Lina Happo

834 total citations
12 papers, 641 citations indexed

About

Lina Happo is a scholar working on Molecular Biology, Oncology and Cancer Research. According to data from OpenAlex, Lina Happo has authored 12 papers receiving a total of 641 indexed citations (citations by other indexed papers that have themselves been cited), including 8 papers in Molecular Biology, 7 papers in Oncology and 2 papers in Cancer Research. Recurrent topics in Lina Happo's work include Cell death mechanisms and regulation (6 papers), Cancer-related Molecular Pathways (5 papers) and Ubiquitin and proteasome pathways (3 papers). Lina Happo is often cited by papers focused on Cell death mechanisms and regulation (6 papers), Cancer-related Molecular Pathways (5 papers) and Ubiquitin and proteasome pathways (3 papers). Lina Happo collaborates with scholars based in Australia, United Kingdom and Netherlands. Lina Happo's co-authors include Andreas Strasser, Suzanne Cory, Clare L. Scott, Ewa M. Michalak, Mark S. Cragg, Gordon K. Smyth, Elisa S. Jansen, Jerry M. Adams, Lin Tai and Marco J. Herold and has published in prestigious journals such as Journal of Biological Chemistry, Nature Communications and Blood.

In The Last Decade

Lina Happo

12 papers receiving 639 citations

Peers

Lina Happo
Comparison fields: 5 of 89
  • Molecular Biology 410
  • Oncology 217
  • Immunology 135
  • Public Health, Environmental and Occupational Health 86
  • Cancer Research 62
Yanwen Zhou Japan
Gustavo Jacob Lourenço Brazil
Ugo Consoli United States
Man Jiang China
Anissa M. Jabbour Australia
Timothy S. Collins United States
Miriam Canavese United States
Rosane Gomes de Paula Queiróz Brazil
Karsten Stahnke Germany
G M Marshall Australia
Yanwen Zhou Japan View profile →
Citations per field, relative to Lina Happo
Lina Happo · 1×
Citations per year, relative to Lina Happo
Lina Happo · 1×

Countries citing papers authored by Lina Happo

Since Specialization
Citations

This map shows the geographic impact of Lina Happo's research. It shows the number of citations coming from papers published by authors working in each country. You can also color the map by specialization and compare the number of citations received by Lina Happo with the expected number of citations based on a country's size and research output (numbers larger than one mean the country cites Lina Happo more than expected).

Fields of papers citing papers by Lina Happo

Since Specialization
Physical SciencesHealth SciencesLife SciencesSocial Sciences

This network shows the impact of papers produced by Lina Happo. Nodes represent research fields, and links connect fields that are likely to share authors. Colored nodes show fields that tend to cite the papers produced by Lina Happo. The network helps show where Lina Happo may publish in the future.

Co-authorship network of co-authors of Lina Happo

This figure shows the co-authorship network connecting the top 25 collaborators of Lina Happo. A scholar is included among the top collaborators of Lina Happo based on the total number of citations received by their joint publications. Widths of edges represent the number of papers authors have co-authored together. Node borders signify the number of papers an author published with Lina Happo. Lina Happo is excluded from the visualization to improve readability, since they are connected to all nodes in the network.

All Works

12 of 12 papers shown
# Title Journal Authors Indexed citations
1 Prevalence and severity of dysmenorrhoea, and management options reported by young Australian women. PubMed Asvini K Subasinghe, Lina Happo et al. 64
2 Therapeutic Response to Non-genotoxic Activation of p53 by Nutlin3a Is Driven by PUMA-Mediated Apoptosis in Lymphoma Cells Cell Reports Liz J. Valente, Brandon J. Aubrey et al. 34
3 BCR-signaling-induced cell death demonstrates dependency on multiple BH3-only proteins in a murine model of B-cell lymphoma Cell Death and Differentiation Matthew Carter, Kerry L. Cox et al. 9
4 Mutually exclusive regulation of T cell survival by IL-7R and antigen receptor-induced signals Nature Communications Susanne Heinzel, Emma M. Carrington et al. 50
5 Caloric restriction modulates Mcl-1 expression and sensitizes lymphomas to BH3 mimetic in mice Blood Ophélie Meynet, Barbara Zunino et al. 43
6 Neither loss of Bik alone, nor combined loss of Bik and Noxa, accelerate murine lymphoma development or render lymphoma cells resistant to DNA damaging drugs Cell Death and Disease Lina Happo, Belinda Phipson et al. 9
7 Transforming Growth Factor-β Directly Induces p53-up-regulated Modulator of Apoptosis (PUMA) during the Rapid Induction of Apoptosis in Myc-driven B-cell Lymphomas Journal of Biological Chemistry Lindsay C. Spender, Matthew Carter et al. 29
8 Translation inhibitors induce cell death by multiple mechanisms and Mcl-1 reduction is only a minor contributor Cell Death and Disease Lisa Lindqvist, Ingela B. Vikstrom et al. 45
9 BH3-only proteins in apoptosis at a glance Journal of Cell Science Lina Happo, Andreas Strasser et al. 131
10 Pharmacological blockade of Bcl-2, Bcl-xL and Bcl-w by the BH3 mimetic ABT-737 has only minor impact on tumour development in p53-deficient mice Cell Death and Differentiation Stephanie Grabow, Paul Waring et al. 15
11 Maximal killing of lymphoma cells by DNA damage–inducing therapy requires not only the p53 targets Puma and Noxa, but also Bim Blood Lina Happo, Mark S. Cragg et al. 86
12 Puma and to a lesser extent Noxa are suppressors of Myc-induced lymphomagenesis Cell Death and Differentiation Ewa M. Michalak, Elisa S. Jansen et al. 126

Rankless uses publication and citation data sourced from OpenAlex, an open and comprehensive bibliographic database. While OpenAlex provides broad and valuable coverage of the global research landscape, it—like all bibliographic datasets—has inherent limitations. These include incomplete records, variations in author disambiguation, differences in journal indexing, and delays in data updates. As a result, some metrics and network relationships displayed in Rankless may not fully capture the entirety of a scholar's output or impact.

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