Evidence map›Paper›PMID 34873486›Full record

ArticleAmerican journal of cancer research2021

Branching clonal evolution patterns predominate mutational landscape in multiple myeloma.

Akanksha Farswan, Lingaraja Jena, Gurvinder Kaur, Anubha Gupta, Ritu Gupta, Lata Rani, Atul Sharma, Lalit Kumar

Open access · greenAbstract read
In one paragraph

Article in American journal of cancer research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.3field-weighted citation impact, top 18% of its field
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

14 citing papers in PubMed, 13 citations in OpenAlex.

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  5. B-cell-specificBlood neoplasia · 2025
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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

8 authors at 3 institutions in 1 country.

Akanksha FarswanSBILab, Department of Electronics and Communication Engineering, Indraprastha Institute of Information Technology-Delhi (IIIT-D) Delhi 110020, India.
Lingaraja JenaLaboratory Oncology Unit, Dr. B.R.A. IRCH, All India Institute of Medical Sciences (AIIMS) New Delhi 110029, India.
Gurvinder KaurLaboratory Oncology Unit, Dr. B.R.A. IRCH, All India Institute of Medical Sciences (AIIMS) New Delhi 110029, India.
Anubha GuptaSBILab, Department of Electronics and Communication Engineering, Indraprastha Institute of Information Technology-Delhi (IIIT-D) Delhi 110020, India.
Ritu GuptaLaboratory Oncology Unit, Dr. B.R.A. IRCH, All India Institute of Medical Sciences (AIIMS) New Delhi 110029, India.
Lata RaniLaboratory Oncology Unit, Dr. B.R.A. IRCH, All India Institute of Medical Sciences (AIIMS) New Delhi 110029, India.
Atul SharmaDepartment of Medical Oncology, Dr. B.R.A. IRCH, All India Institute of Medical Sciences (AIIMS) New Delhi 110029, India.
Lalit KumarDepartment of Medical Oncology, Dr. B.R.A. IRCH, All India Institute of Medical Sciences (AIIMS) New Delhi 110029, India.
DR. B.R.A. Institute Rotary Cancer Hospital · INAll India Institute of Medical Sciences · INIndraprastha Institute of Information Technology Delhi · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Multiple Myeloma (MM) arises from malignant transformation and deregulated proliferation of clonal plasma cells (PCs) harbouring heterogeneous molecular anomalies. The effect of evolving mutations on clone fitness and their cellular prevalence shapes the progressing myeloma genome and impacts clinical outcomes. Although clonal heterogeneity in MM is well established, which subclonal mutations emerge/persist/perish with progression in MM and which of these can be targeted therapeutically remains an open question. In line with this, we have sequenced pairwise whole exomes of 62 MM patients collected at two time points, i.e., at diagnosis and on progression. Somatic variants were called using a novel ensemble approach where a consensus was deduced from four variant callers (Illumina's Dragen, Strelka2, SomaticSniper and SpeedSeq) and actionable/druggable gene targets were identified. A marked intraclonal heterogeneity was observed. Branching evolution was observed among 72.58% patients, of whom 64.51% had low TMBs (<10) and 61.29% had 2 or more founder clones. The hypermutator patients (with high TMB levels ≥10 to ≤100) showed a significant decrease in their TMBs from diagnosis (median TMB 77.11) to progression (median TMB 31.22). A distinct temporal fall in subclonal driver mutations was identified recurrently across diagnosis to progression e.g., in

Indexed as

clonal evolutiondriver genesexome sequencingMultiple myelomamutationsNGSprogressiontumor mutation burden

Identifiers

PMID34873486
PMCPMC8640818
OpenAlexW4206850398

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.