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Rakesh Jain
Director, A.W. Cook Professor of Tumor Biology
Jain Lab

Jain Lab Research

For four decades, my research has focused on one challenge: improving the delivery and efficacy of anti-cancer therapeutics by normalizing the tumor microenvironment. Working on the hypothesis that the abnormal tumor microenvironment fuels tumor progression and treatment resistance, we developed an array of sophisticated imaging technologies and animal models as well as mathematical models to unravel the complex biology of tumors. Using these tools, we demonstrated that the blood and lymphatic vasculature, fibroblasts, immune cells and the extracellular matrix associated with tumors are abnormal, and these collaborate together to create a hostile tumor microenvironment characterized by hypoxia, low pH and high interstitial fluid pressure and solid stress. We next hypothesized that agents that induce “normalization” of the microenvironment can improve the treatment outcome. Indeed, we demonstrated that judicious use of antiangiogenic agents—originally designed to starve tumors—could transiently “normalize” tumor vasculature, alleviate hypoxia, increase delivery of drugs and anti-tumor immune cells, and improve the outcome of various therapies, including immunotherapy (Science 2005, 2019, 2020). In parallel, we provided compelling evidence for vascular normalization in cancer patients treated with antiangiogenic agents. In fact, vascular normalization and the resultant improvement in tumor perfusion and oxygenation associated with longer survival in patients (J Clinical Oncology 2013; Cancer Cell 2014; PNAS 2015). Our preclinical finding that vascular normalization can improve immunotherapy (PNAS 2012) was confirmed by others in randomized phase III trials on combining antiangiogenic therapy with immune-checkpoint inhibitors for lung, kidney, liver and endometrial cancers (New England J Medicine 2018, 2019, 2020), and led to the FDA approvals of six such combinations of antiangiogenic therapy and  immune-checkpoint inhibitors for these cancers (Science 2019).

 The normalization hypothesis also opened doors to treating various non-malignant diseases characterized by abnormal vasculature that afflict >500 million people worldwide, such as, tuberculosis (PNAS 2015) and neurofibromatosis-2 (NF2) (New England J. Medicine 2009). Based on our findings, bevacizumab was approved for NF2-schwannoma patients in UK in 2014. This hypothesis has also been validated by a number of laboratories worldwide and has changed the thinking about how antiangiogenic agents work alone and in combination with conventional and emerging therapeutics (Science 2005; New England J. Medicine 2009; Nature Rev Drug Discovery 2011; Physiological Rev 2011; Cancer Cell 2014; Nature Reviews Clinical Oncology 2018; Science 2019). 

 Finally, we discovered that anti-hypertensive drugs capable of “normalizing” the tumor matrix and stromal cells can reprogram the tumor microenvironment to an immunostimulatory milieu and improve the delivery and efficacy of cancer therapies, including immunotherapy (Nature Comm 2013; Cancer Discovery 2016; Science Translational Medicine 2017; PNAS 2019, 2020). A phase II trial (NCT01821729) led by my clinical collaborators provided compelling evidence in support of this emerging concept for improving the treatment outcome for patients with pancreatic ductal adenocarcinoma – a uniformly fatal disease (JAMA Oncology 2019). 

Rakesh K. Jain receives National Medal of Science at the White House! ->Click here for the webcast.


 Click here for Dr. Jain's CV

Lab News

Rakesh Jain named "Highly Cited Researcher" for 2022
Each year, Clarivate™ identifies the world’s most influential researchers ─ the select few who have been most frequently cited by their peers over the last decade. In 2022, fewer than 7,000, or about 0.1%, of the world's researchers, in 21 research fields and across multiple fields, have earned this exclusive distinction.

Rakesh Jain is among this elite group recognized for  exceptional research influence, demonstrated by the production of multiple highly-cited papers that rank in the top 1% by citations for field and year in the Web of Science™.
Rakesh Jain to Receive 2022 Szent-Györgyi Prize for Progress in Cancer Research

The National Foundation for Cancer Research (NFCR) announced today that Rakesh K. Jain, Ph.D., has been selected to receive the 2022 Szent-Györgyi Prize for Progress in Cancer Research. The blue-ribbon Prize selection committee, consisting of renowned leaders in cancer research, elected Dr. Jain for his pioneering research and breakthrough discoveries on overcoming barriers posed by the tumor microenvironment (TME) which led to the improved delivery and efficacy of anti-cancer medicines. His groundbreaking and innovative research has fundamentally transformed the understanding of tumor biology and directly informed the development and approval of new drug-combinations to treat cancer patients.

Rakesh Jain ranked #82 in the world and #57 in United States by Research.com.

The ranking contains h-index, publications and citations values collected on December 6th, 2021.

Normalizing tumor microenvironment with nanomedicine and metronomic therapy to improve immunotherapy
  • Both nanomedicines and metronomic scheduling—when medications are given at lower, more frequent doses—can correct abnormalities surrounding tumors that help protect cancer cells and foster their growth and spread.

  • Combining nanomedicines and metronomic scheduling may help improve cancer treatment strategies.

MGH Press release

Article link

Renin–angiotensin–aldosterone system inhibitors and survival in patients with hypertension treated with immune checkpoint inhibitors

In this large retrospective study, patients with hypertension who were concomitantly taking a RAAS inhibitor during ICI therapy had better overall survival. This benefit was primarily noted among patients with gastrointestinal and genitourinary cancers. Prospective randomized trials are warranted to further evaluate and specify the benefit of RAAS inhibitors in patients with cancer who receive ICI therapy.

Link to paper

Jain Lab Team

Current Research

The spread of cancer cells from primary tumors to regional lymph nodes is often associated with reduced survival. One prevailing model to explain this association posits that fatal, distant metastases are seeded by lymph node metastases. This view provides a mechanistic basis for the TNM staging system and is the rationale for surgical resection of tumor-draining lymph nodes. Here we examine the evolutionary relationship between primary tumor, lymph node, and distant metastases in human colorectal cancer. Studying 213 archival biopsy samples from 17 patients, we used somatic variants in hypermutable DNA regions to reconstruct high-confidence phylogenetic trees. We found that in 65% of cases, lymphatic and distant metastases arose from independent subclones in the primary tumor, whereas in 35% of cases they shared common subclonal origin. Therefore, two different lineage relationships between lymphatic and distant metastases exist in colorectal cancer.

Science. 2017;357(6346):55-60 - PMID: 28684519 - PMCID: PMC5536201 - DOI: 10.1126/science.aai8515

Angiotensin system inhibitors (ASIs) can improve prognosis in multiple cancer types, including pancreatic ductal adenocarcinoma (PDAC). However, no study has examined the effect of ASIs alone or combined with adjuvant chemotherapy in resected PDAC patients.<br /><br />Experimental Design: We performed an analysis of the records of ASI users and non-user patients with PDAC seen at Massachusetts General Hospital between January 2006 and December 2010. To identify mechanisms of ASIs in PDAC, we performed RNA-Seq of resected primary lesions. <br /><br />Results: 794 consecutive patients were included. In 299 resected patients, ASI-users experienced longer overall survival (OS) in both univariate (median OS: 36.3 vs. 19.3 months, p=0.011) and adjusted multivariate (HR, 0.505; 95%CI, 0.339 – 0.750; p=0.001) analyses. Propensity score adjusted analysis also showed a longer median OS for chronic ASI-users. In unresected patients, the beneficial effect of ASIs was significant in patients with locally advanced disease, but not in metastatic patients. RNA-Seq analysis revealed in tumors of ASI-users (lisinopril) a normalized extracellular matrix, a reduced expression of genes involved in PDAC progression (e.g. WNT and Notch signaling) and an increased expression of genes linked with the activity of T cells and antigen-presenting cells. Finally, chronic use of ASI was associated with a gene expression signature which is predictive of survival in independent validation cohorts.<br /><br />Conclusions: In patients with non-metastatic PDAC, chronic ASI use is associated with longer OS independently of chemotherapy. Our RNA-Seq analysis suggests that ASI reduce the malignant potential of cancer cells and stimulate the immune microenvironment in primary PDAC.

Clin Cancer Res. 2017;23(19):5959-5969 - PMID: 28600474 - PMCID: PMC5856249 - DOI: 10.1158/1078-0432.CCR-17-0256

It remains unclear how obesity worsens treatment outcomes in patients with pancreatic ductal adenocarcinoma (PDAC). In normal pancreas, obesity promotes inflammation and fibrosis. We found in mouse models of PDAC that obesity also promotes desmoplasia associated with accelerated tumor growth and impaired delivery/efficacy of chemotherapeutics through reduced perfusion. Genetic and pharmacological inhibition of angiotensin-II type-1 receptor (AT1) reverses obesity-augmented desmoplasia and tumor growth and improves response to chemotherapy. Augmented activation of pancreatic stellate cells (PSCs) in obesity is induced by tumor-associated neutrophils (TANs) recruited by adipocyte-secreted IL-1ß. PSCs further secrete IL-1ß, and inactivation of PSCs reduces IL-1ß expression and TAN recruitment. Furthermore, depletion of TANs, IL-1ß inhibition, or inactivation of PSCs prevents obesity-accelerated tumor growth. In pancreatic cancer patients, we confirmed that obesity is associated with increased desmoplasia and reduced response to chemotherapy. We conclude that crosstalk between adipocytes, TANs, and PSCs exacerbates desmoplasia and promotes tumor progression in obesity.

Cancer Discov. 2016;6(8):852-69 - PMID: 27246539 - PMCID: PMC4972679 - DOI: 10.1158/2159-8290.CD-15-1177

Polarization of tumor-associated macrophages: a novel strategy for vascular normalization and antitumor immunity.

TAMs with M2-like phenotype lead to abnormal tumor vasculature by producing angiogenic factors, such as PlGF, and M2-cytokines, such as IL10 and CCL22. In addition, M2-cytokines suppress immune cell functions. Elevated levels of HRG polarize TAMs away from an M2-like phenotype to normalize tumor vessels and activate anti-tumor immunity. By fortifying tumor vessels, vascular normalization may decrease shedding of metastatic cells into circulation resulting in decreased metastasis. Normalized vessels may also facilitate delivery of drugs and immune cells. Reduction in hypoxia – known to increase resistance to radiation and a number of therapeutics – also sensitizes tumors to various therapies and decreases selection pressure for more malignant clone, and promotes M1-like TAM phenotype. All these effects of HRG treatment may result in decreased tumor growth and metastasis and increased efficacy of various therapies. PlGF deletion in macrophages can phenocopy many effects of HRG treatment. (Schematics of abnormal and normalized tumor vasculature reproduced from Jain, Nat Med 7:987, 2001).

Cancer Cell. 2011;19(1):1-2 - PMID: 21251607 - PMCID: PMC3037265 - DOI: 10.1016/j.ccr.2011.01.005

Rapid blood perfusion is critical for postimplantation survival of thick, prevascularized bioartificial tissues. Yet the mechanism by which implanted vascular networks inosculate, or anastomose, with the host vasculature has been unknown, making it difficult to develop optimized strategies for facilitating perfusion. Here we show that implanted vascular networks anastomose with host vessels through a previously unidentified process of &quot;wrapping and tapping&quot; between the engrafted endothelial cells (ECs) and the host vasculature. At the host-implant interface, implanted ECs first wrap around nearby host vessels and then cause basement membrane and pericyte reorganization and localized displacement of the underlying host endothelium. In this way, the implanted ECs replace segments of host vessels to divert blood flow to the developing implanted vascular network. The process is facilitated by high levels of matrix metalloproteinase-14 and matrix metalloproteinase-9 expressed by the wrapping ECs. These findings open the door to new strategies for improving perfusion of tissue grafts and may have implications for other physiologic and pathologic processes involving postnatal vasculogenesis.

Blood. 2011;118(17):4740-9 - PMID: 21835951 - PMCID: PMC3208287 - DOI: 10.1182/blood-2011-02-338426

Jain Lab Careers

POSTDOCTORAL RESEARCH FELLOW – TUMOR MICROENVIRONMENT, VASCULR BIOLOGY, MATRIX BIOLOGY, IMMUNOLOGY, MOLECULAR/CELLULAR BIOLOGY, INTRAVITAL MICROSCOPY and BIOMEDICAL ENGINEERING

Investigator: Jain, Rakesh
Date Posted: 2022-01-19
Description
The JAIN LAB in the STEELE LABORATORIES OF TUMOR BIOLOGY at the Massachusetts General Hospital, Harvard Medical School invites applications for Postdoctoral Research Fellow positions. Multiple positions are available in tumor microenvironment, vascular biology, matrix biology, immunology, molecular/cellular biology, intravital microscopy and biomedical engineering. Ideal candidates should have a strong academic background, peer-reviewed publications, strong English language proficiency and writing skills. Candidates with a strong background in single-cell-sequencing, bioinformatics, Python, and R statistical computing are also encouraged to apply. The Steele Labs have a diverse faculty and offer a lively and supportive environment in which to perform cutting-edge interdisciplinary research. Our research goals are (i) to understand how the abnormal tumor microenvironment confers resistance to various cancer treatments (e.g., molecular therapeutics, nanotherapeutics, radiation and immunotherapy), (ii) to develop and test new strategies to overcome this resistance, and (iii) to translate these strategies from bench to bedside through multi-disciplinary clinical trials. This tight integration between bench and bedside and application of engineering/physical science principles to oncology is a hallmark of our research.
Responsibilities
We seek creative thinkers who take risks in defining and addressing important problems, and who use quantitative molecular, genetic, cellular, and computational approaches in their work. Research fellows are encouraged to apply for post-doctoral fellowships and to write their own transition grants to launch their independent research careers following their training period. Salary will be commensurate with qualifications and experience with additional funding for conferences and training seminars.
Requirements
A PhD or MD/PhD is required. To apply, please send your CV, a career statement, a summary of your most significant research accomplishments (300 words) and the contact information of three references to: Steele Labs Recruiting jobs@steele.mgh.harvard.edu.

Postdoctoral fellowship on reprogramming pancreatic ductal adenocarcinoma microenvironment to improve immunotherapy

Investigator: Jain, Rakesh
Date Posted: 2022-01-15
Description
The Steele Laboratories at Massachusetts General Hospital and Harvard Medical School are currently seeking postdoctoral fellow applicants to define the molecular and cellular mechanism underlying the reprogramming of tumor microenvironment to improve immunotherapy. Applicants with a strong training background, experience and publication track record in the following areas are highly encouraged to apply – molecular and cell biology, flow cytometry and FACS, omics (genomics, transcriptomics proteomics and metabolomics), immunohistochemistry and imaging, and/or murine models of cancer.
Responsibilities
Individuals must have a Ph.D. M.D., and/or equivalent degree, appropriate research experience, strong organizational, interpersonal, communication, and computer skills and be prepared to work in a dynamic team environment. To begin the application process, please e-mail a current CV and statement of purpose to jobs@steele.mgh.harvard.edu.
Requirements
The Steele Laboratories at Massachusetts General Hospital and Harvard Medical School are currently seeking postdoctoral fellow applicants to define the molecular and cellular mechanism underlying the reprogramming of tumor microenvironment to improve immunotherapy. Applicants with a strong training background, experience and publication track record in the following areas are highly encouraged to apply – molecular and cell biology, flow cytometry and FACS, omics (genomics, transcriptomics proteomics and metabolomics), immunohistochemistry and imaging, and/or murine models of cancer.

Postdoctoral Fellow

Investigator: Jain, Rakesh
Date Posted: 2022-01-13
Description
The Steele Laboratory is currently seeking a postdoctoral applicant with expertise in breast cancer cell signaling and microenvironment. The position requires a highly motivated and independent researcher to carry out a project aimed at exploring brain-dependent signaling mechanisms to overcome resistance to targeted therapy andto restore anti-tumor immunity. Please see our recent papers for more information about our focus and experimental setup: 1) Askoxylakis et. al., Preclinical Efficacy of Ado-trastuzumab Emtansine in the Brain Microenvironment, JNCI 2015 2) Kodack et. al., Emerging strategies for treating brain metastases from breast cancer, Cancer Cell 2015. Experience in the following technical areas is preferred: molecular and cell biology, biochemistry, flow cytometry and FACS, immunohistochemistry and imaging, and murine models of cancer.
Requirements
Individuals must have a Ph.D. and/or M.D., appropriate research experience, strong organizational, interpersonal, communication, and computer skills and be prepared to work in a dynamic team environment. Applicants with a strong training background and publication track record in brain tumors are highly encouraged to apply. Experience in the following technical areas is preferred: immunohistochemistry, imaging and murine models of cancer. To begin the application process, please e-mail a current CV and statement of purpose to jobs@steele.mgh.harvard.edu

Postdoctoral Fellowship in Tuberculosis Granuloma Microenvironment

Investigator: Jain, Rakesh
Date Posted: 2022-01-13
Description
The Steele Laboratories are currently seeking postdoctoral applicants with expertise in tuberculosis research with extensive experience in immunohistochemistry and tuberculosis pathology. Experience with image analysis is highly preferred. The postdoctoral fellow will participate in an exciting multidisciplinary project aimed at studying the vasculature and matrix of tuberculosis granulomas. The project is funded by the Bill and Melinda Gates Foundation to Prof. Rakesh Jain, with leading tuberculosis collaborators from the NIH and Rutgers University.
Requirements
Individuals must have a Ph.D. and/or M.D., appropriate research experience, strong organizational, interpersonal, communication, and computer skills and be prepared to work in a dynamic team environment. US citizens and permanent US residents are encouraged to apply. To begin the application process, please e-mail a current CV and statement of purpose tojobs@steele.mgh.harvard.edu

Postdoctoral Fellowship in Glioblastoma Microenvironment and Anti-Tumor Immunity

Investigator: Jain, Rakesh
Date Posted: 2022-01-13
Description
The Steele Laboratories are currently seeking postdoctoral applicants with expertise in glioblastoma immunity and microenvironment to explore alternatives to current anti-VEGF treatment and modulation of the associated tumor immune component. Applicants with a strong training background and publication track record in immunology are highly encouraged to apply. Experience in the following technical areas is preferred: molecular and cell biology, flow cytometry and FACS, immunohistochemistry and imaging, and murine models of cancer.
Requirements
Individuals must have a Ph.D. and/or M.D., appropriate research experience, strong organizational, interpersonal, communication, and computer skills and be prepared to work in a dynamic team environment. US citizens and permanent US residents are encouraged to apply. To begin the application process, please e-mail a current CV and statement of purpose to jobs@steele.mgh.harvard.edu

Postdoctoral Fellow in Brain Tumors and Intravital Microscopy

Investigator: Jain, Rakesh
Date Posted: 2022-01-13
Description
The Steele Laboratory is currently seeking a postdoctoral applicant with training and research experience in tumor biology to carry out exciting multidisciplinary projects aimed at understanding tumor microenvironment in brain tumors. Expertise in animal studies and intravital imaging are necessary for the study.
Requirements
Individuals must have a Ph.D. and/or M.D., appropriate research experience, strong organizational, interpersonal, communication, and computer skills and be prepared to work in a dynamic team environment. Applicants with a strong training background and publication track record in brain tumors are highly encouraged to apply. Experience in the following technical areas is preferred: immunohistochemistry, imaging and murine models of cancer. To begin the application process, please e-mail a current CV and statement of purpose to jobs@steele.mgh.harvard.edu

Postdoctoral Fellow in pediatric brain tumors

Investigator: Jain, Rakesh
Date Posted: 2022-01-13
Description
The Steele Laboratory is currently seeking a postdoctoral applicant with training and research experience in tumor biology to carry out exciting multidisciplinary projects aimed at understanding the tumor micro-environment in pediatric brain tumors. Expertise in molecular biology, immunology, animal study and intra-vital imaging are necessary for the study.
Responsibilities
Individuals must have a Ph.D. and/or M.D., appropriate research experience, strong organizational, interpersonal, communication, and computer skills and be prepared to work in a dynamic team environment. Experience in the following technical areas is preferred: molecular and cell biology, flow cytometry and FACS, immunohistochemistry, imaging and murine models of cancer. To begin the application process, please e-mail a current CV and statement of purpose to jobs@steele.mgh.harvard.edu

Selected Publications (from total of 766)

Subudhi S, Voutouri C, Hardin CC, Nikmaneshi MR, Patel AB, Verma A, Khandekar MJ, Dutta S, Stylianopoulos T, Jain RK, Munn LL

Strategies to minimize heterogeneity and optimize
clinical trials in Acute Respiratory Distress Syndrome
(ARDS): Insights from mathematical modelling

EBioMedicine. 2022;75:103809 - PMID: 35033853 - PMCID: PMC8757652 - DOI: 10.1016/j.ebiom.2021.103809
Ho WW, Gomes-Santos IL, Aoki S, Datta M, Kawaguchi K, Talele NP, Roberge S, Ren J, Liu H, Chen IX, Andersson P, Chatterjee S, Kumar AS, Amoozgar Z, Zhang Q, Huang P, Ng MR, Chauhan VP, Xu L, Duda DG, Clark JW, Pittet MJ, Fukumura D, Jain RK

Dendritic cell paucity in mismatch repair-proficient colorectal cancer liver metastases limits immune checkpoint blockade efficacy.

Proc Natl Acad Sci U S A. 2021;118(45):ePub - PMID: 34725151 - PMCID: PMC8609309 - DOI: 10.1073/pnas.2105323118
Wu L, Vasilijic S, Sun Y, Chen J, Landegger LD, Zhang Y, Zhou W, Ren J, Early S, Yin Z, Ho WW, Zhang N, Gao X, Lee GY, Datta M, Sagers JE, Brown A, Muzikansky A, Stemmer-Rachamimov A, Zhang L, Plotkin SR, Jain RK, Stankovic KM, Xu L

Losartan prevents tumor-induced hearing loss and augments radiation efficacy in NF2 schwannoma rodent models.

Sci Transl Med. 2021;13(602):ePub - PMID: 34261799 - PMCID: PMC8409338 - DOI: 10.1126/scitranslmed.abd4816
Siwicki M, Gort-Freitas NA, Messemaker M, Bill R, Gungabeesoon J, Engblom C, Zilionis R, Garris C, Gerhard GM, Kohl A, Lin Y, Zou AE, Cianciaruso C, Bolli E, Pfirschke C, Lin YJ, Piot C, Mindur JE, Talele N, Kohler RH, Iwamoto Y, Mino-Kenudson M, Pai SI, deVito C, Koessler T, Merkler D, Coukos A, Wicky A, Fraga M, Sempoux C, Jain RK, Dietrich PY, Michielin O, Weissleder R, Klein AM, Pittet MJ

Resident Kupffer cells and neutrophils drive liver toxicity in cancer immunotherapy.

Sci Immunol. 2021;6(61):ePub - PMID: 34215680 - PMCID: PMC8845079 - DOI: 10.1126/sciimmunol.abi7083
Amoozgar Z, Kloepper J, Ren J, Tay RE, Kazer SW, Kiner E, Krishnan S, Posada JM, Ghosh M, Mamessier E, Wong C, Ferraro GB, Batista A, Wang N, Badeaux M, Roberge S, Xu L, Huang P, Shalek AK, Fukumura D, Kim HJ, Jain RK

Targeting Treg cells with GITR activation alleviates resistance to immunotherapy in murine glioblastomas

Nat Commun. 2021;12(1):2582 - PMID: 33976133 - PMCID: PMC8113440 - DOI: 10.1038/s41467-021-22885-8
Ferraro GB, Ali A, Luengo A, Kodack DP, Deik A, Abbott KL, Bezwada D, Blanc L, Prideaux B, Jin X, Possada JM, Chen J, Chin CR, Amoozgar Z, Ferreira R, Chen IX, Naxerova K, Ng C, Westermark AM, Duquette M, Roberge S, Lindeman NI, Lyssiotis CA, Nielsen J, Housman DE, Duda DG, Brachtel E, Golub TR, Cantley LC, Asara JM, Davidson SM, Fukumura D, Dartois VA, Clish CB, Jain, RK, Vander Heiden MG

Fatty acid synthesis is required for breast cancer brain metastasis

Nature Cancer. 2021;:ePub
Voutouri C, Nikmaneshi MR, Hardin CC, Patel AB, Verma A, Khandekar MJ, Dutta S, Stylianopoulos T, Munn LL, Jain RK

In silico dynamics of COVID-19 phenotypes for optimizing clinical management.

Proc Natl Acad Sci U S A. 2021;118(3):ePub - PMID: 33402434 - PMCID: PMC7826337 - DOI: 10.1073/pnas.2021642118
Nia HT, Munn LL, Jain RK

Physical traits of cancer.

Science. 2020;370(6516):ePub - PMID: 33122355 - PMCID: PMC8274378 - DOI: 10.1126/science.aaz0868
Chen IX, Newcomer K, Pauken K, Juneja VR, Naxerova K, Wu MW, Pinter M, Singer M, Sharpe AH, Jain RK

A bilateral tumor model identifies transcriptional programs associated with patient response to immune checkpoint blockade

Natl Acad Sci U S A. 2020;117(38):23684-23694 - PMID: 32907939 - PMCID: PMC7519254 - DOI: 10.1073/pnas.2002806117
Nia HT, Datta M, Seano G, Zhang S, Ho WW, Roberge S, Huang P, Munn LL, Jain RK

In vivo compression and imaging in mouse brain to measure the effects of solid stress.

Nat Protoc. 2020;15(8):2321-2340 - PMID: 32681151 - DOI: 10.1038/s41596-020-0328-2
Ngo B, Kim E, Osorio-Vasquez V, Doll S, Bustraan S, Liang RJ, Luengo A, Davidson SM, Ali A, Ferraro GB, Fischer GM, Eskandari R, Kang DS, Ni J, Plasger A, Rajasekhar VK, Kastenhuber ER, Bacha S, Sriram RK, Stein BD, Bakhoum SF, Snuderl M, Cotzia P, Healey JH, Mainolfi N, Suri V, Friedman A, Manfredi M, Sabatini DM, Jones DR, Yu M, Zhao JJ, Jain RK, Keshari KR, Davies MA, Vander Heiden MG, Hernando E, Mann M, Cantley LC, Pacold ME

Limited Environmental Serine and Glycine Confer Brain Metastasis Sensitivity to PHGDH Inhibition.

Cancer Discov. 2020;10(9):1352-1373 - PMID: 32571778 - PMCID: PMC7483776 - DOI: 10.1158/2159-8290.CD-19-1228
Saif M, Kwanten WJ, Carr JA, Chen IX, Posada JM, Srivastava A, Zhang J, Zheng Y, Pinter M, Chatterjee S, Softic S, Kahn CR, van Leyen K, Bruns OT, Jain RK, Bawendi MG

Non-invasive monitoring of chronic liver disease via near-infrared and shortwave-infrared imaging of endogenous lipofuscin.

Nat Biomed Eng. 2020;4(8):801-813 - PMID: 32572196 - PMCID: PMC8310386 - DOI: 10.1038/s41551-020-0569-y
Martin JD, Cabral H, Stylianopoulos T, Jain RK

Improving cancer immunotherapy using nanomedicines: progress, opportunities and challenges.

Nat Rev Clin Oncol. 2020;17(4):251-266 - PMID: 32034288 - PMCID: PMC8272676 - DOI: 10.1038/s41571-019-0308-z
Munn LL, Jain RK

Vascular regulation of antitumor immunity.

Science. 2019;365(6453):544-545 - PMID: 31395771 - PMCID: PMC7321824 - DOI: 10.1126/science.aaw7875
Mitchell MJ, Jain RK, Langer R

Engineering and physical sciences in oncology: challenges and opportunities.

Nat Rev Cancer. 2017;17(11):659-675 - PMID: 29026204 - PMCID: PMC5683724 - DOI: 10.1038/nrc.2017.83
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