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  1. IARC from recognized sources of information on carcinogenesis, including data storage and retrieval systems such as PubMed. Meeting participants who are asked to prepare preliminary working papers for specific sections are expected to supplement the IARC literature searches with their own searches. For most chemicals and some complex

    • Volume 102

      IARC from recognized sources of information on...

    • Volume 108

      Corrigenda to the . IARC Monographs – Volume 108 . Monograph...

  2. IARC from recognized sources of information on carcinogenesis, including data storage and retrieval systems such as PubMed. Meeting participants who are asked to prepare preliminary working papers for specific sections are expected to supplement the IARC literature searches with their own searches. For most chemicals and some complex

  3. Corrigenda to the IARC Monographs – Volumes 1–42 Volume Monograph Section Table/Figure Page Details of Corrigendum 36 Preamble – – 24 In Section (iv), paragraph 1, line 4, replace 00 and 00 with 15–16 and 19. 36 Acetaldehyde 4.3 Table 120 Replace Table with: Genetic activity Cell transformation DNA damage Mutation Chromosomal

  4. Corrigenda to the . IARC Monographs – Volume 108 . Monograph . Section Table/Figure Page Details of Corrigendum Monograph first posted online Correction made to

  5. Jun 28, 2018 · IARC Monographs on the Identification of Carcinogenic Hazards to Humans. Monographs Available. Supplements. Related Publications. IARC Monographs Newsletter.

  6. Sep 11, 2019 · In 2018, IARC convened an Advisory Group to Recommend an Update to the Preamble to the IARC Monographs, with broad expertise across multiple disciplines, to consider progress in the scientific understanding of factors contributing to carcinogenicity as well as in the development of methods for information gathering, evidence assessment, and ...

  7. Dec 1, 2023 · Read the IARC Monographs Q&A for answers to commonly asked questions on the evaluation process. Note: In September 2022, four additional individual Group 1 agents were created by splitting up some existing agent groupings because not all agents in the groups had the same cancer sites with sufficient and limited evidence for cancer in humans.

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