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This is the current revision of this page, as edited by Cewbot (talk | contribs) at 07:17, 20 October 2024 (Maintain {{WPBS}}: 3 WikiProject templates. The article is listed in the level 5 page: Biology.). The present address (URL) is a permanent link to this version.

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Speech Reception

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I see my edits concerning neutrality have been reverted. The stated objection:

This is undue, both in length and in contents. KOFWST asked him to apologise, so acting like the conference organisers were totally fine with his comments is disingenuous

Indeed, KOFWST after the media furore did ask Tim Hunt to apologise, feel free to add that as a result of the social media furore that was the case. However, the fact remains at the time, confirmed by the same anonymous EU official whose quotation is so vital, also confirmed that the speech was well received. They were in fact so pleased with the speech, they asked him to speak again later that evening.

The suggestion that because they later asked him to apologise after the social media frenzy doesn't change that and to remove it doesn't reflect a neutral tone. Nor does the text restored offer the full narrative of the social media outrage, because it wasn't just the speech as reported but the untrue embellishments as well. WCMemail 12:04, 25 March 2024 (UTC)[reply]

"Recording ‘shows Sir Tim was joking’, can't force editors to read sources, and "can't fix stupid", which is the best way to characterize content determined by conflict, ANI, and RfC. fiveby(zero) 15:44, 25 March 2024 (UTC)[reply]

I know this is OR; would someone with the right vocabulary please source it, because it is far more important than a speech ten years ago

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[1] needs to be translated into numbers of patients. And some assessment of impact of the other drugs and conditions involved. And this is just cancers.

Can we pllease stop talking about the speech now?

Thanx Elinruby (talk) 21:39, 11 April 2024 (UTC)[reply]

A little more science-y:

Prognostic importance of cyclin E1 expression in neuroblastic tumors in children. Authors: Taran K; Katarzyna Taran MD, PhD, Department of Pathology, Medical University of Lodz, Pomorska 251, 92-213 Lodz, Poland, e-mail: dr.taran.patho@gmail.com. Owecka A Kobos J Source: Polish journal of pathology : official journal of the Polish Society of Pathologists [Pol J Pathol] 2013 Jun; Vol. 64 (2), pp. 149-52. Publication Type: Journal Article; Research Support, Non-U.S. Gov't Language: English Journal Info: Publisher: Polish Society Of Pathologists Country of Publication: Poland NLM ID: 9437432 Publication Model: Print Cited Medium: Print ISSN: 1233-9687 (Print) Linking ISSN: 12339687 NLM ISO Abbreviation: Pol J Pathol Subsets: MEDLINE Imprint Name(s): Original Publication: Kraków : Polish Society Of Pathologists, 1994- MeSH Terms: Biomarkers, Tumor/*analysis Cyclin E/*biosynthesis Neuroblastoma/*metabolism Oncogene Proteins/*biosynthesis Child ; Child, Preschool ; Cyclin E/analysis ; Female ; Humans ; Immunohistochemistry ; Infant ; Infant, Newborn ; Male ; Neuroblastoma/mortality ; Neuroblastoma/pathology ; Oncogene Proteins/analysis ; Prognosis Abstract: A number of studies have indicated that cyclin E plays an important role in a variety of neoplastic processes. In our study we evaluated cyclin E1 expression and the possible prognostic value of this protein in neuroblastic tumors in children. Cyclin E1 expression was investigated by means of immunohistochemical analysis of 25 neuroblastic tumor tissue samples. We found a significant correlation between high cyclin E1 expression and deaths due to neoplastic disease. The mean values of cyclin E1 indexes in fatal cases were twice as high as in other cases. The results indicate that high cyclin E1 expression may have prognostic importance in neuroblastic tumors in children. Substance Nomenclature: 0 (Biomarkers, Tumor) 0 (CCNE1 protein, human) 0 (Cyclin E) 0 (Oncogene Proteins) Entry Date(s): Date Created: 20130801 Date Completed: 20131118 Latest Revision: 20191112 Update Code: 20240104 DOI: 10.5114/pjp.2013.36016 PMID: 23900874 Database: MEDLINE Complete


and

Are We Prepared for the CDK4/6 Revolution With HR+/HER2− Breast Cancers?: The Importance of Patient Adherence to Adjuvant Therapies. By: Azoz, Seyla, Peters, Martin, Jones, Graham, Breast Cancer: Basic & Clinical Research, 11782234, 11/28/2023 Database: CINAHL Complete


Cancers continue to represent a leading cause of death and major health care burden globally.[ 1] Thanks to enormous and sustained research efforts, many effective therapeutic solutions are now becoming available, including CAR-T, gene therapies, vaccines, and myriad chemotherapeutics.[ 2] In the case of breast cancer, one of the holy grails has been to identify small molecule chemotherapeutic and chemopreventive agents with high efficacy and ease of manufacture. Using precision medicine approaches and targeting the pathways governed by the cyclin-dependent kinase receptors, spectacular breakthroughs have recently been made through CDK4/6 inhibitors which promise to revolutionize prevention and treatment of HR+/HER2− breast cancers.[ 3] No less than 3 effective agents have been fast tracked through regulatory approval: Palbociclib, Abemaciclib, and Ribociclib, the latter being designated by the National Comprehensive Cancer Network (NCCN) as a category 1 preferred first-line treatment.[ 4] Such is the excitement that the entire class has been characterized as "game changing" for oncology patients.[ 5],[ 6] Such expectations however need to be tempered by one of the historical barriers to chemotherapeutics which, while well understood, remains a major obstacle—that of patient medication adherence.[ 7]


These are from Ebsco. I am wildly unqualified to write the explanation of the importance of his discovery, but I am absolutely positive that somebody did do that fifteen or so years ago. And cell growth is also involved in healing, isn't it? 21:54, 11 April 2024 (UTC)

one more

A pancancer analysis of the oncogenic role of cyclin B1 (CCNB1) in human tumors


A pancancer analysis of the oncogenic role of cyclin B1 (CCNB1) in human tumors. By: Dai, Peng, Xiong, Lecai, Wei, Yanhong, Wei, Xiaoyan, Zhou, Xuefeng, Zhao, Jinping, Tang, Hexiao, Scientific Reports, 20452322, 11/20/2023, Vol. 13, Issue 1 Database: Academic Search Complete

Aberrant levels of the G2/M cyclin cyclin B1 (gene CCNB1) have been associated with multiple cancers; however, the literature lacks a focused and comprehensive analysis of the regulation of this important regulator of cell proliferation in cancer. Through this work, we performed a pancancer analysis of the levels of CCNB1 and dissected aspects of regulation and how this correlates with cancer prognosis. We comprehensively evaluated the expression and promoter methylation of CCNB1 across 38 cancers based on RNA sequencing data obtained from the Cancer Genome Atlas (TCGA). The correlation of CCNB1 with prognosis and the tumor microenvironment was explored. Using lung adenocarcinoma data, we studied the potential upstream noncoding RNAs involved in the regulation of CCNB1 and validated the protein levels and prognostic value of CCNB1 for this disease site. CCNB1 was highly expressed, and promoter methylation was reduced in most cancers. Gene expression of CCNB1 correlated positively with poor prognosis of tumor patients, and these results were confirmed at the protein level using lung adenocarcinoma. CCNB1 expression was associated with the infiltration of T helper cells, and this further correlated with poor prognosis for certain cancers, including renal clear cell carcinoma and lung adenocarcinoma. Subsequently, we identified a specific upstream noncoding RNA contributing to CCNB1 overexpression in lung adenocarcinoma through correlation analysis, expression analysis and survival analysis. This study provides a comprehensive analysis of the expression and methylation status of CCNB1 across several forms of cancer and provides further insight into the mechanistic pathways regulating Cyclin B1 in the tumorigenesis process.


smdh

This is really confusingly formatted and I don't understand your point here. Cyclins are fundamental how the cell division of all non-bacteria life works, the fact that some people have found uses for targeting them to fight cancer is unsuprising but does not seem relevant to Hunt's biography unless he was specifically involved in the research. It would be like including mitochondrial replacement therapy on Albert von Kölliker's bio because he discovered the mitochondrion. Hemiauchenia (talk) 22:17, 11 April 2024 (UTC)[reply]
I grant you the formatting. But see, your analogy may be apt but it is lost on me. You can't have the car without the wheel. That is probably too expansive an analogy but you can't understand cyclin dependent kinases if you don't understand cyclins. Or can you? As you say the connection is unsurprising once you see it, but speaking as the non-scirntist in the conversation, "cell replication cycle" sounded important but abstract to me initially. Rather like the ozone layer or the big bang. Certainly did not say "healing" or "years of life extension for millions of cancer patients". And yes, I realize that that's the leap that is OR and that needs a journal cite. We just need something less specific than these. Or have I just eaten one too many rice cakes? I realize you have biology background so you tell me.Elinruby (talk) 22:44, 11 April 2024 (UTC)[reply]


revert of importance of cyclin

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I invite a rewrite if the excerpt is felt to be excessive. I feel the speech is rather excessive actually. But given a few specifics as to what exactly about cyclin is deemed off-topic to the bio of its discoverer, perhaps I can trim off, for example, the list of anti-cancer drugs that it made possible. Elinruby (talk) 00:59, 23 April 2024 (UTC)[reply]