tbuckley/cabot-search huggingface dataset:
Effect of Bevacizumab vs Aflibercept on Visual Acuity Among Patients With Macular Edema Due to Central Retinal Vein Occlusion
Authors: Ingrid U. Scott, Paul C. VanVeldhuisen, Michael S. Ip, Barbara A. Blodi, Neal L. Oden, Carl C. Awh, Derek Y. Kunimoto, Dennis M. Marcus, John J. Wroblewski, Jacqueline King
Journal: JAMA (2017)

Studies have established the efficacy and safety of aflibercept for the treatment of macular edema due to central retinal vein occlusion. Bevacizumab is used off-label to treat this condition despite the absence of supporting data.To investigate whether bevacizumab is noninferior to aflibercept for the treatment of macular edema secondary to central retinal or hemiretinal vein occlusion.The SCORE2 randomized noninferiority clinical trial was conducted at 66 private practice or academic centers in the United States, and included 362 patients with macular edema due to central retinal or hemiretinal vein occlusion who were randomized 1:1 to receive aflibercept or bevacizumab. The first participant was randomized on September 17, 2014, and the last month 6 visit occurred on May 6, 2016. Analyses included data available as of December 30, 2016.Eyes were randomized to receive intravitreal injection of bevacizumab (1.25 mg; n = 182) or aflibercept (2.0 mg; n = 180) every 4 weeks through month 6.The primary outcome was mean change in visual acuity (VA) letter score (VALS) from the randomization visit to the 6-month follow-up visit, based on the best-corrected electronic Early Treatment Diabetic Retinopathy Study VALS (scores range from 0-100; higher scores indicate better VA). The noninferiority margin was 5 letters, and statistical testing for noninferiority was based on a 1-sided 97.5% confidence interval.Among 362 randomized participants (mean [SD] age, 69 [12] years; 157 [43.4%] women; mean [SD] VALS at baseline, 50.3 [15.2] [approximate Snellen VA 20/100]), 348 (96.1%) completed the month 6 follow-up visit. At month 6, the mean VALS was 69.3 (a mean increase from baseline of 18.6) in the bevacizumab group and 69.3 (a mean increase from baseline of 18.9) in the aflibercept group (model-based estimate of between-group difference, -0.14; 97.5% CI, -3.07 to ∞; P = .001 for noninferiority), meeting criteria for noninferiority. Ocular adverse events in the aflibercept group included 4 participants with intraocular pressure (IOP) more than 10 mm Hg greater than baseline; ocular adverse events in the bevacizumab group included 1 participant with endophthalmitis (culture negative), 9 with IOP more than 10 mm Hg greater than baseline, 2 with IOP higher than 35 mm Hg, and 1 with angle-closure glaucoma not attributed to the study drug or procedure.Among patients with macular edema due to central retinal or hemiretinal vein occlusion, intravitreal bevacizumab was noninferior to aflibercept with respect to visual acuity after 6 months of treatment.
Pharmacodynamic effects of regorafenib in metastatic colorectal carcinoma (mCRC).
Authors: Andrea Li Ann Wong, Arvind Sinha, Anil Gopinathan, Robert S.C. Lim, Chee Seng Tan, I Peng Thomas Soh, Sudhakar Venkatesh, Christina Titin, Richie Chuan Teck Soong, Brendan Pang, Nur Sabrina Sapari, Ting Ting Wang, Ying Kiat Zee, Benjamin Chuah, Michael Jeffers, Chetan Lathia, Zuzana Trnkova, Scott Wilhelm, Boon C. Goh
Journal: Journal of Clinical Oncology (2013)

e14507 Background: Regorafenib, an oral multikinase inhibitor of VEGFR2/3, PDGFRb, KIT, FGFR, RET, RAF and TIE2, is efficacious in refractory mCRC but its mechanism of action is unclear and predictive biomarkers are lacking. Methods: We assessed tumor and circulatory biomarkers in a phase 2 study of regorafenib in refractory mCRC patients. Regorafenib was administered orally at 160mg/d for 3 out of 4 weeks. Post cycle 2 response was assessed by RECIST 1.1. Subjects were scheduled for FDG PET-CT scans (pre + D15) and paired core needle tumor biopsies for IHC analysis (pre + D21) in cycle 1. Archival tumor mutations were evaluated using Sequenom MassARRAY OncoCarta Panel V1.0 assay. Results: 35 patients were treated; 49% received &gt; 4 prior therapies and 43% had prior bevacizumab. Median PFS was 3.45 mths (95% CI: 3.40-3.49), ORR was 3% and disease control rate [DCR] (PR + SD at 8 wks) was 57%. Early PET responses (EORTC criteria) were seen in 49%, but did not predict for DCR (p=1.0). Fatigue, hand foot skin reaction (HFSR), voice change and diarrhea occurred in &gt; 30% of subjects. Grade 3-5 toxicities occurred in 46%, the commonest being HFSR and rash (17% each). Median relative dose intensity was 92%; 43% required &gt; 1 dose reduction, 60% required &gt; 1 dose interruption. KRAS (29%), BRAF (9%), EGFR (9%), NRAS (6%) KIT (3%), PIK3CA (3%), PDGFRA (3%) and CDK (3%) mutations were detected in archival tumors. None predicted for ORR or DCR; PFS was identical in KRAS mutant vs wt patients (3.45 mths, p=0.39) and similar in BRAF mutant vs wt patients (3.48 vs 3.45 mths, p=0.10). The patient with the longest PFS (12.6 mths) had a BRAF mutation. Amongst the 10 paired tumor samples available, IHC markers upregulated in &gt;50% cases were pMEK, pERK, pJun and pJNK, whilst those downregulated/ unchanged in &gt;50% were pKIT, pVEGFR2, CD31 [vascular endothelial cells (ECs)] and podoplanin (lymphatic ECs). The greatest change was observed in podoplanin expression, corresponding to a 60% reduction in lymphatic vessel density. Conclusions: FDG-PET responses in cycle 1 did not predict for regorafenib clinical benefit in mCRC patients. Targeting lymphatic/vascular ECs in the tumor microenvironment may be a more significant antitumor mechanism of regorafenib than MAP kinase pathway inhibition. Clinical trial information: NCT01189903.
Impact of beta-catenin mutation status on MDR1/P-glycoprotein expression and chemotherapy response in colon cancer cells
Authors: Ulrike Stein, Claudia Fleuter, Robert Shoemaker, Peter Schlag, Wolfgang Walther
Journal: Cancer Research (2008)

AACR Annual Meeting-- Apr 12-16, 2008; San Diego, CA

3228 

Colorectal cancers are often chemoresistant towards antitumor drugs that are substrates for MDR1/P-glycoprotein-mediated multidrug resistance. Furthermore, activation of the Wnt/beta-catenin pathway is frequently observed in colorectal cancers. Our aim was to elucidate the impact of gain-of-function beta-catenin mutation on expression of the multidrug resistance gene MDR1 in human colon cancer cell lines and tumors. We analyzed cell lines heterozygous for gain-of-function and wild-type beta-catenin, and variants homozygous for gain- or loss-of-function, for MDR1 expression, drug accumulation, and chemosensitivity. Cell lines with gain-of-function beta-catenin expressed up to 5-fold elevated MDR1 levels. Transduction of gain-of-function beta-catenin led to induced MDR1 expression, whereas beta-catenin siRNA knocked down MDR1 expression. Consistent with the presence of functional TCF binding sites within the MDR1 promoter, we confirmed the beta-catenin-induction of MDR1 promoter activity, but with higher activities in cells harboring gain-of-function beta-catenin. Drug accumulation and chemosensitivity towards compounds that are substrates for multiple transporters, were not affected. However, the cytotoxicity of chemotherapeutic drugs, which are major substrates for MDR1/P-glycoprotein, was clearly reduced in gain-of-function beta-catenin harboring and MDR1 overexpressing cancer cells. Extension of these in vitro cell line studies to primary colon tumors heterozygous for gain-of-function beta-catenin showed concomitant nuclear beta-catenin localization and high MDR1 expression. In summary, the mutation status of beta-catenin may impact the MDR1/P-glycoprotein-mediated resistance to chemotherapy in colorectal cancer.
Comparison of clinical prediction rules for detection of cirrhosis in non-alcoholic fatty liver disease: a multicenter, international, collaborative study- NASH CRN (USA) and Newcastle (UK) Cohort
Authors: D. Brandman, M. Boyle, S. McPherson, M. Van Natta, A. Sanyal, K. Kowdley, B. Tetri, N. Chalassani, M. Abdelmalek, N.A. Terrault, A. McCullough, R. Bettencourt, C. Caussy, D. Kleiner, C. Behling, E. Doo, J. Tonascia, Q. Anstee, R. Loomba
Journal: Journal of Hepatology (2017)
Efficacy and safety of the fixed-dose combination regimen of MK3 [MK-3682/grazoprevir/ruzasvir] with or without ribavirin in non-cirrhotic or cirrhotic patients with chronic HCV GT1, 2, 3, 4 or 6 infection (Parts A &amp; B of C-CREST-1 &amp; 2)
Authors: E. Lawitz, E.M. Yoshida, M. Buti, J.M. Vierling, P.L. Almasio, S. Bruno, P.J. Ruane, T.I. Hassanein, B. Mullhaupt, B. Pearlman, L. Jancoriene, W. Gao, H.-C. Huang, A. Shepherd, B. Tannenbaum, D. Fernsler, J.J. Li, A. Grandhi, H. Liu, M. Su, F. Dutko, W.W. Yeh, R. Plank, B.-Y.T. Nguyen, J. Wahl, E. Barr, J.R. Butterton
Journal: Journal of Hepatology (2017)
Barriers to sperm banking in testicular cancer survivors.
Authors: Sagar D. Sardesai, Daniel Sonnenburg, Nasser Hanna, Mary J. Brames, Sommer LeAnn Case-Eads, Lawrence H. Einhorn
Journal: Journal of Clinical Oncology (2015)

e17574 Background: Testicular cancer is the most common malignancy in 15-35 year old men. It is also highly curable with over 95% five-year survival rates. However, forty percent of patients receiving platinum based cytotoxic combination chemotherapy will have oligospermia or azoospermia impairing the ability to father children. Sperm banking is an established option for fertility preservation. The aim of this retrospective survey is to assess the utilization of sperm cryopreservation and potential barriers in this young male population. Methods: Testicular cancer patients 18 years or older with more than 1 year post chemotherapy follow-up were eligible. A 5 item questionnaire including a mix of quantitative and qualitative questions was provided. Results: Two hundred patients enrolled in the study and completed the questionnaire. 139/200 (70%) patients chose not to bank sperm; 71(51%) were not interested, 25(18%) declined due to desire to immediately start chemotherapy, 24(17%) were not offered, 12(9%) declined due to cost and 7(5%) answered
The importance of patient selection in nonmyeloablative stem cell transplant (NMSCT) for acute and chronic leukaemia, myelodysplastic syndrome, and myeloma
Authors: M. Lalancette, M. Michailet, R. Szydlo, Katy Rezvani, S. Mackinnon, D. Biaise, J. Finke, S. Slavin, E. P. Alessandrino, D. Niederwieser, F. Frassoni, G. Gahrton, J. Apperley
Journal: Blood (2000)
Can We Jump from Cross-Sectional to Dynamic Interpretations of Networks Implications for the Network Perspective in Psychiatry
Authors: Fionneke M. Bos, Evelien Snippe, Stijn de Vos, Jessica A. Hartmann, Claudia J.P. Simons, Lian van der Krieke, Peter de Jonge, Marieke Wichers
Journal: Psychotherapy and Psychosomatics (2017)
Has the rising placebo response impacted antidepressant clinical trial outcome? Data from the US Food and Drug Administration 1987‐2013
Authors: Arif Khan, Kaysee Fahl Mar, Jim Faucett, Shirin Khan Schilling, Walter A. Brown
Journal: World Psychiatry (2017)

More than fifteen years ago, it was noted that the failure rate of antidepressant clinical trials was high, and such negative outcomes were thought to be related to the increasing magnitude of placebo response. However, there is considerable debate regarding this phenomenon and its relationship to outcomes in more recent antidepressant clinical trials. To investigate this, we accessed the US Food and Drug Administration (FDA) reviews for sixteen antidepressants (85 trials, 115 trial arms, 23,109 patients) approved between 1987 and 2013. We calculated the magnitude of placebo and antidepressant responses, antidepressant‐placebo differences, as well as the effect sizes and success rates, and compared these measures over time. Exploratory analysis investigated potential changes in trial design and conduct over time. As expected, the magnitude of placebo response has steadily grown in the past 30 years, increasing since 2000 by 6.4% (r=0.46, p&lt;0.001). Contrary to expectations, a similar increase has occurred in the magnitude of antidepressant response (6.0%, r=0.37, p&lt;0.001). Thus, the effect sizes (0.30 vs. 0.29, p=0.42) and the magnitude of antidepressant‐placebo differences (10.5% vs. 10.3%, p=0.37) have remained statistically equivalent. Furthermore, the frequency of positive trial arms has gone up in the past 15 years (from 47.8% to 63.8%), but this difference in frequency has not reached statistical significance. Trial design features that were previously associated with a possible lower magnitude of placebo response were not implemented, and their relationship to the magnitude of placebo response could not be replicated. Of the 34 recent trials, two implemented enhanced interview techniques, but both of them were unsuccessful. The results of this study suggest that the relationship between the magnitude of placebo response and the outcome of antidepressant clinical trials is weak at best. These data further indicate that antidepressant‐placebo differences are about the same for all of the sixteen antidepressants approved by the FDA in the past thirty years.
Prospective Evaluation of Bleeding Incidence in Fibrinogen Deficiency (PRO-RBDD Study)
Authors: Roberta Palla, Marzia Menegatti, Marco Boscarino, Jan Blatny, Ondrej Zapletal, Jean-Francois Schved, Muriel Giansily-Blaizot, Susan Halimeh, Britta Lachmann, Helen Platokouki, Helen Pergantou, Simona Maria Siboni, Marlies van Lent, Paul Brons, Britta A.P. Laros-Van Gorkom, Roger E.G. Schutgens, Monique van Haaften-Spoor, Munira Borhany, Naveena Fatima, Danijela Mikovic, Marko Saracevic, Philippe De Moerloose, Alessandro Casini, Nihal Ozdemir, Yilmaz Ay, Steve Austin, Pearl Quartey, Michael Makris, Sarah Brown, Amy D. Shapiro, Adrianna Williamson, John C. Chapin, Fraustina Hsu, Flora Peyvandi
Journal: Blood (2016)
Abstract A67: Elucidating the impact of zoledronic acid on the bone microenvironment: Implications for breast cancer
Authors: Jessalyn M. Ubellacker, Sandra S. McAllister
Journal: Cancer Research (2016)

Abstract Bisphosphonates, such as zoledronic acid (ZOL), are bone microenvironment modulators that work primarily by inhibiting the activity of bone resorbing osteoclasts and have demonstrated ability to reduce breast cancer risk and recurrence in the bone in clinical trials. Previous work in our laboratory has demonstrated the ability of tumor-derived factors (osteopontin) to activate pro-tumorigenic bone marrow hematopoietic cells, which subsequently promote tumor outgrowth. The aim of this current study is to determine whether ZOL inhibits the impact of such tumor-derived paracrine factors on the bone microenvironment, thus reducing metastatic outgrowth in the bone. A human bone-tropic breast cancer cell line (MDA-MB-231 BO2) was introduced into NU/J mice via intracardiac (IC) and intratibial (IT) injections 72 hours after treating the mice with ZOL. Cell seeding was assessed at 24 hours by CM-DiL staining, and subsequent tumor outgrowth was monitored weekly by bioluminescence. One ZOL pre-dose was sufficient to decrease both tumor cell seeding (via IC) and colonization (via IT) relative to the robust tumor outgrowth observed in mice treated with vehicle control. Additionally, subcutaneous ad-mixtures of MDA-MB-231 BO2 cells with bone marrow cells from ZOL-treated mice demonstrated a decreased incidence of tumor formation relative to control bone marrow cells, indicating that the tumor inhibitory effect of ZOL occurs via modulations to the bone marrow hematopoietic microenvironment. A second MDA-MB-231 bone-tropic cell line similar to the BO2 line, but with higher expression levels of CXCL1, G-CSF, GM-CSF and IL8, was not inhibited by ZOL in the IC and IT bone metastasis models. These results implicate the role of certain tumor-derived paracrine factors in mediating resistance to ZOL treatment. These findings are important for elucidating the therapeutic potential of bisphosphonates for treating at-risk patients in the adjuvant setting before they develop incurable metastatic disease. Citation Format: Jessalyn M. Ubellacker, Sandra S. McAllister. Elucidating the impact of zoledronic acid on the bone microenvironment: Implications for breast cancer. [abstract]. In: Proceedings of the AACR Special Conference on Tumor Metastasis; 2015 Nov 30-Dec 3; Austin, TX. Philadelphia (PA): AACR; Cancer Res 2016;76(7 Suppl):Abstract nr A67.
Hepatitis C virus genotypes are associated with distinct intestinal microbial community structures
Authors: N. Döscher, M. Vital, I. Plumeier, S. Kahl, J. Kirschner, S. Ziegert, A. Potthoff, M.P. Manns, D.H. Pieper, H. Wedemeyer, B. Heidrich, A.G. Heidrich
Journal: Journal of Hepatology (2017)
Key molecular signatures of disease development and progression in non-alcoholic fatty liver disease in humans
Authors: R. Vincent, A. Nefedov, A. Oseini, S. Cazanave, A. Webber, K. Jensen, K. Tanis, L. Wang, B. Banini, D. Kumar, H.-K. Min, P. Santhekadur, M. Seneshaw, K. Daita, P. Bedossa, F. Mirshahi, A. Sanyal
Journal: Journal of Hepatology (2017)
A phase 2 dose-optimization study of lonafarnib with ritonavir for the treatment of chronic delta hepatitis—end of treatment results from the LOWR HDV-2 study
Authors: C. Yurdaydin, R. Idilman, O. Keskin, C. Kalkan, M.F. Karakaya, A. Caliskan, E. Yurdcu, S.C. Karatayli, M. Bozdayi, C. Koh, T. Heller, J. Glenn
Journal: Journal of Hepatology (2017)
Mitomycin C, doxorubicin, and cisplatin: as a safe and effective preoperative chemoradiation cocktail for soft tissue sarcomas.
Authors: Meera Sridharan, Ivy Ann Petersen, Peter S. Rose, Karen Fritchie, Scott H. Okuno, Steven Ian Robinson
Journal: Journal of Clinical Oncology (2014)

10593 Background: Soft tissue sarcomas are rare malignancies, often treated with a multidisciplinary approach at high volume centers. This project investigates one such approach employed at the Mayo Clinic, utilizing mitomycin C 6 mg/m2/day, doxorubicin 30 mg/m2/day, cisplatin 45 mg/m2/day for two cycles concomitantly with radiation prior to surgical resection. Methods: Following institutional review board approval, the charts of 58 patients (39 male) who received the aforementioned regimen from 2008 through 2012 were retrospectively reviewed. Factors relevant to prognosis and survival were analyzed by Kaplan-Meier methods using JMP statistical software. Survival data was censored at 3 years. Patients with sarcomas greater or equal to 5 cm in dimension were selected for this treatment. Results: The histologic subtypes included: undifferentiated sarcoma, liposarcoma, leiomyosarcoma, synovial sarcoma, malignant peripheral nerve sheath tumor, rhabdomyosarcoma, mesenchymal chondrosarcoma and fibrosarcoma. The median age at presentation was 62 years (range 33-78 years) with a median follow up of 37 months (range 6-68 months). Tumors were located primarily in the extremities (44/58; 76%), with a median size of 9.9 cm (range 5 -22 cm). All patients were able to achieve surgical resection. Median tumor necrosis was 72.5% (range 5 -100%) with fibrosarcoma having the poorest response to treatment (median necrosis 20%, n=8). 37 patients (64%) received additional pre- or post-op chemotherapy with doxorubicin and ifosfamide. 23 patients (40%) received intraoperative radiation. The 3-year event free survival (EFS) was 71%. Two of 58 patients (3.4%) suffered a local relapse within 9 (7-11) months. Though not statistically significant, patients who achieved > 90% necrosis or who received pre-or postoperative chemotherapy had superior EFS (84% vs 65% and 78% vs 57% respectively). The postoperative complications included: infection (14), wound dehiscence (1), hematoma (2), and fluid collections (5). Conclusions: Preoperative concomitant chemoradiation with mitomycin C, doxorubicin, and cisplatin is a safe and effective regimen for soft tissue sarcomas.
RNA editing signature during myeloid leukemia cell differentiation
Authors: C Rossetti, E Picardi, M Ye, G Camilli, A M D'Erchia, L Cucina, F Locatelli, L Fianchi, L Teofili, G Pesole, A Gallo, R Sorrentino
Journal: Leukemia (2017)

Adenosine deaminases acting on RNA (ADARs) are key proteins for hematopoietic stem cell self-renewal and for survival of differentiating progenitor cells. However, their specific role in myeloid cell maturation has been poorly investigated. Here we show that ADAR1 is present at basal level in the primary myeloid leukemia cells obtained from patients at diagnosis as well as in myeloid U-937 and THP1 cell lines and its expression correlates with the editing levels. Upon phorbol-myristate acetate or Vitamin D3/granulocyte macrophage colony-stimulating factor (GM-CSF)-driven differentiation, both ADAR1 and ADAR2 enzymes are upregulated, with a concomitant global increase of A-to-I RNA editing. ADAR1 silencing caused an editing decrease at specific ADAR1 target genes, without, however, interfering with cell differentiation or with ADAR2 activity. Remarkably, ADAR2 is absent in the undifferentiated cell stage, due to its elimination through the ubiquitin–proteasome pathway, being strongly upregulated at the end of the differentiation process. Of note, peripheral blood monocytes display editing events at the selected targets similar to those found in differentiated cell lines. Taken together, the data indicate that ADAR enzymes play important and distinct roles in myeloid cells.
Cancer-Associated Mutations in Endometriosis without Cancer
Authors: Michael S. Anglesio, Nickolas Papadopoulos, Ayse Ayhan, Tayyebeh M. Nazeran, Michaël Noë, Hugo M. Horlings, Amy Lum, Siân Jones, Janine Senz, Tamer Seckin, Julie Ho, Ren-Chin Wu, Vivian Lac, Hiroshi Ogawa, Basile Tessier-Cloutier, Rami Alhassan, Amy Wang, Yuxuan Wang, Joshua D. Cohen, Fontayne Wong, Adnan Hasanovic, Natasha Orr, Ming Zhang, Maria Popoli, Wyatt McMahon, Laura D. Wood, Austin Mattox, Catherine Allaire, James Segars, Christina Williams, Cristian Tomasetti, Niki Boyd, Kenneth W. Kinzler, C. Blake Gilks, Luis Diaz, Tian-Li Wang, Bert Vogelstein, Paul J. Yong, David G. Huntsman, Ie-Ming Shih
Journal: New England Journal of Medicine (2017)

Endometriosis, defined as the presence of ectopic endometrial stroma and epithelium, affects approximately 10% of reproductive-age women and can cause pelvic pain and infertility. Endometriotic lesions are considered to be benign inflammatory lesions but have cancerlike features such as local invasion and resistance to apoptosis.
Injectable Supramolecular Hydrogels as Delivery Agents of Bcl‐2 Conversion Gene for the Effective Shrinkage of Therapeutic Resistance Tumors
Authors: Xuan Liu, Xiaohong Chen, Ming Xuan Chua, Zibiao Li, Xian Jun Loh, Yun‐Long Wu
Journal: Advanced Healthcare Materials (2017)

Injectable hydrogels to deliver therapeutic genes in a minimally invasive manner and to achieve long term sustained release at tumor sites to minimize side effects are attractive for cancer therapy and precision medicine, but its rational design remains a challenge. In this report, an injectable supramolecular hydrogel system is designed based on the polypesudorotaxane formation between α‐cyclodextrin (α‐CD) and cationic methoxy‐poly(ethylene glycol)‐ b ‐poly(ε‐caprolactone)‐ b ‐poly(ethylene imine) (MPEG–PCL–PEI) copolymer, with the ability to form polyplexes with anionic plasmid DNA for effective sustained gene delivery. To be mentioned, the MPEG–PCL–PEI copolymers show similar pDNA binding ability, better gene transfection efficiency, lower cytotoxicity than nonviral gene transfection gold standard PEI (25 kDa), due to the formation of micelles and more stable polyplexes. More importantly, this MPEG–PCL–PEI/α‐CD/pDNA supramolecular hydrogel shows a sustained release of pDNA in form of polyplex for up to 7 d. By taking these advantages, this supramolecular hydrogel system is applied as an injectable carrier for sustained Bcl‐2 conversion gene release, in an in vivo rodent model of therapeutic resistant hepatocarcinoma with high expression of antiapoptotic Bcl‐2 protein. This work represents the first time that injectable MPEG–PCL–PEI/α‐CD supramolecular hydrogels possess good controllable release effect of Bcl‐2 conversion genes in the form of polyplex to effectively inhibit in vivo tumor growth and this “enemy to friend” strategy will benefit various applications, including on‐demand gene delivery and personalized medicine.