast cancer) and median duration of PR was 20.5 wks (range: 8.0, 176.0). 19 pts experienced ≥1 Grade 1-5 AE/SAE at least possibly related to tx including 1 death attributed to tx-related kidney injury. Conclusions: C+V demonstrated evidence of anti-tumor activity in pts with advanced solid tumors with BRAF V600E and other muts . Clinical trial information: NCT02693535. [Table: see text]
    Type of Medium: Online Resource
    ISSN: 0732-183X , 1527-7755
    RVK:
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    Language: English
    Publisher: American Society of Clinical Oncology (ASCO)
    Publication Date: 2022
    detail.hit.zdb_id: 2005181-5
    detail.hit.zdb_id: 604914-X
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  • 10
    In: Journal of Clinical Oncology, American Society of Clinical Oncology (ASCO), Vol. 42, No. 16_suppl ( 2024-06-01), p. e23036-e23036
    Abstract: e23036 Background: Acute inpatient hospital care contributes substantially to variation in cancer care costs across the United States. The CMS Hospital Outpatient Quality Reporting Program’s OP-35 rule penalizes health systems for having higher-than-expected rates of emergency department (ED) visits or inpatient admissions for ten potentially preventable conditions within 30 days of receiving chemotherapy. To commence a systematic, automated, risk-adapted program to maximize safety outcomes, we identified independent risk factors specific to cancer patients in the Inova Health System (a 5-hospital, 5 million-patients hospital system in Virginia/greater metropolitan DC). Methods: We identified all cancer patients who received chemotherapy within the previous 30 days and presented to the ED or were admitted between 1/1/2018 to 12/31/2021 for one of the OP-35 toxicities as their primary or secondary diagnoses at the time of the acute care evaluation. Data included demographics, insurance coverage, cancer diagnosis, co-morbidities, and status (alive/dead) at last follow up. A zero-truncated Poisson regression analysis was performed in R v4.1.1. We further performed risk analysis within comorbid conditions by creating a matched cohort of patients by sex, age at first treatment, race, and cancer type who did not have an ED or admission visit due to OP-35 events during this same period. Propensity score matching was performed using R package MatchIt v4.5.1. Results: Among the 1,618 patients identified, the most frequent events were pain, sepsis, and fever. 56% of patients were female with an overall median age of 64 (range = [20, 95]). Men were predicted to have 16% more visits than females. 45% had commercial insurance, 39% were on Medicare, and 15% were on Medicaid or charity care. 39% had two or more visits during the 4 years of the study, and among those patients, the most frequent cancer types were gastrointestinal (32%) and breast (22%). Self-reported latino patients constituted 4% of all patients but had the highest average number of events (median = 2.07, range = [1, 9] ). Patients who reported more-than-one-race or Asian ancestry had the lowest median number of events (1.56 and 1.64, respectively). In the matched cohort analysis, five co-morbidities were statistically significant (p 〈 0.05): a previous history of coagulopathy/pulmonary emboli, myocardial infarction, cardiac arrhythmias, depression, and weight loss (concordance = 0.58). 46% of all patients with an event had at least one of these 5 comorbidities. Conclusions: Demographic factors and specific comorbid conditions were associated with risk for requiring acute care intervention for chemotherapy toxicities. Future interventions will include introduction of risk-reducing monitoring in the outpatient setting for higher risk patients identified in this investigation to reduce the need for ED visits and inpatient hospitalizations.
    Type of Medium: Online Resource
    ISSN: 0732-183X , 1527-7755
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    Language: English
    Publisher: American Society of Clinical Oncology (ASCO)
    Publication Date: 2024
    detail.hit.zdb_id: 2005181-5
    detail.hit.zdb_id: 604914-X
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