Welcome to Dana-Farber's Research News
July 1, 2025
This twice-monthly newsletter highlights recently published research where Dana-Farber faculty are listed as first or senior authors. The information is pulled from PubMed and this issue notes papers published from June 1 through June 15.
If you are a Dana-Farber faculty member and you think your paper is missing from Research News, please let us know by emailing dfciresearchnews@dfci.harvard.edu.
|
Blood Loke J, Kim PG, Nguyen TTP, Boileau M, McConkey M, Miller AP, Shin W, Hergott CB, Ericsson M, Nordstrom A, Montero-Llopis P, Armstrong SA, Mancias JD, Ebert BL TET2 is among the most commonly mutated genes in both clonal hematopoiesis and myeloid malignancies, thus, the ability to identify selective dependencies in TET2 deficient cells has broad translational significance. Here, we identify regulators of Tet2 knockout (KO) hematopoietic stem and progenitor cell (HSPC) expansion using an in vivo CRISPR-Cas9 KO screen, in which nucleotide barcoding enabled large-scale clonal tracing of Tet2 deficient HSPCs in a physiological setting. Our screen identified candidate genes, including Ncoa4, that are selectively required for Tet2 KO clonal outgrowth compared to wild-type (WT). Ncoa4 targets ferritin for lysosomal degradation (ferritinophagy), maintaining intracellular iron homeostasis by releasing labile iron (Fe2+) in response to cellular demands. In Tet2-deficient HSPCs, increased mitochondrial ATP production correlates with increased cellular iron requirements, and in turn, promotes Ncoa4-dependent ferritinophagy. Restricting iron availability reduces Tet2 KO stem cell numbers, revealing a dependency in TET2-mutated myeloid neoplasms. |
|
|
|
Blood TP53-Mutated Acute Myeloid Leukemia: How Can We Improve Outcomes? Stahl M Despite advances in the treatment paradigm of patients with acute myeloid leukemia (AML), TP53-mutated AML represents a molecular subgroup that has failed to improve, with an overall survival of ?6 months that is independent of age and fitness. Notably, there has been significant elucidation in understanding the biology of the disease and key advancements in the classification and prognostication of these patients. International collaborative efforts for novel clinical interventions are urgently needed to change the standard of care. |
|
|
|
Cancer Discovery Nakazawa S, Pecci F, Odintsov I, Gazgalis D, Gottlieb FH, Ricciuti B, Alessi JV, Di Federico A, Aldea M, Garbo E, Gandhi MM, Saini A, Feng WW, Jiang J, Baldacci S, Facchinetti F, Makarem M, Locquet MA, Haratani K, Haradon D, Che J, Sholl LM, Jänne PA, Awad MM Oncogenic translocations involving the MET gene have been reported in several cancer types, but detailed clinicogenomic characterization of these cancers is not well defined. In addition, prospective clinical trials evaluating the antitumor activity of MET inhibitors in MET rearrangement-positive cancers are limited. In this study, in a pan-cancer analysis of >46,000 solid tumors with comprehensive genomic profiling, we identified oncogenic MET rearrangements in ?0.04% of cancers. Preliminary analysis from a phase II clinical trial of the type I MET tyrosine kinase inhibitor (TKI) vebreltinib in MET fusion-positive solid tumors demonstrated an objective response rate of 50% and disease control rate of 79%, with antitumor activity seen in diverse cancer types, including lung adenocarcinoma and intrahepatic cholangiocarcinoma, among others. Similar to MET exon 14-altered lung cancer, secondary mutations in the kinase domain can confer resistance to MET TKIs in MET fusion-positive cancers. Overall, these data categorize MET rearrangements as actionable targets in solid tumors. SIGNIFICANCE: MET rearrangement-positive cancers are not well-characterized, and optimal treatment strategies are yet to be defined. Through comprehensive genomic analysis, preclinical modeling, and preliminary results of a phase II clinical trial, we demonstrate that MET fusions are a unique molecular subtype of cancers targetable with vebreltinib, a TKI in development. |
|
|
|
Cell Stem Cell Bhattacharya S, Tie G, Singh PNP, He R, Kraiczy J, Perlov Y, Shivdasani RA Enterocytes and four classic secretory cell types derive from intestinal epithelial stem cells. Based on morphology, location, and canonical markers, goblet and Paneth cells are considered distinct secretory types. Here, we report high overlap in their transcripts and sites of accessible chromatin, in marked contrast to those of their enteroendocrine or tuft cell siblings. Mouse and human goblet and Paneth cells express extraordinary fractions of few antimicrobial genes, which reflect specific responses to local niches. Wnt signaling retains some ATOH1+ secretory cells in crypt bottoms, where the absence of BMP signaling potently induces Paneth features. Cells that migrate away from crypt bottoms encounter BMPs and thereby acquire goblet properties. These phenotypes and underlying accessible cis-elements interconvert in post-mitotic cells. Thus, goblet and Paneth properties represent alternative phenotypic manifestations of a common signal-responsive terminal cell type. These findings reveal exquisite niche-dependent cell plasticity and cis-regulatory dynamics in likely response to antimicrobial needs. |
|
|
|
Journal of Clinical Oncology Tesch ME, Partridge AH In the early 1990s, an Early Breast Cancer Trialists' Collaborative Group (EBCTCG) meta-analysis of adjuvant tamoxifen trials in patients with early breast cancer demonstrated significant reductions in the risk of death from breast cancer with tamoxifen in postmenopausal women. However, no clear survival advantage was seen in premenopausal women owing to little data in this subgroup, which, in part, led to tamoxifen routinely not being used in younger patients. An updated EBCTCG meta-analysis later established that 5 years of adjuvant tamoxifen substantially improved survival in both postmenopausal and premenopausal women, bringing into harsh focus the number of lives that could have been saved had the benefits of tamoxifen in younger patients been known sooner. Similarly, it was not until the SOFT/TEXT trials investigated adjuvant aromatase inhibitors (AI) in combination with ovarian function suppression (OFS) for premenopausal breast cancer that young patients became eligible, at last, for treatment with AI, over a decade after AIs had become the preferred adjuvant endocrine therapy (ET) for postmenopausal patients with hormone receptor (HR)–positive breast cancer, given their well-established superiority over tamoxifen. These examples underscore the need for dedicated studies in young adults with breast cancer, in whom the incidence of breast cancer has risen more sharply in recent years and whose survival rates remain lower, as compared with older adults. |
|
|
|
Journal of Clinical Oncology Samur MK, Sperling AS, Raje NS, Ghobrial IM, Anderson KC, Munshi NC Despite significant improvements in survival of patients with multiple myeloma (MM), outcomes remain heterogeneous, and a significant proportion of patients experience suboptimal outcomes. Importantly, traditional prognostic factors based on data from patients treated with older therapies no longer capture prognosis accurately in the contemporary era of novel triplet or quadruplet therapies. Therefore, risk stratification requires refinement in the context of available and investigational treatment options in routine practice and clinical trials, respectively. The current identification of high-risk MM (HRMM) in routine practice is based on the Revised International Staging System, which stratifies patients using a combination of widely available serum biomarkers and chromosomal abnormalities assessed via fluorescence in situ hybridization. In recent years, a substantial body of evidence concerning additional clinical, biological, and molecular/genomic prognostic factors has accumulated, along with new MM risk stratification tools and consensus reports. The International Myeloma Society, along with the International Myeloma Working Group, convened an Expert Panel with the primary aim of revisiting the definition of HRMM and formulating a practical and data-driven consensus definition, based on new evidence from molecular/genomic assays, updated clinical data, and contemporary risk stratification concepts. The Panel proposes the following Consensus Genomic Staging (CGS) of HRMM which relies upon the presence of at least one of these abnormalities: (1) del(17p), with a cutoff of >20% clonal fraction, and/or TP53 mutation; (2) an IgH translocation including t(4;14), t(14;16), or t(14;20) along with 1q+ and/or del(1p32); (3) monoallelic del(1p32) along with 1q+ or biallelic del(1p32); or (4) ?2 microglobulin ?5.5 mg/L with normal creatinine (<1.2 mg/dL). |
|
|
|
JAMA Why Good Palliative Care Clinicians Get Fired Rosenberg AR, Rabinowitz E Even the most seasoned palliative care clinician gets fired. In the past year, one of us was fired after asking whether a patient endorsing suicidal ideation had access to a gun; the patient requested not to see the palliative care team because we asked intrusive questions and documented the encounter. One of us was fired after supporting a family’s decision to discontinue life-sustaining therapies for their loved one with multisystem organ failure; the primary intensivist suggested palliative care overstepped in discussing options for which the family (and clinical teams) was not ready. And one of us was fired after sharing the impression that a patient with cancer was dying; the family suggested they preferred the oncologist’s version of a more hopeful future. |
|
|
|
JAMA Oncology Caring for Fasting Patients with Cancer During Ramadan Mora J, Bakhtiar M, Saeed NA, Balboni TA Ramadan is the ninth month of the Islamic lunar calendar and represents a holy time for Muslims worldwide to dedicate themselves to prayer, fasting, and community. During Ramadan, some observant Muslim patients with cancer may elect to fast. While some studies explore the impact of intentional caloric restriction on cancer therapy, the effect of repetitive daytime fasting for religious purposes has not been well characterized. Nevertheless, oncology clinicians should familiarize themselves with this cultural practice due to the potential clinical implications for patients. |
|
|
|
JAMA Oncology What Age Is the Best "FIT" for Colorectal Cancer Screening? Jayakrishnan T, Ng K Early-onset colorectal cancer (eoCRC), defined as colorectal cancer (CRC) diagnosed in individuals younger than 50 years, is one of the most rapidly increasing malignancies among young adults globally.1 The highest incidence rates of eoCRC have been reported in Australia, with an age-standardized rate (ASR) of 16.5 per 100?000 population (95% CI, 16.1-16.9), followed by New Zealand (ASR, 14.8; 95% CI, 14.0-15.6), the US (ASR, 14.8; 95% CI, 14.7-14.9), and South Korea (ASR, 14.3; 95% CI, 14.0-14.5). While the overall incidence of CRC in the US has declined by approximately 1.3% to 4.2% annually since the mid-1990s, the incidence of eoCRC has increased by about 2% per year during this timeframe. In parallel, CRC-related mortality among individuals younger than 50 years has also risen by approximately 1% per year between 2011 and 2020, with CRC now being the leading cause of cancer-related death in men aged 20 to 49 years in the US and the second leading cause in women of the same age group. The alarming rise of eoCRC prompted the US Preventive Services Task Force to lower the recommended starting age for CRC screening in average-risk individuals from age 50 to 45 years in 2021. However, most screening programs in other countries initiate screening at age 50 years. Furthermore, unlike the US, which largely relies on colonoscopy as the primary screening modality, most other countries rely on less resource-intensive, noninvasive stool-based tests such as the fecal immunochemical test (FIT) and fecal occult blood test. Thus, as the burden of eoCRC continues to grow around the world, there is an urgent need to better understand the effectiveness of these noninvasive tools in younger populations. |
|
|
|
Nature Biotechnology A CAR Enhancer Increases the Activity and Persistence of CAR T Cells Rakhshandehroo T, Mantri SR, Moravej H, Louis BBV, Salehi Farid A, Munaretto L, Khan RMM, Wolff A, Farkash Z, Cong M, Kuhnast A, Nili A, Lee UJ, Allen HH, Berland L, Simkova E, Uslu SC, Tavakolpour S, Rowley JE, Codet E, Shahbazian H, Baral J, Pyrdol J, Jacobson CA, Nadeem O, Wucherpfennig KW, Rashidian M Although chimeric antigen receptor (CAR) T cell therapies have demonstrated promising clinical outcomes, durable remissions remain limited. To extend the efficacy of CAR T cells, we develop a CAR enhancer (CAR-E), comprising a CAR T cell antigen fused to an immunomodulatory molecule. Here we demonstrate this strategy using B cell maturation antigen (BCMA) CAR T cells for the treatment of multiple myeloma, with a CAR-E consisting of the BCMA fused to a low-affinity interleukin 2 (IL-2). This selectively induces IL-2 signaling in CAR T cells upon antigen-CAR binding, enhancing T cell activation and antitumor activity while reducing IL-2-associated toxicities. We show that the BCMA CAR-E selectively binds CAR T cells and increases CAR T cell proliferation, clearance of tumor cells and development of memory CAR T cells. The memory cells retain the ability to re-expand upon restimulation, effectively controlling tumor growth upon rechallenge. Mechanistic studies reveal the involvement of both CAR and IL-2 receptor endodomains in the CAR-E mechanism of action. The CAR-E approach avoids the need for specific engineering and enables CAR T cell therapy with lower cell doses. |
|
|
|
Nature Biotechnology Cieri N, Hookeri N, Stromhaug K, Li L, Keating J, Stevens J, Kfuri-Rubens R, Shao Y, Kooshesh KA, Powell K, Ji H, Hernandez GM, Abelin J, Klaeger S, Forman C, Clauser KR, Sarkizova S, Braun DA, Penter L, Kim HT, Lane WJ, Oliveira G, Kean LS, Li S, Livak KJ, Carr SA, Keskin DB, Ho VT, Ritz J, Soiffer RJ, Neuberg D, Stewart C, Getz G, Wu CJ T cell alloreactivity against minor histocompatibility antigens (mHAgs)-polymorphic peptides resulting from donor-recipient (D-R) disparity at sites of genetic polymorphisms-is at the core of the therapeutic effect of allogeneic hematopoietic cell transplantation (allo-HCT). Despite the crucial role of mHAgs in graft-versus-leukemia (GvL) and graft-versus-host disease (GvHD) reactions, it remains challenging to consistently link patient-specific mHAg repertoires to clinical outcomes. Here we devise an analytic framework to systematically identify mHAgs, including their detection on HLA class I ligandomes and functional verification of their immunogenicity. The method relies on the integration of polymorphism detection by whole-exome sequencing of germline DNA from D-R pairs with organ-specific transcriptional- and proteome-level expression. Application of this pipeline to 220 HLA-matched allo-HCT D-R pairs demonstrated that total and organ-specific mHAg load could independently predict the occurrence of acute GvHD and chronic pulmonary GvHD, respectively, and defined promising GvL targets, confirmed in a validation cohort of 58 D-R pairs, for the prevention or treatment of post-transplant disease recurrence. |
|
|
|
Nature Genetics Genomic Landscape of Multiple Myeloma and Its Precursor Conditions Alberge JB, Dutta AK, Poletti A, Coorens THH, Lightbody ED, Toenges R, Loinaz X, Wallin S, Dunford A, Priebe O, Dagan J, Boehner CJ, Horowitz E, Su NK, Barr H, Hevenor L, Towle K, Beesam R, Beckwith JB, Perry J, Cordas Dos Santos DM, Bertamini L, Kübler K, Hess J, Sklavenitis-Pistofidis R, Stewart C, Getz G, Ghobrial IM Reliable strategies to capture patients at risk of progression from precursor stages of multiple myeloma (MM) to overt disease are still missing. We assembled a comprehensive collection of MM genomic data comprising 1,030 patients (218 with precursor conditions) that we used to identify recurrent coding and non-coding candidate drivers as well as significant hotspots of structural variation. We used those drivers to define and validate a simple 'MM-like' score, which we could use to place patients' tumors on a gradual axis of progression toward active disease. Our MM precursor genomic map provides insights into the time of initiation and cell-of-origin of the disease, order of acquisition of genomic alterations and mutational processes found across the stages of transformation. Taken together, we highlight here the potential of genome sequencing to better inform risk assessment and monitoring of MM precursor conditions. |
|
|
|
Nature Genetics Li Z, Peluffo G, Stevens LE, Qiu X, Seehawer M, Tawawalla A, Huang XY, Egri SB, Raval S, McFadden M, Kingston NL, Nishida J, Evans KE, Seo JH, Clement K, Temko D, Ekram M, Li R, Rees MG, Ronan MM, Roth JA, SMichor F, Meissner A, Freedman ML, Jaffe JD, Papanastasiou M, Long HW, Polyak K Basal breast cancer is a subtype with a poor prognosis in need of more effective therapeutic approaches. Here we describe a unique role for the KDM4C histone lysine demethylase in KDM4C-amplified basal breast cancers, where KDM4C inhibition reshapes chromatin and transcriptomic landscapes without substantial alterations of its canonical substrates, trimethylated histone H3 lysine 9 (H3K9me3) and lysine 36 (H3K36me3). Rather, KDM4C loss causes proteolytic cleavage of histone H3 mediated by cathepsin L (CTSL), resulting in decreased glutamate-cysteine ligase expression and increased reactive oxygen species. CTSL is recruited to the chromatin by the grainyhead-like 2 (GRHL2) transcription factor that is methylated at lysine 453 following KDM4C inhibition, triggering CTSL histone clipping activity. Deletion of CTSL rescued KDM4-loss-mediated tumor suppression. Our study reveals a function for KDM4C that connects cellular redox regulation and chromatin remodeling. |
|
|
|
New England Journal of Medicine Menopausal Symptom Management in Breast Cancer Survivors - A Promising New Option Among women with a history of early breast cancer treated with endocrine therapy (tamoxifen or aromatase inhibitors), vasomotor symptoms are common, occurring in up to 90% of this population, and often severe. These symptoms are attributable to mainstay treatments used to reduce disease recurrence and improve survival. Two such treatments are chemotherapy, which causes temporary or permanent ovarian suppression and is associated with precipitously low levels of estradiol in premenopausal women, and endocrine therapy, which is used to decrease or block estrogen in breast cancer survivors of all ages. Menopausal symptoms not only affect quality of life among survivors of breast cancer but also may have indirect adverse effects on disease-free and overall survival, especially if the symptoms lead to nonadherence to risk-reducing endocrine therapy. In a large cross-sectional study involving breast cancer survivors, half the participants reported nonadherence to endocrine therapy; nonadherence was significantly more likely among participants reporting more-severe vasomotor symptoms than those with less-severe symptoms, which suggests that improved symptom management is a vital issue in breast cancer care. |
|
|
|
New England Journal of Medicine The Fetal-to-Adult Hemoglobin Switch - Mechanism and Therapy Orkin SH The evolution of biomedical science can be appreciated through studies of hemoglobin, the oxygen-carrying protein in red cells. Before molecular cloning, the geneticist Arno Motulsky noted, “Many fundamental concepts have become clarified by investigations on human hemoglobins.” Half a century into the recombinant-DNA era, these words are even more apt. From gene cloning to editing, hemoglobin-related research has embraced emerging technologies and uncovered general principles. The accessibility of red cells for study, their extraordinary specialization for hemoglobin production, and the global burden of the major hemoglobin disorders, ?-thalassemia and sickle cell disease, sustain interest in the field. |
|
|
|
ACS Chemical Biology High-Throughput Screening Tool to Identify Small Molecule Inhibitors of Telomerase Aquilanti E, Barkho S, Bozinov V, Kageler L, Garrity-Janger M, Mesleh MF, Horner S, Ranaghan MJ, Meyerson M |
|
|
|
American Journal of Hematology Kim HT, Liney DJ, Rizza K, Cutler CS, Koreth J, Nikiforow S, Shapiro RM, Kelkar AH, Gooptu M, Romee R, Wu CJ, Antin JH, Ritz J, Soiffer RJ, Ho VT |
|
|
|
American Society of Clinical Oncology Educational Book Corti C, Tolaney SM |
|
|
|
American Society of Clinical Oncology Educational Book Liu Y, Nadeem O |
|
|
|
Annals of Surgical Oncology Gait Speed as a Measure of Frailty and Outcomes After Lung Resection Singh A, Xie Y, Mazzola E, Wang S, McAllister M, Pezeshkian F, Frain LN, Wilder FG, Steimer D, Jaklitsch MT, DuMontier C |
|
|
|
Annals of Surgical Oncology Weiss A, Rosito MS, Braun D, Barton B, McGrath M, Stokes S, Laws A, Warren L, Morganti S, Lynce F, Bychkovsky B, Rana HQ, Davis D, Stopfer J, Garber JE, King TA |
|
|
|
Blood Advances Yoon JT, Zhou Y, Mikhaleva M, Choi DS, Fernandes SM, Armand P, Bessnow AC, Crombie JL, Fisher DC, Jacobsen ED, Jacobson CA, Kim AI, LaCasce AS, Merryman RW, Odejide OO, Parry EM, Qualls DA, Ryan CE, Sekar A, Soumerai JD, Arnason J, Tyekucheva S, Davids MS, Brown JR, Ahn IE |
|
|
|
Blood Advances Branagan AR, Mo CC, Lei MM, Gustine J, Yee AJ, O'Donnell E, Castillo JJ, Nadeem O, Flynn C, Bernstein Z, Nakamoto-Matsubara R, Meid KE, Verma R, Hunter ZR, Guerrera ML, Alter G, Burke JN, Harrington CC, Agyemang EA, Gammon MT, Lively KJ, Packer L, Horick N, Laubach JP, Mitsiades CS, Munshi NC, Anderson KC, Treon SP, Richardson PG, Raje NS, Sarosiek S |
|
|
|
British Journal of Haematology Liu S, Liu X, Yusuf CFB, Kofides A, Soroko KM, Penailillo J, Canning AG, Cao Y, Yang G, Xu L, Tsakmaklis N, Sun H, Guijosa A, Guerrera ML, Patterson CJ, Carrasco RD, Gokhale PC, Sarosiek SR, Castillo JJ, Hatcher JM, Hunter ZR, Treon SP |
|
|
|
British Journal of Haematology Sorial MN, Lei MM, MacVicar CT, Freydman J, Malespini J, Aniagboso KN, McCabe SM, Singh S, Iwasaki M, Eche-Ugwu IJ, Gabler J, Fernandez Turizo MJ, Garg A, Disciullo A, Chopra K, Ford J, Lenart A, Nwodo E, Barnes J, Koh MJ, Merrill M, Jacobsen E, Kariya KM, Bhanushali F, Meharwal A, Mistry D, Kosovsky M, Jain S |
|
|
|
Breast Cancer Research and Treatment Wehbe A, Katlin F, Sharma E, Hans M, Graichen MK, Bychkovsky BL, Scheib R, Garber JE, Pace LE, King TA, Laws A |
|
|
|
Cell Reports Medicine Yates J, Mathey-Andrews C, Park J, Garza A, Gagné A, Hoffman S, Bi K, Titchen B, Remland J, Carnes M, Shannon E, Camp S, Balamurali S, Cavale SK, Li Z, Raghawan AK, Boland G, Aguirre AJ, Sethi NS, Van Allen EM |
|
|
|
Cell Reports Medicine Olsen SN, Anderson B, Hatton C, Wen Y, Bourgeois W, Haarer EL, Brown M, Jeselsohn R, Armstrong SA |
|
|
|
Chemical Science Advances in Sulfonyl Exchange Chemical Biology: Expanding Druggable Target Space Jones LH |
|
|
|
|
|
Clinical Cancer Research Pecci F, Alden SL, Ricciuti B, Alessi JV, Wang X, Jeng M, Vaz VR, Barrichello A, Lamberti G, Di Federico A, Santo V, Rossato de Almeida G, Gandhi M, Nishino M, Johnson BE, Awad MM |
|
|
|
Clinical Breast Cancer Factors Associated with Short- and Long-Term Survival in Metastatic HER2-Positive Breast Cancer Leone JP, Moges R, Parsons HA, Hassett MJ, Lin NU |
|
|
|
Clinical Breast Cancer Trapani D, Jin Q, Ligibel J, Chen W, Come S, Nohria A, Ryabin N, Tayob N, Tolaney SM, Burstein HJ, Mayer EL |
|
|
|
Clinical Cancer Research Paweletz CP, Ha M, Janne PA |
|
|
|
Clinical Genitourinary Cancer CDK4/6 Inhibition with Abemaciclib in Patients with Previously Treated Advanced Renal Cell Carcinoma McGregor BA, Xie W, Berg SA, Xu W, Viswanathan SR, McDermott D, Signoretti S, Kaelin WG Jr, Choueiri TK |
|
|
|
Clinical Lung Cancer Saraf A, He J, Shin KY, Weiss J, Awad MM, Gainor J, Kann BH, Christiani DC, Aerts HJWL, Mak RH |
|
|
|
Clinical Lung Cancer Barrichello APC, Ricciuti B, Wang X, Lotter W, Lindsay J, Santo V, Sharma B, Felt K, Pfaff K, Lamberti G, Pecci F, Federico AD, Makarem M, Gandhi MM, Nguyen T, Haradon D, Vaz VR, Johnson BE, Rodig SJ, Awad MM, Alessi JV |
|
|
|
Current Treatment Options in Oncology Epithelioid Hemangioendothelioma: Treatment Landscape and Innovations for an Ultra-Rare Sarcoma Pimenta EM, Goyal A, Farber ON, Lilley E, Shyn PB, Wang J, Wagner MJ |
|
|
|
European Journal of Haematology Outcomes of Melflufen Treatment in Patients with Relapsed/Refractory Multiple Myeloma Hossain S, Mo C, Patches S, Leblebjian H, Goodrich K, Regan E, O'Neill K, Noonan K, Richardson PG, Laubach J |
|
|
|
European Urology Ravi P, Kwak L, Rastogi S, Xie W, Abdelnaser A, Einstein DJ, Chang P, Wagner AA, Kibel AS, Taplin ME |
|
|
|
European Urology Refining the Role of Androgen Deprivation Therapy After Radical Prostatectomy Sayan M, Nguyen PL |
|
|
|
European Urology Oncology Ravi P, Zhong C, Xie W, Kelly E, Whelpley B, Kuczmarski K, Beltran H, Kilbridge KL, King MT, McGregor BA, Morgans AK, Pomerantz M, Taplin ME, Tewari AK, Viswanathan SR, Wei XX, Anh Huynh M, Choudhury AD |
|
|
|
Gynecologic Oncology Fitzgerald KJ, Konstantinopoulos P, Matulonis U, Liu J, Horowitz N, Lee E, Kolin DL, Lee L, King M |
|
|
|
Haematologica Blinatumomab and Better BCR::ABL1 Inhibition Begets Better Bone Marrow Transplant Outcomes Luskin MR |
|
|
|
Health Communication The Relationship Between News Coverage of COVID-19 Misinformation and Online Search Behavior Douglas-Durham E, Emmons KM, Viswanath K |
|
|
|
Hematology Oncology Advances in the Management of Relapsed/Refractory CLL and Richter Transformation Javidi-Sharifi N, Davids MS |
|
|
|
Hematology Oncology Diagnosis and Management of Waldenstrom's Macroglobulinemia Treon SP, Sarosiek S, Castillo JJ |
|
|
|
Hematology/Oncology Clinics of North America Histiocytic Disorders in Pediatric and Adult Patients Berliner N, Degar BA |
|
|
|
Hematology/Oncology Clinics of North America Clinical Characteristics and Treatment of Histiocytic Disorders in Children Degar BA, Huang JT, Bledsoe J |
|
|
|
Hematology/Oncology Clinics of North America Nikiforow S, Duncan CN |
|
|
|
International Journal of Radiation Oncology, Biology, Physics D'Amico AV, Nguyen PL |
|
|
|
Journal of Geriatric Oncology Newman AB, Martin AR, Hughes ME, Higgins A, Kirkner GJ, Files J, Skeffington M, Moore M, Strauss S, Kuhnly N, Crowley L, Tolaney SM, Lin NU, Freedman RA |
|
|
|
Journal of Geriatric Oncology Ruderman K, Simo S, McGrath B, Snow C, Rigby K, Arnaout A, Hshieh TT, Minami C, Freedman RA |
|
|
|
Journal of Thoracic Oncology Gandhi MM, Moore CG, Ricciuti B, Alessi JV, Williams J, Lamberti G, Pecci F, Di Federico A, Makarem M, Johnson BE, Nishino M, Sholl LM |
|
|
|
JCO Oncology Practice Beyond Opioids: A Multidisciplinary Approach to Cancer Pain Management Azizoddin DR, Enzinger AC |
|
|
|
JCO Oncology Practice Yu L, Espiritu J, Patel K, Rosner BA, Rompelman GH, Rubinson DA, Jacobson JO |
|
|
|
JCO Precision Oncology Gariazzo E, Laaksonen S, Canty S, De Almeida GR, Odintsov I, Santo V, Garbo E, Pecci F, Aldea M, Oser MG, Sholl L, Sands JM, Ricciuti B |
|
|
|
JCO Precision Oncology Incidental Diffuse Midline Glioma, H3 K27-Altered of the Pons Without Significant Coalterations Yeo KK, Power P, Lidov H, Rosenberg T, Warren KE, Smith ER, Haas-Kogan D, Bandopadhayay P |
|
|
|
Lancet Regional Health Europe Enhancing Existing Tumour Biobanks in European Prospective Cohort Studies Ugai T, Mucci LA, Ogino S |
|
|
|
Nature Chemistry Boeszoermenyi A, Schindler S, Valadares V, Padmanabha Das KM, Dubey A, Viennet T, Ficarro S, Marto J, Geffken EA, Dhe-Paganon S, Seo HS, Arthanari H |
|
|
|
Nature Review Immunology CD45-PET Imaging Gives a Panoramic View of in Vivo Immune Activity Djafari Rouhani S, Rashidian M |
|
|
|
NPJ Digital Medicine Riaz IB, Ashraf N, Harris GJ, Kehl KL |
|
|
|
Nucleic Acids Research Singh PK, Engelman AN |
|
|
|
Oncology and Therapy Morganti S, Partridge AH, Lynce F |
|
|
|
Pediatric Blood and Cancer DuBois SG, George RE, Majzner RG |
|
|
|
Pediatrics Psychosocial Experiences of African American Parents of Children with Cancer Eche-Ugwu IJ, Wolfe J, Feraco AM |
|
|
|
Prostate Losee M, Kavanaugh M, Liu M, Borges N, Haberman V, Ritzer J, Wolanski A, Bhimaniya S, Choudhury AD, Hyun H, Stoltenberg H, Kilbridge KL, Morgans A, Pomerantz M, Robertson M, Sakellis C, Shah H, Taplin ME, Wei XX, Ng T, Ravi P, Jacene H |
|
|
|
Prostate Cancer and Prostatic Diseases Kang DW, Dieli-Conwright CM |
|
|
|
Radiotherapy and Oncology Adleman J, McLaughlin PY, Tsui JMG, Buzurovic I, Harris T, Hudson J, Urribarri J, Cail DW, Nguyen PL, Orio PF, Lee LK, King MT |
|
|
|
Seminars in Oncology Nursing Moraitis AM, Hammer MJ |
|
|
|
Seminars in Oncology Nursing Moraitis AM, Hammer MJ |
|
|
|
Transplantation and Cellular Therapy Guo M, Keane EP, Mate-Kole MN, Boardman AC, Larizza IS, Song MT, Schaefer DA, Cutler C, El-Jawahri A, Amonoo HL |
|
|
|
Transplantation and Cellular Therapy Frigault MJ, Nikiforow S |
|
|
|
Trends in Cancer Mixing It Up: Boosting Responses with Immunotherapy Combinations Komatsuda H, Sim ES, Uppaluri R |