Evidence map›Paper›PMID 41824051›Full record

ReviewInnere Medizin (Heidelberg, Germany)2026

[New ways in interdisciplinarity: internal medicine meets human genetics : When frequent conditions become rare and rare conditions become frequent].

Lars Möller, Ann-Kathrin Schörding, Frank Kaiser, Markus Nöthen, Elisabeth Mack, Andreas Neubauer

Abstract readEnglish AbstractReview
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In one paragraph

Review in Innere Medizin (Heidelberg, Germany), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors.

Lars MöllerKlinik für Endokrinologie, Diabetologie und Stoffwechsel, Centrum für Endokrine Medizin, Universitätsklinikum Essen, Universität Duisburg-Essen, Hufelandstr. 55, 45147, Essen, Deutschland. lars.moeller@uk-essen.de.
Ann-Kathrin SchördingKlinik für Endokrinologie, Diabetologie und Stoffwechsel, Centrum für Endokrine Medizin, Universitätsklinikum Essen, Universität Duisburg-Essen, Hufelandstr. 55, 45147, Essen, Deutschland.
Frank KaiserInstitut für Humangenetik, Universitätsklinikum Essen, Zentrum für seltene Erkrankungen (ESZE) Essen, Essen, Deutschland.
Markus NöthenInstitut für Humangenetik, Universitätsklinikum Bonn, Bonn, Deutschland.
Elisabeth MackZentrum Innere Medizin m.S. Hämatologie, Onkologie und Immunologie, Universitätsklinikum Marburg, Baldingerstraße, 35043, Marburg, Deutschland.
Andreas NeubauerZentrum Innere Medizin m.S. Hämatologie, Onkologie und Immunologie, Universitätsklinikum Marburg, Baldingerstraße, 35043, Marburg, Deutschland.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Molecular findings have led to a deeper understanding of the pathophysiology of numerous diseases and now form the basis for targeted treatment. An example of this is chronic myeloid leukemia (CML). The identification of the BCR::ABL1 translocation enabled the development of specific tyrosine kinase inhibitors. While the median survival time used to be 4 years, CML is now often a chronic disease with a near-normal life expectancy thanks to targeted treatment; however, most tumor diseases are more complex at the molecular level. Advances in genome analysis enable increasingly more refined molecular characterization. Common tumor diseases are thus divided into increasingly smaller molecularly distinct segments, which become rarer as individual entities but can also be treated in a more targeted and individualized manner. The concept of personalized medicine is manifested in molecular tumor boards. A similar approach can start from rare genetic syndromes. In this case, understanding the underlying pathophysiology does not necessarily lead to a causal treatment of the syndrome itself but it does enable new treatment options for frequent diseases. An example is thyroid hormone resistance (RTH)β. Findings on the effect of thyroid hormone receptor β in the liver have contributed to the development of analogues that can now be used specifically to treat metabolic dysfunction-associated steatohepatitis (MASH) with fibrosis and can possibly also have the potential to reduce the progression of liver cirrhosis. Overall, close cooperation between human genetics and internal medicine can substantially contribute to an improvement in treatment success. A better understanding of molecular disease mechanisms enables an increasingly more precise, individualized and effective treatment.

Indexed as

Genetics, MedicalInterdisciplinary CommunicationInternal MedicinePrecision MedicineRare DiseasesHumansLeukemia, Myelogenous, Chronic, BCR-ABL PositiveChronic myeloid leukemiaMetabolic dysfunction-associated steatohepatitisMolecular tumor boardsPersonalized medicineThyroid hormone resistance β

Identifiers

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.