CoChat
Sign Up
Cited by 37Metabolism, Diabetes, and CancerPI3K/AKT/mTOR signaling in cancerAdvanced Breast Cancer Therapies

Management of phosphatidylinositol-3-kinase inhibitor-associated hyperglycemia

Open access
Goncalves, Marcus D., Farooki, Azeez·2022·Integrative Cancer Therapies
DOI 10.1177/15347354211073163PMC PMC8793384
Open this paper in CoChat — free accountOpen PDF

Abstract

Phosphatidylinositol-3-kinase (PI3K) pathway hyperactivation has been associated with the development of cancer and treatment resistance. PI3K inhibitors are now used to treat hormone receptor-positive (HR+), human epidermal growth factor receptor-2–negative (HER2−), PIK3CA-mutated advanced breast cancer. Hyperglycemia, a frequently observed adverse event with PI3K inhibitors (PI3Ki), is regarded as an on-target effect because inhibition of the PI3K pathway has been shown to decrease glucose transport and increase glycogenolysis and gluconeogenesis. PI3Ki-induced hyperglycemia results in a compensatory increase in insulin release, which has been shown to reduce the efficacy of treatment by reactivating the PI3K pathway in preclinical models. Patients with an absolute or relative deficiency in insulin, and those with insulin resistance or pancreatic dysfunction, may experience exacerbated or prolonged hyperglycemia. Therefore, the effective management of PI3Ki-associated hyperglycemia depends on early identification of patients at risk, frequent monitoring to allow prompt recognition of hyperglycemia and its sequelae, and initiating appropriate management strategies. Risk factors for the development of hyperglycemia include older age (≥75 years), overweight/obese at baseline, and family history of diabetes. Consultation with an endocrinologist is recommended for patients considered high risk. The management of PI3Ki-induced hyperglycemia requires an integrative approach that combines diets low in carbohydrates and glucose-lowering medications. Medications that do not affect the PI3K pathway are preferred as the primary and secondary agents for the management of hyperglycemia. These include metformin, sodium-glucose co-transporter 2 inhibitors, thiazolidinediones, and α-glucosidase inhibitors. Insulin should only be considered as a last-line agent for PI3Ki-associated hyperglycemia due to its stimulatory effect of PI3K signaling. Clinical studies show that alpelisib-associated hyperglycemia is reversible and manageable, rarely leading to treatment discontinuation. Management of PI3Ki-associated hyperglycemia in patients with breast cancer should focus on the prevention of acute and subacute complications of hyperglycemia, allowing patients to remain on anticancer treatment longer.

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.1177/15347354211073163

Cites

8 of 8 references verified0 citation errors · 0 not checkable

Statistics

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • Insulin can reactivate the PI3K pathway, negating the effects of alpelisib.

    “Insulin and sulfonylureas should be considered last-line agents, as insulin can reactivate the PI3K pathway, negating the effects of alpelisib (223,224).”

    From 9. Pharmacologic Approaches to Glycemic Treatment: Standards of Care in Diabetes—2025 (2025) · cites this paper as [224]

    The “Insulin as Last Line of Therapy” section says insulin can partially reactivate the PI3K pathway despite PI3K-inhibitor treatment. The Concluding Remarks say insulin may theoretically curb antitumor activity; the paper does not say it negates alpelisib’s effects. Page numbers were not available in our copy. (LLM, conf=0.88)

    Experimental — accuracy not yet measured

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Cites

Flagged first, then by citations

Research works printed but not linked: 69

  1. [1]Yang J Nie J Ma X Wei Y Peng Y Wei X. Targeting PI3K in cancer: mechanisms and advances in clinical trials. Mol Cancer. 2019; 18: 26. doi: 10.1186/s12943-019-0954-x 30782187 PMC6379961 · DOI
  2. [2]Paplomata E O’Regan R. The PI3K/AKT/mTOR pathway in breast cancer: targets, trials and biomarkers. Ther Adv Med Oncol. 2014; 6: 154- 166. 25057302 PMC4107712
  3. [3]Thorpe LM Yuzugullu H Zhao JJ. PI3K in cancer: divergent roles of isoforms, modes of activation and therapeutic targeting. Nat Rev Cancer. 2015; 15: 7- 24. doi: 10.1038/nrc3860 25533673 PMC4384662 · DOI
  4. [4]Fruman DA Chiu H Hopkins BD Bagrodia S Cantley LC Abraham RT. The PI3K pathway in human disease. Cell. 2017; 170: 605- 635. doi: 10.1016/j.cell.2017.07.029 28802037 PMC5726441 · DOI · Paper page
  5. [5]Hoxhaj G Manning BD. The PI3K-AKT network at the interface of oncogenic signalling and cancer metabolism. Nat Rev Cancer. 2019; 20: 74- 88. doi: 10.1038/s41568-41019-40216-41567 31686003 PMC7314312 · DOI
  6. [7]Vasan N Toska E Scaltriti M. Overview of the relevance of PI3K pathway in HR-positive breast cancer. Ann Oncol. 2019; 30:x3-x11. doi: 10.1093/annonc/mdz281 PMC6923788 31859348 · DOI
  7. [8]Engelman JA Luo J Cantley LC. The evolution of phosphatidylinositol 3-kinases as regulators of growth and metabolism. Nat Rev Genet. 2006; 7: 606- 619. doi: 10.1038/nrg1879 16847462 · DOI · Paper page
  8. [9]Qin H Liu L Sun S, et al The impact of PI3K inhibitors on breast cancer cell and its tumor microenvironment. PeerJ. 2018; 6:e5092. doi: 10.7717/peerj.5092 PMC6014315 29942710 · DOI
  9. [10]Razavi P Chang MT Xu G, et al The genomic landscape of endocrine-resistant advanced breast cancers. Cancer Cell. 2018; 34: 427- 438. doi: 10.1016/j.ccell.2018.08.008 30205045 PMC6327853 · DOI
  10. [11]The Cancer Genome Atlas Network. Comprehensive molecular portraits of human breast tumours. Nature. 2012; 490: 61- 70. 23000897 PMC3465532
  11. [12]Di Leo A Johnston S Lee KS, et al Buparlisib plus fulvestrant in postmenopausal women with hormone-receptor-positive, HER2-negative, advanced breast cancer progressing on or after mTOR inhibition (BELLE-3): a randomised, double-blind, placebo-controlled, phase 3 trial. Lancet Oncol. 2018; 19: 87- 100. 29223745
  12. [13]Moynahan ME Chen D He W, et al Correlation between PIK3CA mutations in cell-free DNA and everolimus efficacy in HR(+), HER2(-) advanced breast cancer: results from BOLERO-2. Br J Cancer. 2017; 116: 726- 730. 28183140 PMC5355930
  13. [14]Garrido-Castro AC Lin NU Polyak K. Insights into molecular classifications of triple-negative breast cancer: improving patient selection for treatment. Cancer Discov. 2019; 9: 176- 198. 30679171 PMC6387871
  14. [15]Mollon LE Anderson EJ Dean JL, et al A systematic literature review of the prognostic and predictive value of PIK3CA mutations in HR(+)/HER2(-) metastatic breast cancer. Clin Breast Cancer. 2020; 20:e232-e243. 32234362
  15. [16]Spangle JM Von T Pavlick DC Khotimsky A Zhao JJ Roberts TM. PIK3CA C-terminal frameshift mutations are novel oncogenic events that sensitize tumors to PI3K-α inhibition. Proc Natl Acad Sci U S A. 2020; 117: 24427- 24433. doi: 10.1073/pnas.2000060117 32929011 PMC7533832 · DOI
  16. [20]Aronoff SL Berkowitz K Shreiner B Want L. Glucose metabolism and regulation: beyond insulin and glucagon. Diabetes Spectr. 2004; 17: 183- 190. doi: 10.2337/diaspect.17.3.183 · DOI
  17. [21]Drullinsky PR Hurvitz SA. Mechanistic basis for PI3K inhibitor antitumor activity and adverse reactions in advanced breast cancer. Breast Cancer Res Treat. 2020; 181: 233- 248. doi: 10.1007/s10549-020-05618-1 32274666 · DOI
  18. [22]Goldman JW Mendenhall MA Rettinger SR. Hyperglycemia associated with targeted oncologic treatment: mechanisms and management. Oncologist. 2016; 21: 1326- 1336. doi: 10.1634/theoncologist.2015-0519 27473045 PMC5189614 · DOI
  19. [23]Huang X Liu G Guo J Su Z. The PI3K/AKT pathway in obesity and type 2 diabetes. Int J Biol Sci. 2018; 14: 1483- 1496. doi: 10.7150/ijbs.27173 30263000 PMC6158718 · DOI · Paper page
  20. [25]Goncalves MD Hopkins BD Cantley LC. Phosphatidylinositol 3-kinase, growth disorders, and cancer. N Engl J Med. 2018; 379: 2052- 2062. doi: 10.1056/NEJMra1704560 30462943 · DOI · Paper page
  21. [27]Gallagher EJ Fierz Y Vijayakumar A Haddad N Yakar S LeRoith D. Inhibiting PI3K reduces mammary tumor growth and induces hyperglycemia in a mouse model of insulin resistance and hyperinsulinemia. Oncogene. 2011; 31: 3213- 3222. doi: 10.1038/onc.2011.3495 22037215 PMC3275680 · DOI
  22. [28]du Rusquec P Blonz C Frenel JS Campone M. Targeting the PI3K/Akt/mTOR pathway in estrogen-receptor positive HER2 negative advanced breast cancer. Ther Adv Med Oncol. 2020; 12: 1758835920940939. doi: 10.1177/1758835920940939 32782489 PMC7388095 · DOI
  23. [29]Juric D de Bono JS LoRusso PM, et al A first-in-human, phase I, dose-escalation study of TAK-117, a selective PI3Kα isoform inhibitor, in patients with advanced solid malignancies. Clin Cancer Res. 2017; 23: 5015- 5023. doi: 10.1158/1078-0432.CCR-16-2888 28490463 PMC6858996 · DOI
  24. [30]Janku F. Phosphoinositide 3-kinase (PI3K) pathway inhibitors in solid tumors: from laboratory to patients. Cancer Treat Rev. 2017; 59: 93- 101. doi: 10.1016/j.ctrv.2017.07.005 28779636 · DOI
  25. [31]Vuylsteke P Huizing M Petrakova K, et al Pictilisib PI3Kinase inhibitor (a phosphatidylinositol 3-kinase [PI3K] inhibitor) plus paclitaxel for the treatment of hormone receptor-positive, HER2-negative, locally recurrent, or metastatic breast cancer: interim analysis of the multicentre, placebo-controlled, phase II randomised PEGGY study. Ann Oncol. 2016; 27: 2059- 2066. 27573562
  26. [32]Dent S Cortés J Im YH, et al Phase III randomized study of taselisib or placebo with fulvestrant in estrogen receptor-positive, PIK3CA-mutant, HER2-negative, advanced breast cancer: the SANDPIPER trial. Ann Oncol. 2021; 32: 197- 207. 33186740 PMC8457522
  27. [33]Moore AM Einhorn LH Estes D, et al Gefitinib in patients with chemo-sensitive and chemo-refractory relapsed small cell cancers: a Hoosier Oncology Group phase II trial. Lung Cancer. 2006; 52: 93- 97. doi: 10.1016/j.lungcan.2005.1012.1002 16488055 · DOI
  28. [34]Blow T Hyde PN Falcone JN, et al Treating alpelisib-induced hyperglycemia with very low carbohydrate diets and sodium-glucose co-transporter 2 inhibitors: a case series. Integr Cancer Ther. 2021; 20: 15347354211032283. 34259084 PMC8283040
  29. [35]Ando Y Iwasa S Takahashi S, et al Phase I study of alpelisib (BYL719), an α-specific PI3K inhibitor, in Japanese patients with advanced solid tumors. Cancer Sci. 2019; 110: 1021- 1031. 30588709 PMC6398875
  30. [36]Sarker D Ang JE Baird R, et al First-in-human phase I study of pictilisib (GDC-0941), a potent pan-class I phosphatidylinositol-3-kinase (PI3K) inhibitor, in patients with advanced solid tumors. Clin Cancer Res. 2015; 21: 77- 86. 25370471 PMC4287394
  31. [37]Patnaik A Appleman LJ Tolcher AW, et al First-in-human phase I study of copanlisib (BAY 80-6946), an intravenous pan-class I phosphatidylinositol 3-kinase inhibitor, in patients with advanced solid tumors and non-Hodgkin's lymphomas. Ann Oncol. 2016; 27: 1928- 1940. 27672108 PMC5035790
  32. [38]Rugo HS André F Yamashita T, et al Time course and management of key adverse events during the randomized phase III SOLAR-1 study of PI3K inhibitor alpelisib plus fulvestrant in patients with HR-positive advanced breast cancer. Ann Oncol. 2020; 31: 1001- 1010. doi: 10.1016/j.annonc.2020.05.001 32416251 · DOI · Paper page
  33. [39]American Diabetes Association. Standards of medical care in diabetes-2020. Diabetes Care. 2020; 43:S1-S212. 31862741
  34. [41]Peairs KS Barone BB Snyder CF, et al Diabetes mellitus and breast cancer outcomes: a systematic review and meta-analysis. J Clin Oncol. 2011; 29: 40- 46. doi: 10.1200/JCO.2009.27.3011 21115865 PMC3055858 · DOI
  35. [42]Ribeiro RT Macedo MP Raposo JF. HbA1c, fructosamine, and glycated albumin in the detection of dysglycaemic conditions. Curr Diabetes Rev. 2016; 12: 14- 19. doi: 10.2174/1573399811666150701143112 26126638 · DOI
  36. [43]Shai I Schwarzfuchs D Henkin Y, et al Weight loss with a low-carbohydrate, Mediterranean, or low-fat diet. N Engl J Med. 2008; 359: 229- 241. doi: 10.1056/NEJMoa0708681 18635428 · DOI · Paper page
  37. [45]Nuttall FQ Almokayyad RM Gannon MC. Comparison of a carbohydrate-free diet vs. fasting on plasma glucose, insulin and glucagon in type 2 diabetes. Metabolism. 2015; 64: 253- 262. doi: 10.1016/j.metabol.2014.10.004 25458830 · DOI
  38. [46]Crouthamel MC Kahana JA Korenchuk S, et al Mechanism and management of AKT inhibitor-induced hyperglycemia. Clin Cancer Res. 2009; 15: 217- 225. doi: 10.1158/1078-0432.CCR-08-1253 19118049 · DOI
  39. [47]Zou Y Fineberg S Pearlman A Feinman RD Fine EJ. The effect of a ketogenic diet and synergy with rapamycin in a mouse model of breast cancer. PLoS One. 2020; 15:e0233662. doi: 10.0231371/journal.pone.0233662 PMC7714189 33270630 · DOI
  40. [48]Fine EJ Feinman RD. Insulin, carbohydrate restriction, metabolic syndrome and cancer. Expert Rev Endocrinol Metab. 2015; 10: 15- 24. doi: 10.1586/17446651.2014.960392 30289045 · DOI
  41. [49]Warburg O Wind F Negelein E. The metabolism of tumors in the body. J Gen Physiol. 1927; 8: 519- 530. doi: 10.1085/jgp.8.6.519 19872213 PMC2140820 · DOI · Paper page
  42. [50]Fine EJ Segal-Isaacson CJ Feinman RD, et al Targeting insulin inhibition as a metabolic therapy in advanced cancer: a pilot safety and feasibility dietary trial in 10 patients. Nutrition. 2012; 28: 1028- 1035. doi: 10.1016/j.nut.2012.05.001 22840388 · DOI
  43. [51]Xia S Lin R Jin L, et al Prevention of dietary-fat-fueled ketogenesis attenuates BRAF V600E tumor growth. Cell Metab. 2017; 25: 358- 373. doi: 10.1016/j.cmet.2016.12.010 28089569 PMC5299059 · DOI
  44. [52]Liśkiewicz AD Kasprowska D Wojakowska A, et al Long-term high fat ketogenic diet promotes renal tumor growth in a rat model of tuberous sclerosis. Sci Rep. 2016; 6: 21807. doi: 10.21038/srep21807 26892894 PMC4759602 · DOI
  45. [54]von Geijer L Ekelund M. Ketoacidosis associated with low-carbohydrate diet in a non-diabetic lactating woman: a case report. J Med Case Rep. 2015; 9: 224. 26428083 PMC4591635
  46. [55]Marzban S Arbee M Vorajee N Richards GA. Non-diabetic ketoacidosis associated with a low carbohydrate, high fat diet in a postpartum lactating female. Oxf Med Case Reports. 2020; 2020:omz026. PMC7416821 32793371
  47. [56]Westerberg DP. Diabetic ketoacidosis: evaluation and treatment. Am Fam Physician. 2013; 87: 337- 346. 23547550
  48. [57]Fayfman M Pasquel FJ Umpierrez GE. Management of hyperglycemic crises: diabetic ketoacidosis and hyperglycemic hyperosmolar state. Med Clin North Am. 2017; 101: 587- 606. 28372715 PMC6535398
  49. [59]Cartee GD. Mechanisms for greater insulin-stimulated glucose uptake in normal and insulin-resistant skeletal muscle after acute exercise. Am J Physiol Endocrinol Metab. 2015; 309:E949-E959. doi: 10.1152/ajpendo.00416.2015 PMC4816200 26487009 · DOI
  50. [61]Pfeiffer AF Klein HH. The treatment of type 2 diabetes. Dtsch Arztebl Int. 2014; 111: 69- 82. doi: 10.3238/arztebl.2014.0069 24612534 PMC3952010 · DOI
  51. [62]Bowman C Abramson V Wellons M. Ketoacidosis with canagliflozin prescribed for phosphoinositide 3-kinase inhibitor-induced hyperglycemia: a case report. J Investig Med High Impact Case Rep. 2017; 5: 2324709617725351. doi: 10.1177/2324709617725351 PMC5571767 28856166 · DOI
  52. [64]Torimoto K Okada Y Koikawa K Tanaka Y. Early effects of sodium-glucose co-transporter 2 inhibitors in type 2 diabetes: study based on continuous glucose monitoring. Diabetol Metab Syndr. 2017; 9: 60. 28785316 PMC5544992
  53. [65]Rendell M. Advances in diabetes for the millennium: drug therapy of type 2 diabetes. MedGenMed. 2004; 6: 9. PMC1474831 15647714
  54. [66]Hanefeld M. Cardiovascular benefits and safety profile of acarbose therapy in prediabetes and established type 2 diabetes. Cardiovasc Diabetol. 2007; 6: 20. 17697384 PMC2040135
  55. [67]Hinnen D. Glucagon-like peptide 1 receptor agonists for type 2 diabetes. Diabetes Spectr. 2017; 30: 202- 210. 28848315 PMC5556578
  56. [68]Pathak R Bridgeman MB. Dipeptidyl peptidase-4 (DPP-4) inhibitors in the management of diabetes. P T. 2010; 35: 509- 513. 20975810 PMC2957740
  57. [69]Klein-Schwartz W Stassinos GL Isbister GK. Treatment of sulfonylurea and insulin overdose. Br J Clin Pharmacol. 2016; 81: 496- 504. 26551662 PMC4767194
  58. [70]Luna B Feinglos MN. Oral agents in the management of type 2 diabetes mellitus. Am Fam Physician. 2001; 63: 1747- 1756. 11352285
  59. [71]Marín-Peñalver JJ Martín-Timón I Sevillano-Collantes C Del Cañizo-Gómez FJ. Update on the treatment of type 2 diabetes mellitus. World J Diabetes. 2016; 7: 354- 395. 27660695 PMC5027002
  60. [72]Basu R Chandramouli V Dicke B Landau B Rizza R. Obesity and type 2 diabetes impair insulin-induced suppression of glycogenolysis as well as gluconeogenesis. Diabetes. 2005; 54: 1942- 1948. doi: 10.2337/diabetes.54.7.1942 15983193 · DOI
  61. [73]Madiraju AK Erion DM Rahimi Y, et al Metformin suppresses gluconeogenesis by inhibiting mitochondrial glycerophosphate dehydrogenase. Nature. 2014; 510: 542- 546. doi: 10.1038/nature13270 24847880 PMC4074244 · DOI · Paper page
  62. [74]Yang X Xu Z Zhang C Cai Z Zhang J. Metformin, beyond an insulin sensitizer, targeting heart and pancreatic β cells. Biochim Biophys Acta Mol Basis Dis. 2017; 1863: 1984- 1990. doi: 10.1016/j.bbadis.2016.09.019 27702625 · DOI
  63. [75]Kawanami D Takashi Y Tanabe M. Significance of metformin use in diabetic kidney disease. Int J Mol Sci. 2020; 21: 4239. doi: 10.3390/ijms21124239 PMC7352798 32545901 · DOI
  64. [78]Unnikrishnan AG Kalra S Purandare V Vasnawala H. Genital infections with sodium glucose cotransporter-2 inhibitors: occurrence and management in patients with type 2 diabetes mellitus. Indian J Endocrinol Metab. 2018; 22: 837- 842. doi: 10.4103/ijem.IJEM_159_17 30766827 PMC6330876 · DOI
  65. [80]Danne T Garg S Peters AL, et al International consensus on risk management of diabetic ketoacidosis in patients with type 1 diabetes treated with sodium-glucose cotransporter (SGLT) inhibitors. Diabetes Care. 2019; 42: 1147- 1154. doi: 10.2337/dc18-2316 30728224 PMC6973545 · DOI · Paper page
  66. [82]Hwangbo Y Lee EK. Acute hyperglycemia associated with anti-cancer medication. Endocrinol Metabol. 2017; 32: 23- 29. doi: 10.3803/EnM.2017.32.1.23 PMC5368117 28345313 · DOI
  67. [83]Flory J Farooki A. Diabetes management in cancer patients. Oncology. 2016; 30: 565- 570. 27306711
  68. [84]Carrillo M Rodriguez RM Walsh CL Mcgarvey M. Alpelisib-induced diabetic ketoacidosis: a case report and review of literature. AACE Clin Case Rep. 2021; 7: 127- 131. 34095470 PMC8053625
  69. [85]Farah SJ Masri N Ghanem H Azar M. Diabetic ketoacidosis associated with alpelisib treatment of metastatic breast cancer. AACE Clin Case Rep. 2020; 6:e349-e351. PMC7685409 33244501

Cited by

Sorted by citations

Authors
Goncalves, M. D., & Farooki, A.
Affiliations
  • Weill Cornell Medicine (US)
  • Memorial Sloan Kettering Cancer Center (US)
Corresponding author
Goncalves, Marcus D.
ORCID
Venue
Integrative Cancer Therapies
Publisher
SAGE Publications
Published
2022-01
Volume
21
Pages
15347354211073163-15347354211073163
ISSN
  • 1534-7354 (ISSN-L)
  • 1552-695X
DOI
10.1177/15347354211073163
PMC
PMC8793384
OpenAlex
W4210528495
Cited by
37
References
8
Citations by year
2026: 14 · 2025: 9 · 2024: 10 · 2023: 4
FWCI
1.88
Type
journal article
Language
en
Open access
Licence
Locations
  • Integrative Cancer Therapies (publishedVersion, cc-by-nc)
  • PubMed Central (publishedVersion, cc-by-nc)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Funders
Novartis Pharmaceuticals Corporation
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › PI3K/AKT/mTOR signaling in cancer
  • Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Advanced Breast Cancer Therapies
Keywords
PI3K inhibitors, hyperglycemia, alpelisib, breast cancer, hyperglycemia management, insulin resistance, metformin, SGLT2 inhibitors, thiazolidinediones, alpha-glucosidase inhibitors, insulin therapy, risk factors, adverse drug reactions, glucose-lowering medications
MeSH terms
Phosphoinositide-3 Kinase Inhibitors, Breast Neoplasms, Female, Glucose, Humans, Hyperglycemia, Insulin, Phosphatidylinositol 3-Kinases

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review